Researchers find that combining novel gene-editing CRISPR technology with CAR T therapy could simplify and improve CAR T therapy in one fell swoop.

Traditional CAR T Therapy 

A remarkable feat in cancer care, today people with difficult-to-treat blood cancers can receive CAR T therapy, a personalized “drug” made from their own immune cells. Chimeric Antigen Receptor T cell (CAR T) therapy relies on extracting a patient’s immune cells and modifying them in the lab with a new, synthetic receptor.

The new receptor allows the white blood cell to target and destroy cancer cells once re-infused back in the bloodstream. Evoking the patched image of a mythical chimera, these receptors merge signaling machinery typical of a T cell with an antibody-derived detection region to create a powerful “living drug” which continually expands inside the body. Figure 1 highlights the basic design of a CAR T cell, while Figure 2 illustrates the step-by-step process in more depth.

Gene Editing with Viral Vectors 

To craft CAR T cells, the very genes of the T cells must be altered to express the chimeric antigen receptor. Gene editing, therefore, provides the foundation for the therapy.

Integrating CAR genes normally requires the use of a viral vector. Retroviruses in particular have the unique ability to insert and meld their own foreign genetic material into human cells permanently. This allows viruses to use host machinery to produce viral proteins.

Scientists have repurposed this strength to deliver CAR genes into T cells. An inactivated form of the virus is filled with genetic material which encodes for CAR. The desired genes are then transferred from the virus into the T cells through a process called transduction (see Figure 3). As if reading biological instructions, the T cell uses the genetic information to construct the receptor before expressing it onto the cell surface.

MORGAN AND BOYERINAS

The industry standard may depend on viral vectors, but the procedure lacks in some aspects. This stage of the CAR T process is the most time-consuming and expensive; it can take a year or longer to produce a batch of viral vectors, and can cost up to $50,000 per dose. For these reasons researchers now hope to turn to CRISPR technology, a recent scientific breakthrough in gene editing, to resolve these issues.

Enter CRISPR/Cas9 Gene Editing 

CRISPR originates from organisms such as bacteria and plays a major role in their defense. The acronym CRISPR stands for Clustered Regularly Interspaced Short Palindromic Repeats—in essence, they are short, repeating DNA sequences which read the same forwards or backwards, similarly to words such as “MADAM” or “DEED.” Sandwiched between these repeats are protospacers, a genetic history of viruses the bacteria encounters (see Figure 5).

When a virus tries to insert its genetic information into the bacteria, the bacteria can recognize the sequence from its protospacer catalog. The bacteria transcribes the protospacer DNA into RNA; this RNA guides enzymes such as Cas9 to the viral DNA to cut and deactivate it.

The same CRISPR/Cas9 interface can also snip human DNA. As seen in Figure 6, an RNA guide can be made to cut DNA at a specific site. The broken DNA, eager to repair itself, can easily adopt a new DNA sequence in that location.

Translating this concept to CAR T therapy, researchers could modify T cell DNA directly to express a new receptor. Synthesizing an RNA guide is cheaper and more efficient than cultivating retroviral vectors. If successful, CRISPR could simply solve two major drawbacks associated with CAR T therapy: price and time-to-delivery.

LABIOTECH

Conclusion 

CAR T therapy, although a triumph of human engineering in its own regard, still has room for improvement. There is potential to propel CAR T design forward by integrating contemporary innovations such as CRISPR/Cas9 technology. Although this method still requires T cell manipulation outside the body, this change could streamline the process while becoming more accessible. The most critical step now is to test the feasibility of this concept. The next installment in the series will explore the latest clinical results from PACT Pharma and the University of California, Los Angeles on their CRISPR/CAR T dual interface.

The post CRISPR Technology To Simplify And Enhance CAR T Cancer Treatment appeared first on Medika Life.

CAR T is an effective treatment for some hard to treat cancers. This “living drug” is made by extracting killer T cells from the body, manipulating them to target cancer cells, multiplying the newly engineered cells and infusing them back into the body. Development over the last forty years has evolved the precision, efficiency and safety of this technology. Arguably the best example is the treatment of  B cell cancers.

B cells to B cell cancers

CUSABIO Link Added

Figure 1 illustrates the development of antibody cells. B cell maturation begins with stem cells in the bone marrow and is completed with the antibody producing plasma B cells.

Typically, threats to the body leave trails of foreign antigen which can be followed. B cells detect these antigens and proliferate to eliminate pathogens, but these numbers quickly subside. This is done by design. The body regulates this process to ensure the bloodstream is not flooded with too many antibodies to prevent normal function. However, this system can go awry at any point. B cell precursors, intermediate cells or plasma cells can mutate and grow uncontrollably, causing damage to the body rather than shielding from it. When this happens, the immune system weakens and B cell cancers result.

LYMPHOMA CANADA

B cell lymphomas originate from the lymphatic system organs, vessels and tissues, such as the lymph nodes or the spleen. In contrast, leukemias circulate in the bone marrow and blood instead of the lymph organs. Although multiple myeloma is also a cancer of the bone marrow, it entails the abnormal growth of plasma B cells in particular.

Treating B cell cancers

Chemotherapy and radiation most successfully reduce the size and quantity of B cell tumors. Partial remission is very achievable, but complete remission—the total absence of cancer— is much more difficult to attain. For many, the cancer may temporarily recede for months or years after treatment before recurring. And when the cancer recurs, it can be resistant to treatment.

CAR T cell therapy addresses this problem by transforming patient immune cells into an anti-cancer drug. Cells are taken from the body and modified to detect the tumor cells. CAR T cells are fitted with a fusion protein (scFV, Figure 3) made from antigen-recognizing regions of antibodies. This component is typically engineered to target CD19, a B cell antigen known for its role in B cell signaling. This protein is found in B cells of all stages and is present on the surface of many B cell cancers. CD19 is not found on hematopoietic stem cells—those which have yet to mature and gain purpose; as a result, the therapy is less likely to target non-cancerous immune cells, an ideal quality in a therapeutic target.

FIGURE 3: CD19 is an antigen expressed on cancer cells. CAR T cells are fitted with an antigen recognition domain, a single chain variable fragment (scFV), to target the CD19 on the surface of these cancer cells. Once the antigen domain binds to the cancer cell, the CAR T cell can induce apoptosis to eliminate the tumor cell.

BRITTEN, OLIVER, ET AL. 2019 Link Added

Once the CAR T cell binds to CD19 on the tumor cell, several signals are released from the endodomain that trigger cell death of the tumor cell through apoptosis. The co-stimulatory molecules found in the interior of the CAR T cell allow it to multiply and persist in the body.

Normal T cells from the body lack the precision of this antigen recognizing protein and usually require specific proteins—major histocompatibility complexes—to present the antigen and facilitate similar binding. CAR T cells forgo these steps, producing superior hybrid molecules which combine antibody detection with T cell signal transduction. This synthetic engineering defines the chimeric nature of Chimeric Antigen Receptor T cells.

Why CAR T therapy?

As of publication, CAR T is only considered after standard cancer treatments have run their course. Why, then, do people turn to CAR T therapy if it is only considered after several other lines of treatment?

For those who have B cancers which are unresponsive to alternative anti-cancer treatments, CAR T can deliver lasting remission and extend life expectancy by several years—sometimes without additional treatment.

NOVARTIS

For example, one study revealed that 44% of young patients with acute lymphoblastic leukemia (ALL) live at least five years without relapse after CAR T therapy. This is especially remarkable given how difficult it can be to treat the condition and the less than 10% five-year survival rate. Approved CAR T therapies also exist for patients with diffuse large B cell lymphoma (DLCL), follicular lymphoma, mantle cell lymphoma and multiple myeloma.

ACCELERATING CANCER IMMUNOTHERAPY RESEARCH

There is a caveat—it is possible to experience relapse after CAR T therapy. One contributing factor is CD19 antigen escape, a type of CAR T resistance. As illustrated in Figure 5, patients with antigen escape develop cancer cells which no longer express CD19 and thus escape recognition by CAR T cells. So while CD19 targeting has proven effective, this phenomena highlights the need to find alternative antigen targets to improve the drug’s efficiency.

One possible solution is dual targeting CAR T cells. By engineering T cells which detect more than one antigen on cancer cells, the therapy has a greater chance of attacking tumor-only cells and overcoming antigen escape. Current contenders include dual targeting of antigens CD19 and CD22, as well as CD19 and CD20.

Summary 

CAR T shines best in solving what other therapies cannot. When other lines of cancer treatments such as chemotherapy or radiation cause relapse, CAR T therapy often provides a more lasting remission. There’s promise for these engineered T cells to become even more effective in the future with the advent of dual-targeting CAR T cells. And while none of the six FDA approved CAR T therapies are currently used as first-line treatment, developments are underway to establish this innovative technology as a primary line of defense. This is a major step forward for treating B cell cancers, and we can anticipate more to come.

The post The Remarkable Research Of CAR T Therapy: B Cell Cancers appeared first on Medika Life.

Do I think that the research is good enough to have our patients adopt the practice of a fasting-mimicking diet? No, the study does not conclude that such an approach to nutrition has antitumor effects. Let’s look at the study’s merits.

The study authors begin with this observation: In mice with cancer, cyclic fasting or fasting-mimicking diets (FMDs) enhance the activity of anti-cancer treatments by changing systemic metabolism and boosting anti-cancer immunity.

But what about humans? Can a similar dietary approach yield similar effects? To find out, researchers examined 101 patients undergoing treatment for either breast cancer or melanoma. They asked the study participants to do this:

Consume 1800 kilocalories in five days (more specifically, 600 on the first day and up to 300 kilocalories for the remaining four days). The subjects repeated the cycle every three to four weeks. The patients had no diet restrictions in-between cycles, but the investigators recommended a healthy diet and lifestyle.

Here are the results of an interim analysis of the ongoing DIgesT trial, testing a 5-day fasting-mimicking cycle seven to ten days before surgery.

First, dietary interventions (such as fasting) are often challenging for patients to follow. Not for this study: 92 percent complied with the diet approach.

The patients successfully modified both body and within-tumor metabolism and immune response with compliance high.

The average blood sugar concentrations dropped by 19 percent, and insulin levels dropped by 51 percent. Serum insulin-like growth factor-1 levels went down by 30 percent. These changes held over several dietary cycles.

I was concerned about body weight, but the weight loss appeared reversible during the healthy-eating periods between fasting cycles.

That’s a brief overview of this very recent study. It is only in abstract form, but I wanted to share it with you now. I love that the fasting-mimicking diet had a broad and favorable effect on immune system function. The diet approach led to many anti-cancer programs in the cancer cells.

I have recently been thinking more about out-of-the-box approaches for my patients at high risk for cancer-related recurrence or death. I am especially interested in approaches that modulate insulin-like growth factor-1 (IGF-1).

In summary, the new study reveals that a fasting-mimicking diet is associated with a significant rise in tumor-infiltrating CD8-positive T cells. This diet leads to an anti-cancer immune microenvironment at cancer cell and systemic levels.

Let’s close with the words of research team member Licia Rivoltini, MD, head of the immunotherapy of human tumors unit at the National Cancer Institute in Milan:

“Severe calorie restriction generated a metabolic shock that activated several populations of immune cells that could boost the antitumor activity of standard antineoplastic treatments.”

I look forward to seeing results from new clinical research, including the BREAKFAST trial. This experiment is the next step in understanding the anti-cancer effects caused by calorie restriction.

Oh, I cannot resist this shot of me in fabulous Milan:

Thank you for joining me today. I hope you have a joy-filled next year.

The post Fasting May Fight Cancer appeared first on Medika Life.

Here are the numbers — Among patients found to have breast, colorectal, or prostate cancer:

• 40 percent reported dietary supplement use
• 19 percent believed dietary supplements could reduce cancer recurrence risk

Researchers recently reported these findings in the journal Cancer.

There appeared to be differences in supplement use by subgroups. Females appeared nearly 2.5-times more likely to take supplements. Perhaps not surprisingly, a belief in the importance of supplements to reduce cancer recurrence risk led to a 3.1-times higher chance of supplement use. Obese individuals were nearly half as likely to use dietary supplements.

What are the most common supplements? Thirteen percent reported fish oil use, while 9 percent used calcium (with or without vitamin D). Over eight percent consumed multivitamins and minerals. For those with breast cancer, 15 percent used calcium (with or without vitamin D).

Do supplements improve cancer outcomes?

Study author Rana E. Conway, BSc (Hons), Ph.D., RNutr, research fellow in the obesity group at the research department of behavioral science and health at University College London, offers this:

“There is no evidence that self-prescribed supplements reduce the risks of cancer coming back, and they could interfere with treatment.”

There is good evidence that a healthy diet and physical activity are beneficial; supplements appear to be an easier option, but we don’t have evidence that they prevent cancer from coming back.

On the other hand, mixing supplements with chemotherapy comes with peril. While common, such supplement use can lead to serious potential medication interactions. A 2021 study demonstrates this problem.

Prescription medications are most often associated with drug interactions, followed by herb and supplement-related interactions. Over one-third of potential medication interactions are considered significant.

Moreover, supplements may lead to poorer outcomes for those receiving chemotherapy for cancer. In a study of patients with breast cancer, patients who took vitamin B12 before and during chemotherapy had poorer disease-free and overall survival odds.

Iron consumption before and during chemotherapy appeared associated with a higher probability of a return of cancer. On the other hand, multivitamin use did not seem linked to changes in survival.

Certain antioxidants may help you fight cancer (or provide protection for your normal cells). However, we know that some supplements may make cancer treatment less successful. If you have cancer management, please ensure that your care team knows about any supplements you are taking.

Do supplements improve life length?

Moving beyond the realm of cancer, do supplements improve mortality? Do we live longer if we add this form of nutrients into our diets? While adequate intake of specific nutrients derived from food appears associated with lower all-cause mortality, nutrients derived from supplements are not helpful.

When Fang Fang Zhang, MD, Ph.D. (of Tufts University) evaluated data from the 1999 to 2010 National Health and Nutrition Examination Survey (NHANES) and National Death Index to determine how dietary supplement use and levels of nutrient intake from foods affect all-cause, cardiovascular disease, and cancer mortality among adults in the U.S. aged 20 years or older, she discovered:

• There appeared to be no association between the ever-use of dietary supplements and mortality outcomes.
• Participants with adequate vitamin A, vitamin K, magnesium, zinc, and copper via foods, not supplements, had lower all-cause and cardiovascular disease mortality rates.

Dr. Zhang offers this: “The general U.S. population should aim for achieving adequate nutrition through a healthy and balanced diet rather than counting on dietary supplements.

She adds: “For certain subgroups such as individuals with medical conditions that lead to malabsorption of nutrients from foods or those who have specific dietary practices that could cause nutritional deficiency, their nutritional needs including the use of dietary supplements shall be evaluated separately.”

These findings remind us that we health care professionals should review the use of dietary supplements with our patients. Thank you for joining me today.

The post Got Cancer? Supplements May Be Dangerous appeared first on Medika Life.

More than 30 preeminent experts to present virtually; vast degree of structural disease change, high speed of cancer evolution, rarely considered until now

Date of Release:  Sept. 21, 2020

BOSTON, /PRNewswire/ — Evolutionary processes have made cancer supremely difficult to treat and cure – but evolutionary thinking could hold the fundamental keys to stopping cancer in its tracks. 

That premise, rapidly gaining momentum with outside-the-box cancer trailblazers, is the thrust behind a global “Cancer & Evolution Symposium,” held virtually October 14, 15 and 16.  

More than 30 leading scientific researchers, oncologists, and biopharma experts will participate as speakers and panelists from 8:30 am to 2 pm ET each day.

“We are not winning the war on advanced-stage cancers, when therapy resistance and disease spread often emerge suddenly,” said Frank H. Laukien, a lead organizer of the conference.  “The fact that tumors are constantly, rapidly transforming their genetic makeup is one reason late-stage cancers are difficult to cure.  This has spurred thoughtful leaders to take an evolutionary approach to tackling cancer.”

“We have yet to adequately capture the evolutionary capacity of cancer cells,” said Professor Henry Heng, Wayne State University. “Advanced stages of disease can be different from initial stages.  This massive genome reorganization produces treatment-resistant and more ‘fit’ species of cancer cells in just weeks.  We need adaptive therapies to combat this evolution process.” 

The symposium and marriage between evolution and cancer is expected to mark an inflection point for physicians and patients, addressing difficult but important issues:

• Does the standard “maximum tolerable dose” of one single therapy, despite initial benefits, cause the disease to make a rapid evolutionary transition that inevitably does more long-term harm to patients, as resistance evolves?
• Does the present treatment paradigm of not following up with secondary or tertiary therapies until after tumors reemerge demand reconsideration to extend more lives?
• What are the critical biomarkers for screening to identify tumors before they have evolved beyond treatable stages?
• Does this deeper understanding of these major evolutionary transitions in cancer offer new molecular targets for treatment? 

Registration is $250 for corporate participants; $95 for government, nonprofit or academic research; $25 for students, post-docs or retired/emeritus individuals.  A detailed agenda can be found at the conference website www.cancerevolution.org.  Press may contact diane.ferrucci@brucker.com for free access. 

“Beating cancer means understanding how it evolves, especially in response to treatments,” said University of Chicago’s James Shapiro.  “If you hammer someone’s advancing cancer, you may eliminate 99% of the cells but the stressed 1% that survive shift into a rapid evolution mode and produce a tumor population resistant to your therapy.  Knowing how this tumor evolution happens is key to preventing it.”

The 2020 Cancer & Evolution Symposium is organized by a committee including:  Frank H. Laukien, Ph.D., Chairman and CEO of Bruker Corporation; James A. Shapiro, University of Chicago, Biochemistry and Molecular Biology; Henry H. Heng, Center for Molecular Medicine and Genetics, Wayne State University; Denis Noble, Oxford University Physiology, Anatomy and Genetics; and Perry Marshall, Founder, $10 M Evolution 2.0 Prize.  Notable participants include Veracyte CEO Bonnie Anderson; Anna Barker, Chief Strategy Officer, USC Institute for Transformative Medicine; Steven Carr, Broad Institute of Harvard and MIT; George Church, Genetics, Harvard and MIT; and Azra Raza, M.D. Columbia University and Author, The First Cell:  And the Human Costs of Pursuing Cancer to the Last.  More information is www.cancerevolution.org.

SOURCE Natural Code LLC

Related Links

evo2.org

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If your only takeaway from this article is the following, the it has served its purpose.

Chemo is not a cure for cancer. It is not a magic bullet that can be used to rid your body of cancer. Do not rely on it for that purpose, Chemo is simply a tool in the fight against cancer, a treatment that is occasionally met with some success.

Worth noting is that this article relates only to chemo in terms of cancer treatment and not antimicrobial chemotherapy.

This article is over 25 minutes long and if there are certain sections that are not of interest, the list below will help you navigate the article.

Article Contents

1. The origins of Chemotherapy

Not unsurprisingly perhaps, this treatment traces it’s routes back to World War I and the German introduction of chemical warfare. Among the chemical agents used, mustard gas was particularly devastating. Although banned by the Geneva Protocol in 1925, the advent of World War II caused concerns over the possible re-introduction of chemical warfare. Such concerns led to the discovery of nitrogen mustard, a chemical warfare agent, as an effective treatment for cancer.

Two pharmacologists from the Yale School of Medicine, Louis S. Goodman and Alfred Gilman, were recruited by the US Department of Defense to investigate the potential therapeutic applications of chemical warfare agents.

(Authors note — there is so much wrong with the sentence above that reading it now raises a smile. It is, however, the official explanation given by the DOD and we’ll leave it there)

Goodman and Gilman observed that mustard gas was too volatile and they subsequently developed a more stable compound called nitrogen mustard. A year into the start of their research, a German air raid in Bari, Italy led to the exposure of more than 1000 people to the SS John Harvey’s* secret cargo of mustard gas bombs.

• read the unlikely story behind the SS John Harvey in the footer

Dr. Stewart Francis Alexander, a lieutenant colonel who was an expert in chemical warfare, was subsequently deployed to investigate the aftermath. Autopsies of the victims suggested that profound lymphoid and myeloid suppression had occurred after exposure. In his report, Dr. Alexander theorized that since mustard gas all but ceased the division of certain types of somatic cells whose nature is to divide rapidly, it could also potentially be put to use in helping to suppress the division of certain types of cancerous cells.

Goodman and Gilman reasoned that this agent could be used to treat lymphoma, a tumor of lymphoid cells. In collaboration with a thoracic surgeon, Gustaf Lindskog, they injected a related agent, mustine (the prototype nitrogen mustard anticancer chemotherapeutic), into a patient with non-Hodgkin’s lymphoma. A dramatic reduction in the patient’s tumor masses were observed but the effect lasted only a few weeks, and the patient had to return for another set of treatment, This was, in effect the first step to the realization that cancer could be treated by pharmacological agents.

Publication of the first clinical trials was reported in 1946 in the New York Times and chemotherapy was born.

2. How does chemo work?

Chemotherapy is considered a systemic therapy as drugs are introduced into the blood stream and are therefore, in principle, able to address cancer at any anatomic location in the body. Systemic therapy is often used in conjunction with other local therapies (i.e. treatments whose efficacy is confined to the anatomic area where they are applied) for cancer such as radiation therapy, surgery or hyperthermia therapy.

Traditional chemotherapeutic agents are cytotoxic — i.e. they are toxic to our cells, effectively a poison, a natural equivalent would be snake venom which can destroy human cells — and this is they reason they are able to destroy cancer cells. However, we remain unable to fashion traditional agents to specifically target and attack only cancerous cells. Chemotherapeutic agents also destroy healthy cells and therein lies the quandary.

Scientifically we would describe chemotherapy as connoting non-specific usage of intracellular poisons to inhibit mitosis (cell division) or induce DNA damage, which is why inhibition of DNA repair can augment chemotherapy

Chemotherapy can, in its simplest form, be thought of as a way to damage or stress cells, which may then lead to cell death if apoptosis is initiated. Many of the side effects of chemotherapy can be traced to the damage of normal cells that divide rapidly and are therefor, as with cancerous cells, sensitive to anti-mitotic drugs: cells in the bone marrow, digestive tract and hair follicles.

This results in the more common side-effects of chemotherapy:

• myelosuppression (decreased production of blood cells, resulting in immunosuppression)
• mucositis (inflammation of the lining of the digestive tract)
• and alopecia (hair loss).

3. Understanding treatment protocols

Chemotherapeutics are used in two settings, curative or palliative. The first is self-explanatory, the second, palliative, relates to treatments designed to extend life expectancy, management rather than cure of the disease in question. It is a last ditch effort to buy a patient that “extra over” at the end of their innings. Sadly, the quality of this extra time is often compromised by the side effects of chemo and the real world implications of opting for late-stage palliative chemotherapy are often not adequately discussed with the recipient or family.

Combinations of drugs are used in treatment as these have proven more effective in combatting cancers. Cancerous cells have proven themselves immensely adaptive and able to deflect, adapt to and overcome the efforts of a single chemotherapeutical to destroy them, so doctors opt for combinations, determined by the type of cancer in question. There is now a growing debate in the medical community over how aggressive treatment protocols may serve to encourage cancers to metastasize.

If you’ve or a family member has been exposed to or will undergo chemo, you will hear the following terms;

• Induction chemotherapy: The first line treatment of cancer with a chemotherapeutic drug. This type of chemotherapy is used for curative intent.
• Combined modality chemotherapy: The use of drugs with other cancer treatments, such as surgery, radiation therapy, or hyperthermia therapy.
• Consolidation chemotherapy: Given after remission in order to prolong the overall disease-free time and improve overall survival. The drug that is administered is the same as the drug that achieved remission.
• Intensification chemotherapy: Identical to consolidation chemotherapy but a different drug than the induction chemotherapy is used.
• Combination chemotherapy: Thisinvolves treating a person with a number of different drugs simultaneously. The drugs differ in their mechanism and side-effects. The biggest advantage is minimizing the chances o;f resistance developing to any one agent. Also, the drugs can often be used at lower doses, reducing toxicity.
• Neoadjuvant chemotherapy: This is given prior to a local treatment such as surgery, and is designed to shrink the primary tumor. It is also given for cancers with a high risk of micrometastatic disease.
• Adjuvant chemotherapy: Given after a local treatment (radiotherapy or surgery). It can be used when there is little evidence of cancer present, but there is risk of recurrence. It is also useful in killing any cancerous cells that have spread to other parts of the body. These micrometastases can be treated with adjuvant chemotherapy and can reduce relapse rates caused by these disseminated cells.
• Maintenance chemotherapy: A repeated low-dose treatment to prolong remission.
• Salvage chemotherapy: Palliative chemotherapy is given without curative intent, but simply to decrease tumor load and increase life expectancy. For these regimens, in general, a better toxicity profile is expected.

4. Types of Chemotherapeutics

This section if included for the more technically mined. Page down to carry on reading issues relating to dosing and the side effects of chemotherapy.

Alkylating agents

Alkylating agents are the oldest group of chemotherapeutics in use today. Originally derived from mustard gas used in World War I, there are now many types of alkylating agents in use. They are so named because of their ability to alkylate many molecules, including proteins, RNA and DNA. This ability to bind covalently to DNA via their alkyl group is the primary cause for their anti-cancer effects. Read more…

Antimetabolites

Anti-metabolites are a group of molecules that impede DNA and RNA synthesis. Many of them have a similar structure to the building blocks of DNA and RNA. These drugs exert their effect by either blocking the enzymes required for DNA synthesis or becoming incorporated into DNA or RNA. By inhibiting the enzymes involved in DNA synthesis, they prevent mitosis because the DNA cannot duplicate itself. Read more…

Anti-microtubule agents

Anti-microtubule agents are plant-derived chemicals that block cell division by preventing microtubule function. Microtubules are an important cellular structure composed of two proteins, α-tubulin and β-tubulin. They are hollow, rod-shaped structures that are required for cell division, among other cellular functions. Read more…

Topoisomerase inhibitors

Topoisomerase inhibitors are drugs that affect the activity of two enzymes: topoisomerase I and topoisomerase II. When the DNA double-strand helix is unwound, during DNA replication or transcription, for example, the adjacent unopened DNA winds tighter (supercoils), like opening the middle of a twisted rope. The stress caused by this effect is in part aided by the topoisomerase enzymes. Read more…

Cytotoxic antibiotics

The cytotoxic antibiotics are a varied group of drugs that have various mechanisms of action. The common theme that they share in their chemotherapy indication is that they interrupt cell division. The most important subgroup is the anthracyclines and the bleomycins; other prominent examples include mitomycin C and actinomycin. Read more…

5. Dosages and outdated systems

Chemotherapeutical dosage strengths are critical to ensure optimal treatment. Too little and the cancer will continue to grow, to much and the treatment can kill the patient.. It’s a delicate balance and strengths of dosage are determined by an archaic system that ignores various factors, considering only the height and weight of the patient. It is called the BSA or body surface area. The BSA is usually calculated with a mathematical formula or a nomogram, using the recipient’s weight and height, rather than by direct measurement of body area.

The BSA formula was originally developed in a 1916 study and attempted to translate medicinal doses established with laboratory animals to equivalent doses for humans and only included nine human subjects. When chemotherapy was introduced in the 1950s, the BSA formula was adopted as the official standard for chemotherapy dosing for lack of a better option.

Drug absorption and clearance are influenced by multiple factors, including age, sex, metabolism, disease state, organ function, drug-to-drug interactions, genetics, and obesity, which have major impacts on the actual concentration of the drug in the person’s bloodstream. There is high variability in the systemic chemotherapy drug concentration in people dosed by BSA, and this variability has been demonstrated to be more than ten-fold for many drugs

To explain this properly, in two individuals of identical body weight given identical dosages using BSA, concentrations of the drug can be up to ten times higher in one individual than the other. Both patients are at risk, one from under dosage and the other from the potential of being fatally poisoned. Clearly, BSA is not fit for purpose.

In a randomized clinical trial, investigators found 85% of metastatic colorectal cancer patients treated with 5-fluorouracil (5-FU) did not receive the optimal therapeutic dose when dosed by the BSA standard — 68% were under dosed and 17% were overdosed. The problem is exacerbated by rising rates of obesity. We need to do far better to ensure optimal treatment.

Several clinical studies have demonstrated that when chemotherapy dosing is individualized to achieve optimal systemic drug exposure, treatment outcomes are improved and toxic side effects are reduced. In the 5-FU clinical study cited above, people whose dose was adjusted to achieve a pre-determined target exposure realized an 84% improvement in treatment response rate and a six-month improvement in overall survival (OS) compared with those dosed by BSA.

6. The Side Effects of Chemo

Chemotherapeutic techniques have a broad range of well documented side-effects. These side-effects depend largely on the type of medications used in treatment. The most common medications affect mainly the fast-dividing cells of the body, such as blood cells and the cells lining the mouth, stomach, and intestines. Toxicities can occur acutely after administration, within hours or days, or chronically, from weeks to years. As discussed above, correct dosage strengths for treatments are perhaps the best tool to prevent or reduce these side effects.

Immunosuppression and myelosuppression

Virtually all chemotherapeutic regimens can cause depression of the immune system, often by paralysing the bone marrow and leading to a decrease of white blood cells, red blood cells, and platelets. Anemia and thrombocytopenia may require blood transfusion.

In very severe myelosuppression, which occurs in some regimens, almost all the bone marrow stem cells (cells that produce white and red blood cells) are destroyed, meaning allogenic or autologous bone marrow cell transplants are necessary. In some instances treatment has to be halted as immune suppression poses serious risk to the patients life.

Although people receiving chemotherapy are encouraged to wash their hands, avoid sick people, and take other infection-reducing steps, about 85% of infections are due to naturally occurring microorganisms in the person’s own gastrointestinal tract (including the mouth) and skin. The risk of illness and death can be reduced by taking common antibiotics such as quinolones or trimethoprim/sulfamethoxazole before any fever or sign of infection appears. Quinolones show effective prophylaxis mainly with hematological cancer.

In Japan, the government has approved the use of some medicinal mushrooms like Trametes versicolor, to counteract depression of the immune system in people undergoing chemotherapy.

Neutropenic enterocolitis

Due to immune system suppression, neutropenic enterocolitis (typhlitis) is a “life-threatening gastrointestinal complication of chemotherapy”. Typhlitis is an intestinal infection which may manifest itself through symptoms including nausea, vomiting, diarrhea, a distended abdomen, fever, chills, or abdominal pain and tenderness. Typhlitis is a medical emergency. It has a very poor prognosis and is often fatal unless promptly recognized and aggressively treated.

Gastrointestinal distress

Nausea, vomiting, anorexia, diarrhoea, abdominal cramps, and constipation are common side-effects of chemotherapeutic medications that kill fast-dividing cells. Malnutrition and dehydration can result when the recipient does not eat or drink enough, or when the person vomits frequently, because of gastrointestinal damage. This can result in rapid weight loss, or occasionally in weight gain, if the person eats too much in an effort to allay nausea or heartburn. Weight gain can also be caused by some steroid medications. These side-effects can frequently be reduced or eliminated with antiemetic drugs.

Anemia

Anemia can be a combined outcome caused by myelosuppressive chemotherapy, and possible cancer-related causes such as bleeding, blood cell destruction (hemolysis), hereditary disease, kidney dysfunction, nutritional deficiencies or anemia of chronic disease. Treatments to mitigate anemia include hormones to boost blood production (erythropoietin), iron supplements, and blood transfusions.

Nausea and vomiting

Nausea and vomiting are two of the most known and feared cancer treatment-related side-effects. In 1983, Coates et al. found that people receiving chemotherapy ranked nausea and vomiting as the first and second most severe side-effects, respectively. Up to 20% of people receiving highly emetogenic agents in this era postponed, or even refused, potentially curative treatments.

Chemotherapy-induced nausea and vomiting (CINV) are common with many treatments and some forms of cancer. Since the 1990s, several novel classes of antiemetics have been developed and commercialized, becoming a nearly universal standard in chemotherapy regimens, and helping to successfully manage these symptoms in many people. Ensuring accurate levels of dosage also greatly reduce these side-effects. Read more…

Hair loss

Hair loss (alopecia) can be caused by chemotherapy that kills rapidly dividing cells; other medications may cause hair to thin. These are most often temporary effects: hair usually starts to regrow a few weeks after the last treatment, but sometimes with a change in color, texture, thickness or style. Sometimes hair has a tendency to curl after regrowth, resulting in “chemo curls.” Severe hair loss occurs most often with drugs such as doxorubicin, daunorubicin, paclitaxel, docetaxel, cyclophosphamide, ifosfamide and etoposide. Permanent thinning or hair loss can result from some standard chemotherapy regimens.

Secondary neoplasm

Development of secondary neoplasia after successful chemotherapy or radiotherapy treatment can occur. The most common secondary neoplasm is secondary acute myeloid leukemia, which develops primarily after treatment with alkylating agents or topoisomerase inhibitors. Survivors of childhood cancer are more than 13 times as likely to get a secondary neoplasm during the 30 years after treatment than the general population, however not all of this increase can be attributed to chemotherapy.

Infertility

Some types of chemotherapy are gonadotoxic and may cause infertility. Chemotherapies with high risk include procarbazine and other alkylating drugs such as cyclophosphamide, ifosfamide, busulfan, melphalan, chlorambucil, and chlormethine. Drugs with medium risk include doxorubicin and platinum analogs such as cisplatin and carboplatin.

Female infertility by chemotherapy appears to be secondary to premature ovarian failure by loss of primordial follicles. This loss is not necessarily a direct effect of the chemotherapeutic agents, but could be due to an increased rate of growth initiation to replace damaged developing follicles. People can choose between several methods of fertility preservation prior to chemo, including cryopreservation of semen, ovarian tissue, oocytes, or embryos.

Teratogenicity

Chemotherapy is teratogenic ( an agent that can disturb the development of the embryo or fetus) during pregnancy, especially during the first trimester, to the extent that abortion usually is recommended if pregnancy in this period is found during chemotherapy. Second- and third-trimester exposure does not usually increase the teratogenic risk and adverse effects on cognitive development, but it may increase the risk of various complications of pregnancy and fetal myelosuppression.

In males previously having undergone chemotherapy or radiotherapy, there appears to be no increase in genetic defects or congenital malformations in their children conceived after therapy. In females previously having undergone chemotherapy, miscarriage and congenital malformations are not increased in subsequent conceptions. However, when in vitro fertilization and embryo cryopreservation is practised between or shortly after treatment, possible genetic risks to the growing oocytes exist, and it is recommended that the babies be screened.

Peripheral neuropathy

Between 30 and 40 percent of people undergoing chemotherapy experience chemotherapy-induced peripheral neuropathy (CIPN), a progressive, enduring, and often irreversible condition, causing pain, tingling, numbness and sensitivity to cold, beginning in the hands and feet and sometimes progressing to the arms and legs. Read more…

Cognitive impairment

Some people receiving chemotherapy report fatigue or non-specific neurocognitive problems, such as an inability to concentrate; this is sometimes called post-chemotherapy cognitive impairment, referred to as “chemo brain” in popular and social media.

Tumor lysis syndrome

Large tumors and cancers with high white cell counts, such as lymphomas, teratomas, and some leukemias, can lead to some people develop tumor lysis syndrome. The rapid breakdown of cancer cells causes the release of chemicals from the inside of the cells. Following this, high levels of uric acid, potassium and phosphate are found in the blood. High levels of phosphate induce secondary hypoparathyroidism, resulting in low levels of calcium in the blood. This causes kidney damage and the high levels of potassium can cause cardiac arrhythmia. Potentially fatal if untreated.

Organ damage

Cardiotoxicity (heart damage) is especially prominent with the use of anthracycline drugs (doxorubicin, epirubicin, idarubicin, and liposomal doxorubicin).

Hepatotoxicity (liver damage) can be caused by many cytotoxic drugs. The susceptibility of an individual to liver damage can be altered by other factors such as the cancer itself, viral hepatitis, immunosuppression and nutritional deficiency. The liver damage can consist of damage to liver cells, hepatic sinusoidal syndrome (obstruction of the veins in the liver), cholestasis (where bile does not flow from the liver to the intestine) and liver fibrosis.

Nephrotoxicity (kidney damage) can be caused by tumor lysis syndrome and also due direct effects of drug clearance by the kidneys. Different drugs will affect different parts of the kidney and the toxicity may be asymptomatic (only seen on blood or urine tests) or may cause acute kidney injury.

Ototoxicity (damage to the inner ear) is a common side effect of platinum based drugs that can produce symptoms such as dizziness and vertigo. Children treated with platinum analogues have been found to be at risk for developing hearing loss.

Other side-effects

Less common side-effects include red skin (erythema), dry skin, damaged fingernails, a dry mouth (xerostomia), water retention, and sexual impotence. Some medications can trigger allergic or pseudoallergic reactions.

Specific chemotherapeutic agents are associated with organ-specific toxicities, including cardiovascular disease (e.g., doxorubicin), interstitial lung disease (e.g., bleomycin) and occasionally secondary neoplasm (e.g., MOPP therapy for Hodgkin’s disease).

Hand-foot syndrome is another side effect to cytotoxic chemotherapy.

7. What do the outcomes look like for chemo patients?

Not brilliant, and this has as much to do with dosing as with the nature of the treatments themselves. Getting the dosage right and hitting that sweet spot of balancing the efficacy of the attack on the cancer against the toxicity experienced by the patient matters hugely. Because of the reduced toxicity, dose-adjusted patients in the 5-FU trial referenced above were able to be treated for longer periods of time. BSA-dosed people were treated for a total of 680 months while people in the dose-adjusted group were treated for a total of 791 months.

Similar results were found in a study involving people with colorectal cancer who were treated with the popular FOLFOX regimen. The incidence of serious diarrhea was reduced from 12% in the BSA-dosed group of patients to 1.7% in the dose-adjusted group, and the incidence of severe mucositis was reduced from 15% to 0.8%.

Chemo is not a cure for cancer, it is a treatment. Expectations for patients receiving chemo present an issue. Chemotherapy does not always work, and even when it is useful, it may not completely destroy the cancer. People frequently fail to understand its limitations. In one study of people who had been newly diagnosed with incurable, stage 4 cancer, more than two-thirds of people with lung cancer and more than four-fifths of people with colorectal cancer still believed that chemotherapy was likely to cure their cancer.

Fault can be laid squarely at the door of the healthcare profession in this instance, with lack of proper educational materials and poor or absent doctor patient interaction. What the medical profession view as success within the narrow scope of chemotherapeutics and what the public perceive are worlds apart. Success can translate to extending life expectancy by two months or remission. It is the duty of the caregiver to ensure that expectations are shared and understood and that both parties are mutually aware of desired outcomes.

If your doctor or healthcare provider does not offer you total transparency in terms of the above along with access to relevant information pertaining to you your treatment, seek alternate advice.

Despite all the side effects, many of which are life threatening, chemo does still have its place in the medical arsenal against cancer and there are success stories of ‘successful’ outcomes for patients, whether that be extension of life or remission. It is however critical that your doctor evaluates your cancer against all the potential treatments available and assess you correctly in terms of chemo as an appropriate treatment.

8. What are the alternatives to chemo?

Chemotherapeutical’s suffer two basic and telling shortcomings that lead to far from ideal outcomes. They are, at the end of the day, a toxin and toxins are not well tolerated. Their biggest issue however is the lack of cell specificity of the drugs. They cannot distinguish between healthy cells and cancerous cells.

Certain cancers will respond to treatment from chemo whilst others simply shrug off the drugs and acquired resistances renders drugs useless. Newer drugs however, work in a far more targeted fashion that hugely reduce many of the serious side effects associated with chemo treatment.

Targeted Therapies

Targeted therapies are a relatively new class of cancer drugs that can overcome many of the issues seen with the use of cytotoxics. They are divided into two groups: small molecule and antibodies. The massive toxicity seen with the use of cytotoxics is due to the lack of cell specificity of the drugs. They will kill any rapidly dividing cell, tumor or normal. Targeted therapies are designed to affect cellular proteins or processes that are utilized by the cancer cells.

This allows a high dose to cancer tissues with a relatively low dose to other tissues. Although the side effects are often less severe than that seen of cytotoxic chemotherapeutics, life-threatening effects can still occur. Initially, targeted therapeutics were designed to be solely selective for one protein.

Now it is clear that there is often a range of protein targets that the drug can bind. An example for targeted therapy is the BCR-ABL1 protein produced from the Philadelphia chromosome, a genetic lesion found commonly in chronic myelogenous leukemia and in some patients with acute lymphoblastic leukemia. This fusion protein has enzyme activity that can be inhibited by imatinib, a small molecule drug.

Steroids

Steroids are drugs that act like your body’s own hormones. They can help treat many types of cancer, and they can keep you from having nausea and vomiting after a round of chemo. They can also prevent allergic reactions to other drugs. They are not however without risk of their own and prolonged use has been linked to an increased risk of developing nonmelanoma-type skin malignancies and non-Hodgkin’s lymphoma.

Typical steroids prescribed for cancer inlude;

• prednisolone
• methylprednisolone
• dexamethasone
• hydrocortisone

Depending on the type of cancer, it is well worth exploring steroids as an alternative form of treatment. You can learn more about the topic by following this link.

Clinical Trials

There a continuous raft of clinical trials for cancer treatments and you can find an exhaustive list of these on the Cancer.org website for American patients. These can often provide an alternative to individuals who are not comfortable with the option of chemo as a treatment and whose cancer may not lend itself to any of the treatments mentioned above.

Follow the link below to keep updated on trials as they become available and discuss this option with your doctor if you feel a trial may offer you a better outcome.Clinical Trials Information for Patients and CaregiversClinical trials are research studies that involve people. Any time you or a loved one need treatment for cancer…www.cancer.gov

9. The financial incentive for chemo treatment

I’ve left the controversy for last and it is a topic most doctors skirt around, but it is an important issue to address as it helps one to understand the dynamics at play and the eagerness to enroll patients for chemo.

Brand-name chemotherapy is often incredibly expensive, in excess of $100,000 per patient.

Healthcare requires funding to keep its doors open. This is true for a small private practice and applies equally to large hospitals and clinics. Pharmaceutical companies incentivize the sale of their chemotherapeutics to ensure their profitability. Incentives are financial in nature and benefit the prescribing individual or organization. As chemo treatments can last over extensive periods of time and the drugs are costly, the returns can generate a solid revenue stream.

Oncologists were placed in the spotlight by the NYT as early as 2003.

Cancer specialists (oncologists) are pocketing hundreds of millions of dollars each year by selling drugs to patients — a practice that almost no other doctors follow.

The practice of purchasing drugs directly from pharmaceutical companies, often at hugely discounted prices to administer to your patients in the setting of your practice is unique to Oncology and creates an environment for ethical abuse, a potential conflict of interest for these doctors, who must help patients decide whether to undergo or continue chemotherapy if it is not proving to be effective, and which drugs to use.

Another study raised this issue. The cost of cancer care continues to increase at an unprecedented rate. Concerns have been raised about financial incentives associated with the chemotherapy concession in oncology practices and their impact on treatment recommendations.

Oncologists receive a 6% markup, meaning when they infuse a patient with a branded $10,000 monthly course of chemotherapy, their practice yields an extra $600. This reduces the desire to prescribe cheaper generics and places additional stress on insurers, who are actively trying to restrict the profits of oncologists. Last month, in August, Forbes ran an article on the topic.

Finally, in an aptly entitled piece from 2019, ny StaffNews, The Cancer in Cancer Medicine; pharma money paid to doctors

If anything gives you pause for thought when your are prescribed chemo, this one single aspect should be at the forefront of your mind. It is a sad reflection on the medical profession that at a point in the patients life, when they are most in need of unbiased, caring, patient focused treatment, they need to be watching their backs — and their wallets.

As promised, we’re at the end and the story below is of little relevance, but of historical interest in the development of chemotherapeutics.

The SS John Henry

In August 1943, Roosevelt approved the shipment of chemical munitions containing mustard agent to the Mediterranean theater. On 18 November 1943 the John Harvey, commanded by Captain Elwin F. Knowles, sailed from Oran, Algeria, to Italy, carrying 2,000 M47A1 mustard gas bombs, each of which held 60–70 lb of sulfur mustard, in clear contravention of the Geneva Convention. After stopping for an inspection by an officer of the 7th Chemical Ordnance Company at Augusta, Sicily on 26 November, the John Harvey sailed through the Strait of Otranto to arrive at Bari.

Bari was packed with ships waiting to be unloaded, and the John Harvey had to wait for several days. Captain Knowles wanted to tell the British port commander about his deadly cargo and request it be unloaded as soon as possible, but secrecy prevented him doing so. (Again the official version. Transporting chemical weapons was a punishable offence under the Geneva Convention)

On 2 December 1943 German aircraft attacked Bari, killing over 1,000 people, and sinking 28 ships, including the John Harvey, which was destroyed in a huge explosion, causing liquid sulfur mustard to spill into the water, mixing with oil from the sunken ships, and a cloud of sulfur mustard vapor to blow over the city. Nearly all crewmen of John Harvey perished in the sinking, this prevented the rescuers from knowing the real nature of the danger until a M47A1 bomb fragment was retrieved from the wreckage.

A total of 628 military victims were hospitalized with mustard gas symptoms, and by the end of the month, 83 of them had died. The number of civilian casualties, thought to have been even greater, could not be accurately gauged since most had left the city to seek shelter with relatives.

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Melanoma is a disease in which malignant cancer cells form in melanocytes (cells that color the skin)

The skin is the body’s largest organ. It protects against heat, sunlight, injury, and infection. Skin also helps control body temperature and stores water, fat, and vitamin D. The skin has several layers, but the two main layers are the epidermis (upper or outer layer) and the dermis (lower or inner layer). Skin cancer begins in the epidermis, which is made up of three kinds of cells:

• Squamous cells: Thin, flat cells that form the top layer of the epidermis.
• Basal cells: Round cells under the squamous cells.
• Melanocytes: Cells that make melanin and are found in the lower part of the epidermis. Melanin is the pigment that gives skin its natural color. When skin is exposed to the sun or artificial light, melanocytes make more pigment and cause the skin to darken.

The number of new cases of melanoma has been increasing over the last 30 years. Melanoma is most common in adults, but it is sometimes found in children and adolescents. 

There are different types of cancer that start in the skin.

There are two main forms of skin cancer: melanoma and nonmelanoma.

Melanoma is a rare form of skin cancer. It is more likely to invade nearby tissues and spread to other parts of the body than other types of skin cancer. When melanoma starts in the skin, it is called cutaneous melanoma. Melanoma may also occur in mucous membranes (thin, moist layers of tissue that cover surfaces such as the lips). This article is about cutaneous (skin) melanoma and melanoma that affects the mucous membranes.

The most common types of skin cancer are basal cell carcinoma and squamous cell carcinoma. They are nonmelanoma skin cancers. Nonmelanoma skin cancers rarely spread to other parts of the body.

Melanoma can occur anywhere on the skin.

In men, melanoma is often found on the trunk (the area from the shoulders to the hips) or the head and neck. In women, melanoma forms most often on the arms and legs.

When melanoma occurs in the eye, it is called intraocular or ocular melanoma.

Unusual moles, exposure to sunlight, and health history can affect the risk of melanoma.

Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn’t mean that you will not get cancer. Talk with your doctor if you think you may be at risk.

Risk factors for melanoma include the following:

• Having a fair complexion, which includes the following:
  • Fair skin that freckles and burns easily, does not tan, or tans poorly.
  • Blue or green or other light-colored eyes.
  • Red or blond hair.
• Being exposed to natural sunlight or artificial sunlight (such as from tanning beds).
• Being exposed to certain factors in the environment (in the air, your home or workplace, and your food and water). Some of the environmental risk factors for melanoma are radiation, solvents, vinyl chloride, and PCBs.
• Having a history of many blistering sunburns, especially as a child or teenager.
• Having several large or many small moles.
• Having a family history of unusual moles (atypical nevus syndrome).
• Having a family or personal history of melanoma.
• Being white.
• Having a weakened immune system.
• Having certain changes in the genes that are linked to melanoma.

Being white or having a fair complexion increases the risk of melanoma, but anyone can have melanoma, including people with dark skin.

Signs of melanoma include a change in the way a mole or pigmented area looks.

These and other signs and symptoms may be caused by melanoma or by other conditions. Check with your doctor if you have any of the following:

• A mole that:
  • changes in size, shape, or color.
  • has irregular edges or borders.
  • is more than one color.
  • is asymmetrical (if the mole is divided in half, the 2 halves are different in size or shape).
  • itches.
  • oozes, bleeds, or is ulcerated (a hole forms in the skin when the top layer of cells breaks down and the tissue below shows through).
• A change in pigmented (colored) skin.
• Satellite moles (new moles that grow near an existing mole).

Tests that examine the skin are used to diagnose melanoma.

If a mole or pigmented area of the skin changes or looks abnormal, the following tests and procedures can help find and diagnose melanoma:

• Physical exam and health history: An exam of the body to check general signs of health, including checking for signs of disease, such as lumps or anything else that seems unusual. A history of the patient’s health habits and past illnesses and treatments will also be taken.
• Skin exam: A doctor or nurse checks the skin for moles, birthmarks, or other pigmented areas that look abnormal in color, size, shape, or texture.
• Biopsy: A procedure to remove the abnormal tissue and a small amount of normal tissue around it. A pathologist looks at the tissue under a microscope to check for cancer cells. It can be hard to tell the difference between a colored mole and an early melanoma lesion. Patients may want to have the sample of tissue checked by a second pathologist. If the abnormal mole or lesion is cancer, the sample of tissue may also be tested for certain gene changes.There are four main types of skin biopsies. The type of biopsy done depends on where the abnormal area formed and the size of the area.
  • Shave biopsy: A sterile razor blade is used to “shave-off” the abnormal-looking growth.
  • Punch biopsy: A special instrument called a punch or a trephine is used to remove a circle of tissue from the abnormal-looking growth.

• • Incisional biopsy: A scalpel is used to remove part of a growth.
  • Excisional biopsy: A scalpel is used to remove the entire growth.

Certain factors affect prognosis (chance of recovery) and treatment options.

The prognosis and treatment options depend on the following:

• The thickness of the tumor and where it is in the body.
• How quickly the cancer cells are dividing.
• Whether there was bleeding or ulceration of the tumor.
• How much cancer is in the lymph nodes.
• The number of places cancer has spread to in the body.
• The level of lactate dehydrogenase (LDH) in the blood.
• Whether the cancer has certain mutations (changes) in a gene called BRAF.
• The patient’s age and general health.

Stages of Melanoma

After melanoma has been diagnosed, tests may be done to find out if cancer cells have spread within the skin or to other parts of the body.

The process used to find out whether cancer has spread within the skin or to other parts of the body is called staging. The information gathered from the staging process determines the stage of the disease. It is important to know the stage in order to plan treatment.

For melanoma that is not likely to spread to other parts of the body or recur, more tests may not be needed. For melanoma that is likely to spread to other parts of the body or recur, the following tests and procedures may be done after surgery to remove the melanoma:

• Lymph node mapping and sentinel lymph node biopsy: The removal of the sentinel lymph node during surgery. The sentinel lymph node is the first lymph node in a group of lymph nodes to receive lymphatic drainage from the primary tumor. It is the first lymph node the cancer is likely to spread to from the primary tumor. A radioactive substance and/or blue dye is injected near the tumor. The substance or dye flows through the lymph ducts to the lymph nodes. The first lymph node to receive the substance or dye is removed. A pathologist views the tissue under a microscope to look for cancer cells. If cancer cells are not found, it may not be necessary to remove more lymph nodes. Sometimes, a sentinel lymph node is found in more than one group of nodes.
• CT scan (CAT scan): A procedure that makes a series of detailed pictures of areas inside the body taken from different angles. The pictures are made by a computer linked to an x-ray machine. A dye may be injected into a vein or swallowed to help the organs or tissues show up more clearly. This procedure is also called computed tomography, computerized tomography, or computerized axial tomography. For melanoma, pictures may be taken of the neck, chest, abdomen, and pelvis.
• PET scan (positron emission tomography scan): A procedure to find malignant tumor cells in the body. A small amount of radioactive glucose (sugar) is injected into a vein. The PET scanner rotates around the body and makes a picture of where glucose is being used in the body. Malignant tumor cells show up brighter in the picture because they are more active and take up more glucose than normal cells do.
• MRI (magnetic resonance imaging) with gadolinium: A procedure that uses a magnet, radio waves, and a computer to make a series of detailed pictures of areas inside the body, such as the brain. A substance called gadolinium is injected into a vein. The gadolinium collects around the cancer cells so they show up brighter in the picture. This procedure is also called nuclear magnetic resonance imaging (NMRI).
• Ultrasound exam: A procedure in which high-energy sound waves (ultrasound) are bounced off internal tissues, such as lymph nodes, or organs and make echoes. The echoes form a picture of body tissues called a sonogram. The picture can be printed to be looked at later.
• Blood chemistry studies: A procedure in which a blood sample is checked to measure the amounts of certain substances released into the blood by organs and tissues in the body. For melanoma, the blood is checked for an enzyme called lactate dehydrogenase (LDH). High LDH levels may predict a poor response to treatment in patients with metastatic disease.

The results of these tests are viewed together with the results of the tumor biopsy to find out the stage of the melanoma.

There are three ways that cancer spreads in the body.

Cancer can spread through tissue, the lymph system, and the blood:

• Tissue. The cancer spreads from where it began by growing into nearby areas.
• Lymph system. The cancer spreads from where it began by getting into the lymph system. The cancer travels through the lymph vessels to other parts of the body.
• Blood. The cancer spreads from where it began by getting into the blood. The cancer travels through the blood vessels to other parts of the body.

Cancer may spread from where it began to other parts of the body.

When cancer spreads to another part of the body, it is called metastasis. Cancer cells break away from where they began (the primary tumor) and travel through the lymph system or blood.

• Lymph system. The cancer gets into the lymph system, travels through the lymph vessels, and forms a tumor (metastatic tumor) in another part of the body.
• Blood. The cancer gets into the blood, travels through the blood vessels, and forms a tumor (metastatic tumor) in another part of the body.

The metastatic tumor is the same type of cancer as the primary tumor. For example, if melanoma spreads to the lung, the cancer cells in the lung are actually melanoma cells. The disease is metastatic melanoma, not lung cancer.

The stage of melanoma depends on the thickness of the tumor, whether cancer has spread to lymph nodes or other parts of the body, and other factors.

To find out the stage of melanoma, the tumor is completely removed and nearby lymph nodes are checked for signs of cancer. The stage of the cancer is used to determine which treatment is best. Check with your doctor to find out which stage of cancer you have.

The stage of melanoma depends on the following:

The thickness of the tumor. The thickness of the tumor is measured from the surface of the skin to the deepest part of the tumor.

Whether the tumor is ulcerated (has broken through the skin).

Whether cancer is found in lymph nodes by a physical exam, imaging tests, or a sentinel lymph node biopsy

Whether the lymph nodes are matted (joined together).

Whether there are:

• Satellite tumors: Small groups of tumor cells that have spread within 2 centimeters of the primary tumor.
• Microsatellite tumors: Small groups of tumor cells that have spread to an area right beside or below the primary tumor.
• In-transit metastases: Tumors that have spread to lymph vessels in the skin more than 2 centimeters away from the primary tumor, but not to the lymph nodes.

Whether the cancer has spread to other parts of the body, such as the lung, liver, brain, soft tissue (including muscle), gastrointestinal tract, and/or distant lymph nodes. Cancer may have spread to places in the skin far away from where it first formed.

The following stages are used for melanoma:

Stage 0 (Melanoma in Situ)

In stage 0, abnormal melanocytes are found in the epidermis. These abnormal melanocytes may become cancer and spread into nearby normal tissue. Stage 0 is also called melanoma in situ.

Stage I

In stage I, cancer has formed. Stage I is divided into stages IA and IB.

• Stage IA: The tumor is not more than 1 millimeter thick, with or without ulceration.
• Stage IB: The tumor is more than 1 but not more than 2 millimeters thick, without ulceration.

Stage II

Stage II is divided into stages IIA, IIB, and IIC.

Stage IIA: The tumor is either:

• more than 1 but not more than 2 millimeters thick, with ulceration; or
• more than 2 but not more than 4 millimeters thick, without ulceration.

Stage IIB: The tumor is either:

• more than 2 but not more than 4 millimeters thick, with ulceration; or
• more than 4 millimeters thick, without ulceration.

Stage IIC: The tumor is more than 4 millimeters thick, with ulceration.

Stage III

Stage III is divided into stages IIIA, IIIB, IIIC, and IIID.

• Stage IIIA: The tumor is not more than 1 millimeter thick, with ulceration, or not more than 2 millimeters thick, without ulceration. Cancer is found in 1 to 3 lymph nodes by sentinel lymph node biopsy.
• Stage IIIB:
  • (1) It is not known where the cancer began or the primary tumor can no longer be seen, and one of the following is true:
    • cancer is found in 1 lymph node by physical exam or imaging tests; or
    • there are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.or
  • (2) The tumor is not more than 1 millimeter thick, with ulceration, or not more than 2 millimeters thick, without ulceration, and one of the following is true:
    • cancer is found in 1 to 3 lymph nodes by physical exam or imaging tests; or
    • there are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.or
  • (3) The tumor is more than 1 but not more than 2 millimeters thick, with ulceration, or more than 2 but not more than 4 millimeters thick, without ulceration, and one of the following is true:
    • cancer is found in 1 to 3 lymph nodes; or
    • there are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.
• Stage IIIC:
  • (1) It is not known where the cancer began, or the primary tumor can no longer be seen. Cancer is found:
    • in 2 or 3 lymph nodes; or
    • in 1 lymph node and there are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin; or
    • in 4 or more lymph nodes, or in any number of lymph nodes that are matted together; or
    • in 2 or more lymph nodes and/or in any number of lymph nodes that are matted together. There are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.or
  • (2) The tumor is not more than 2 millimeters thick, with or without ulceration, or not more than 4 millimeters thick, without ulceration. Cancer is found:
    • in 1 lymph node and there are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin; or
    • in 4 or more lymph nodes, or in any number of lymph nodes that are matted together; or
    • in 2 or more lymph nodes and/or in any number of lymph nodes that are matted together. There are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.or
  • (3) The tumor is more than 2 but not more than 4 millimeters thick, with ulceration, or more than 4 millimeters thick, without ulceration. Cancer is found in 1 or more lymph nodes and/or in any number of lymph nodes that are matted together. There may be microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.or
  • (4) The tumor is more than 4 millimeters thick, with ulceration. Cancer is found in 1 or more lymph nodes and/or there are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.
• Stage IIID: The tumor is more than 4 millimeters thick, with ulceration. Cancer is found:
  • in 4 or more lymph nodes, or in any number of lymph nodes that are matted together; or
  • in 2 or more lymph nodes and/or in any number of lymph nodes that are matted together. There are microsatellite tumors, satellite tumors, and/or in-transit metastases on or under the skin.

Stage IV

In stage IV, the cancer has spread to other parts of the body, such as the lung, liver, brain, spinal cord, bone, soft tissue (including muscle), gastrointestinal (GI) tract, and/or distant lymph nodes. Cancer may have spread to places in the skin far away from where it first started.

Melanoma can recur (come back) after it has been treated.

The cancer may come back in the area where it first started or in other parts of the body, such as the lungs or liver.

There are different types of treatment for patients with melanoma.

Different types of treatment are available for patients with melanoma. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Five types of standard treatment are used:

Surgery

Surgery to remove the tumor is the primary treatment of all stages of melanoma. A wide local excision is used to remove the melanoma and some of the normal tissue around it. Skin grafting (taking skin from another part of the body to replace the skin that is removed) may be done to cover the wound caused by surgery.

Sometimes, it is important to know whether cancer has spread to the lymph nodes. Lymph node mapping and sentinel lymph node biopsy are done to check for cancer in the sentinel lymph node (the first lymph node in a group of lymph nodes to receive lymphatic drainage from the primary tumor). It is the first lymph node the cancer is likely to spread to from the primary tumor. A radioactive substance and/or blue dye is injected near the tumor. The substance or dye flows through the lymph ducts to the lymph nodes. The first lymph node to receive the substance or dye is removed. A pathologist views the tissue under a microscope to look for cancer cells. If cancer cells are found, more lymph nodes will be removed and tissue samples will be checked for signs of cancer. This is called a lymphadenectomy. Sometimes, a sentinel lymph node is found in more than one group of nodes.

After the doctor removes all the melanoma that can be seen at the time of the surgery, some patients may be given chemotherapy after surgery to kill any cancer cells that are left. Chemotherapy given after the surgery, to lower the risk that the cancer will come back, is called therapy.

Surgery to remove cancer that has spread to the lymph nodes, lung, gastrointestinal (GI) tract, bone, or brain may be done to improve the patient’s quality of life by controlling symptoms.

Chemotherapy

Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy).

One type of regional chemotherapy is hyperthermic isolated limb perfusion. With this method, anticancer drugs go directly to the arm or leg the cancer is in. The flow of blood to and from the limb is temporarily stopped with a tourniquet. A warm solution with the anticancer drug is put directly into the blood of the limb. This gives a high dose of drugs to the area where the cancer is.

The way the chemotherapy is given depends on the type and stage of the cancer being treated.

Radiation therapy

Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. External radiation therapy uses a machine outside the body to send radiation toward the area of the body with cancer. External radiation therapy is used to treat melanoma and may also be used as palliative therapy to relieve symptoms and improve quality of life.

Immunotherapy

Immunotherapy is a treatment that uses the patient’s immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the body’s natural defenses against cancer. This type of cancer treatment is also called biotherapy or biologic therapy.

The following types of immunotherapy are being used in the treatment of melanoma:

• Immune checkpoint inhibitor therapy: Some types of immune cells, such as T cells, and some cancer cells have certain proteins, called checkpoint proteins, on their surface that keep immune responses in check. When cancer cells have large amounts of these proteins, they will not be attacked and killed by T cells. Immune checkpoint inhibitors block these proteins and the ability of T cells to kill cancer cells is increased. They are used to treat some patients with advanced melanoma or tumors that cannot be removed by surgery.There are two types of immune checkpoint inhibitor therapy:
  • CTLA-4 inhibitor: CTLA-4 is a protein on the surface of T cells that helps keep the body’s immune responses in check. When CTLA-4 attaches to another protein called B7 on a cancer cell, it stops the T cell from killing the cancer cell. CTLA-4 inhibitors attach to CTLA-4 and allow the T cells to kill cancer cells. Ipilimumab is a type of CTLA-4 inhibitor.

PD-1 inhibitor: PD-1 is a protein on the surface of T cells that helps keep the body’s immune responses in check. When PD-1 attaches to another protein called PDL-1 on a cancer cell, it stops the T cell from killing the cancer cell. PD-1 inhibitors attach to PDL-1 and allow the T cells to kill cancer cells. Pembrolizumab and nivolumab are types of PD-1 inhibitors.

• Interleukin-2 (IL-2): IL-2 boosts the growth and activity of many immune cells, especially lymphocytes (a type of white blood cell). Lymphocytes can attack and kill cancer cells.
• Tumor necrosis factor (TNF) therapy: TNF is a protein made by white blood cells in response to an antigen or infection. TNF is made in the laboratory and used as a treatment to kill cancer cells. It is being studied in the treatment of melanoma.

Targeted therapy

Targeted therapy is a type of treatment that uses drugs or other substances to attack cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do. The following types of targeted therapy are used or being studied in the treatment of melanoma:

• Signal transduction inhibitor therapy: Signal transduction inhibitors block signals that are passed from one molecule to another inside a cell. Blocking these signals may kill cancer cells. They are used to treat some patients with advanced melanoma or tumors that cannot be removed by surgery. Signal transduction inhibitors include:
  • BRAF inhibitors (dabrafenib, vemurafenib, encorafenib) that block the activity of proteins made by mutant BRAF genes; and
  • MEK inhibitors (trametinib, cobimetinib, binimetinib) that block proteins called MEK1 and MEK2 which affect the growth and survival of cancer cells.Combinations of BRAF inhibitors and MEK inhibitors used to treat melanoma include:
  • Dabrafenib plus trametinib.
  • Vemurafenib plus cobimetinib.
  • Encorafenib plus binimetinib.
• Oncolytic virus therapy: A type of targeted therapy that is used in the treatment of melanoma. Oncolytic virus therapy uses a virus that infects and breaks down cancer cells but not normal cells. Radiation therapy or chemotherapy may be given after oncolytic virus therapy to kill more cancer cells. Talimogene laherparepvec is a type of oncolytic virus therapy made with a form of the herpesvirus that has been changed in the laboratory. It is injected directly into tumors in the skin and lymph nodes.
• Angiogenesis inhibitors: A type of targeted therapy that is being studied in the treatment of melanoma. Angiogenesis inhibitors block the growth of new blood vessels. In cancer treatment, they may be given to prevent the growth of new blood vessels that tumors need to grow.

New targeted therapies and combinations of therapies are being studied in the treatment of melanoma.

Vaccine therapy

Vaccine therapy is a cancer treatment that uses a substance or group of substances to stimulate the immune system to find the tumor and kill it. Vaccine therapy is being studied in the treatment of stage III melanoma that can be removed by surgery.

Treatment of Stage 0 (Melanoma in Situ)

Treatment of stage 0 is usually surgery to remove the area of abnormal cells and a small amount of normal tissue around it.

Treatment of Stage I Melanoma

Treatment of stage I melanoma may include the following:

• Surgery to remove the tumor and some of the normal tissue around it. Sometimes lymph node mapping and removal of lymph nodes is also done.
• A clinical trial of new ways to find cancer cells in the lymph nodes.

Treatment of Stage II Melanoma

Treatment of stage II melanoma may include the following:

• Surgery to remove the tumor and some of the normal tissue around it. Sometimes lymph node mapping and sentinel lymph node biopsy are done to check for cancer in the lymph nodes at the same time as the surgery to remove the tumor. If cancer is found in the sentinel lymph node, more lymph nodes may be removed.
• A clinical trial of new types of treatment to be used after surgery.

Treatment of Stage III Melanoma That Can Be Removed By Surgery

Treatment of stage III melanoma that can be removed by surgery may include the following:

• Surgery to remove the tumor and some of the normal tissue around it. Skin grafting may be done to cover the wound caused by surgery. Sometimes lymph node mapping and sentinel lymph node biopsy are done to check for cancer in the lymph nodes at the same time as the surgery to remove the tumor. If cancer is found in the sentinel lymph node, more lymph nodes may be removed.
• Surgery followed by immunotherapy with immune checkpoint inhibitors (nivolumab, pembrolizumab, or ipilimumab) if there is a high risk that the cancer will come back.
• Surgery followed by targeted therapy with signal transduction inhibitors (dabrafenib and trametinib) if there is a high risk that the cancer will come back.
• A clinical trial of immunotherapy with or without vaccine therapy.
• A clinical trial of surgery followed by therapies that target specific gene changes.

Use the clinical trial search [NCI Website] to find NCI-supported cancer clinical trials that are accepting patients. You can search for trials based on the type of cancer, the age of the patient, and where the trials are being done. General information [NCI Websites] about clinical trials is also available.

Treatment of Stage III Melanoma That Cannot Be Removed By Surgery, Stage IV Melanoma, and Recurrent Melanoma

Treatment of stage III melanoma that cannot be removed by surgery, stage IV melanoma, and recurrent melanoma may include the following:

• Oncolytic virus therapy (talimogene laherparepvec) injected into the tumor.
• Immunotherapy with ipilimumab, pembrolizumab, nivolumab, or interleukin-2 (IL-2). Sometimes ipilimumab and nivolumab are given together.
• Targeted therapy with signal transduction inhibitors (dabrafenib, trametinib, vemurafenib, cobimetinib, encorafenib, binimetinib). These may be given alone or in combination.
• Chemotherapy.
• Palliative therapy to relieve symptoms and improve the quality of life. This may include:
  • Surgery to remove lymph nodes or tumors in the lung, gastrointestinal (GI) tract, bone, or brain.
  • Radiation therapy to the brain, spinal cord, or bone.

Treatments that are being studied in clinical trials for stage III melanoma that cannot be removed by surgery, stage IV melanoma, and recurrent melanoma include the following:

• Immunotherapy alone or in combination with other therapies such as targeted therapy.
• For melanoma that has spread to the brain, immunotherapy with nivolumab plus ipilimumab.
• Targeted therapy, such as signal transduction inhibitors, angiogenesis inhibitors, oncolytic virus therapy, or drugs that target certain gene mutations. These may be given alone or in combination.
• Surgery to remove all known cancer.
• Regional chemotherapy (hyperthermic isolated limb perfusion). Some patients may also have immunotherapy with tumor necrosis factor.
• Systemic chemotherapy.

The post Melanoma, a skin cancer appeared first on Medika Life.

SCC of the skin is also known as cutaneous squamous cell carcinoma (cSCC). Adding the word “cutaneous” identifies it as a skin cancer and differentiates it from squamous cell cancers that can arise inside the body, in places like the mouth, throat or lungs. It is the second most common form of skin cancer, characterized by abnormal, accelerated growth of squamous cells. When caught early, most SCCs are curable.

One of three main types of cells in the top layer of the skin (the epidermis), squamous cells are flat cells located near the surface of the skin that shed continuously as new ones form.

SCC occurs when DNA damage from exposure to ultraviolet radiation or other damaging agents trigger abnormal changes in the squamous cells.

What does SCC look like?

SCCs can appear as scaly red patches, open sores, rough, thickened or wart-like skin, or raised growths with a central depression. At times, SCCs may crust over, itch or bleed. The lesions most commonly arise in sun-exposed areas of the body.

SCCs can also occur in other areas of the body, including the genitals.

The following stages are used for basal cell carcinoma and squamous cell carcinoma of the skin that is on the head or neck but not on the eyelid:

Stage 0 (Carcinoma in situ)

In stage 0, abnormal cells are found in the squamous cell or basal cell layer of the epidermis. These abnormal cells may become cancer and spread into nearby normal tissue. Stage 0 is also called carcinoma in situ.

Stage I

In stage I, cancer has formed and the tumor is 2 centimeters or smaller.

Stage II

In stage II, the tumor is larger than 2 centimeters but not larger than 4 centimeters.

Stage III

or

In stage III, one of the following is found:

• the tumor is larger than 4 centimeters, or cancer has spread to tissue covering the nerves below the dermis, or has spread below the subcutaneous tissue, or has spread to the bone and the bone has minor damage. Cancer may have also spread to one lymph node on the same side of the body as the tumor and the node is 3 centimeters or smaller, and cancer has not spread through to the outside covering of the lymph node; or
• the tumor is 4 centimeters or smaller. Cancer has spread to one lymph node on the same side of the body as the tumor and the node is 3 centimeters or smaller.

Stage IV

or

or

In stage IV, one of the following is found:

• the tumor is any size and cancer may have spread to the bone and the bone has minor damage, or to tissue covering the nerves below the dermis, or below the subcutaneous tissue. Cancer has spread to the lymph nodes as follows:
  • one lymph node on the same side of the body as the tumor, the affected node is 3 centimeters or smaller, and cancer has spread through to the outside covering of the lymph node; or
  • one lymph node on the same side of the body as the tumor, the affected node is larger than 3 centimeters but not larger than 6 centimeters, and cancer has not spread through to the outside covering of the lymph node; or
  • more than one lymph node on the same side of the body as the tumor, the affected nodes are 6 centimeters or smaller, and cancer has not spread through to the outside covering of the lymph nodes; or
  • one or more lymph nodes on the opposite side of the body as the tumor or on both sides of the body, the affected nodes are 6 centimeters or smaller, and cancer has not spread through to the outside covering of the lymph nodes.
• the tumor is any size and cancer may have spread to tissue covering the nerves below the dermis, or below the subcutaneous tissue, or to bone marrow or to bone, including the bottom of the skull. Also:
  • cancer has spread to one lymph node that is larger than 6 centimeters and cancer has not spread through to the outside covering of the lymph node; or
  • cancer has spread to one lymph node on the same side of the body as the tumor, the affected node is larger than 3 centimeters, and cancer has spread through to the outside covering of the lymph node; or
  • cancer has spread to one lymph node on the opposite side of the body as the tumor, the affected node is any size, and cancer has spread through to the outside covering of the lymph node; or
  • cancer has spread to more than one lymph node on one or both sides of the body and cancer has spread through to the outside covering of the lymph nodes.
• the tumor is any size and cancer has spread to bone marrow or to bone, including the bottom of the skull, and the bone has been damaged. Cancer may have also spread to the lymph nodes; or
• cancer has spread to other parts of the body, such as the lung.

The following stages are used for basal cell carcinoma and squamous cell carcinoma of the skin on the eyelid:

Stage 0 (Carcinoma in situ)

In stage 0, abnormal cells are found in the epidermis, usually in the basal cell layer. These abnormal cells may become cancer and spread into nearby normal tissue. Stage 0 is also called carcinoma in situ.

Stage I

In stage I, cancer has formed. Stage I is divided into stages IA and IB.

• Stage IA: The tumor is 10 millimeters or smaller and may have spread to the edge of the eyelid where the lashes are, to the connective tissue in the eyelid, or to the full thickness of the eyelid.
• Stage IB: The tumor is larger than 10 millimeters but not larger than 20 millimeters and the tumor has not spread to the edge of the eyelid where the lashes are, or to the connective tissue in the eyelid.

Stage II

Stage II is divided into stages IIA and IIB.

• In stage IIA, one of the following is found:
  • the tumor is larger than 10 millimeters but not larger than 20 millimeters and has spread to the edge of the eyelid where the lashes are, to the connective tissue in the eyelid, or to the full thickness of the eyelid; or
  • the tumor is larger than 20 millimeters but not larger than 30 millimeters and may have spread to the edge of the eyelid where the lashes are, to the connective tissue in the eyelid, or to the full thickness of the eyelid.
• In stage IIB, the tumor may be any size and has spread to the eye, eye socket, sinuses, tear ducts, or brain, or to the tissues that support the eye.

Stage III

Stage III is divided into stages IIIA and IIIB.

• Stage IIIA: The tumor may be any size and may have spread to the edge of the eyelid where the lashes are, to the connective tissue in the eyelid, or to the full thickness of the eyelid, or to the eye, eye socket, sinuses, tear ducts, or brain, or to the tissues that support the eye. Cancer has spread to one lymph node on the same side of the body as the tumor and the node is 3 centimeters or smaller.
• Stage IIIB: The tumor may be any size and may have spread to the edge of the eyelid where the lashes are, to the connective tissue in the eyelid, or to the full thickness of the eyelid, or to the eye, eye socket, sinuses, tear ducts, or brain, or to the tissues that support the eye. Cancer has spread to lymph nodes as follows:
  • one lymph node on the same side of the body as the tumor and the node is larger than 3 centimeters; or
  • more than one lymph node on the opposite side of the body as the tumor or on both sides of the body.

Stage IV

In stage IV, the tumor has spread to other parts of the body, such as the lung or liver.

Treatment depends on the type of skin cancer or other skin condition diagnosed:

Squamous cell carcinoma occurs on areas of the skin that have been damaged by the sun, such as the ears, lower lip, and the back of the hands. Squamous cell carcinoma may also appear on areas of the skin that have been sunburned or exposed to chemicals or radiation. Often this cancer looks like a firm red bump. The tumor may feel scaly, bleed, or form a crust. Squamous cell tumors may spread to nearby lymph nodes. Squamous cell carcinoma that has not spread can usually be cured.

There are different types of treatment for patients with basal cell carcinoma, squamous cell carcinoma of the skin, and actinic keratosis.

Different types of treatment are available for patients with basal cell carcinoma, squamous cell carcinoma of the skin, and actinic keratosis. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

Eight types of standard treatment are used:

Surgery

One or more of the following surgical procedures may be used to treat basal cell carcinoma, squamous cell carcinoma of the skin, or actinic keratosis:

• Simple excision: The tumor, along with some of the normal tissue around it, is cut from the skin.
• Mohs micrographic surgery: The tumor is cut from the skin in thin layers. During the procedure, the edges of the tumor and each layer of tumor removed are viewed through a microscope to check for cancer cells. Layers continue to be removed until no more cancer cells are seen. This type of surgery removes as little normal tissue as possible. It is often used to remove skin cancer on the face, fingers, or genitals and skin cancer that does not have a clear border.

• Shave excision: The abnormal area is shaved off the surface of the skin with a small blade.
• Curettage and electrodesiccation: The tumor is cut from the skin with a curette (a sharp, spoon-shaped tool). A needle-shaped electrode is then used to treat the area with an electric current that stops the bleeding and destroys cancer cells that remain around the edge of the wound. The process may be repeated one to three times during the surgery to remove all of the cancer. This type of treatment is also called electrosurgery.
• Cryosurgery: A treatment that uses an instrument to freeze and destroy abnormal tissue, such as carcinoma in situ. This type of treatment is also called cryotherapy.

• Laser surgery: A surgical procedure that uses a laser beam (a narrow beam of intense light) as a knife to make bloodless cuts in tissue or to remove a surface lesion such as a tumor.
• Dermabrasion: Removal of the top layer of skin using a rotating wheel or small particles to rub away skin cells.

Simple excision, Mohs micrographic surgery, curettage and electrodesiccation, and cryosurgery are used to treat basal cell carcinoma and squamous cell carcinoma of the skin. Laser surgery is rarely used to treat basal cell carcinoma. Simple excision, shave excision, curettage and desiccation, dermabrasion, and laser surgery are used to treat actinic keratosis.

Radiation therapy

Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. External radiation therapy uses a machine outside the body to send radiation toward the area of the body with cancer.

External radiation therapy is used to treat basal cell carcinoma and squamous cell carcinoma of the skin.

Chemotherapy

Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing.

Chemotherapy for basal cell carcinoma, squamous cell carcinoma of the skin, and actinic keratosis is usually topical (applied to the skin in a cream or lotion). Topical fluorouracil (5-FU) is used to treat basal cell carcinoma.

Photodynamic therapy

Photodynamic therapy (PDT) is a cancer treatment that uses a drug and a certain type of light to kill cancer cells. A drug that is not active until it is exposed to light is injected into a vein or put on the skin. The drug collects more in cancer cells than in normal cells. For skin cancer, laser light is shined onto the skin and the drug becomes active and kills the cancer cells. Photodynamic therapy causes little damage to healthy tissue.

Photodynamic therapy is also used to treat actinic keratoses.

Immunotherapy

Immunotherapy is a treatment that uses the patient’s immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the body’s natural defenses against cancer. This type of cancer treatment is also called biotherapy or biologic therapy.

Interferon and imiquimod are immunotherapy drugs used to treat skin cancer.

• Interferon (by injection) may be used to treat squamous cell carcinoma of the skin.
• Topical imiquimod therapy (a cream applied to the skin) may be used to treat some basal cell carcinomas.

Targeted therapy

Targeted therapy is a type of treatment that uses drugs or other substances to attack cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do.

• Signal transduction inhibitors therapy: This treatment block signals that are passed from one molecule to another inside a cell. Blocking these signals may kill cancer cells. Vismodegib and sonidegib are signal transduction inhibitors used to treat basal cell carcinoma.

Chemical peel

A chemical peel is a procedure used to improve the way certain skin conditions look. A chemical solution is put on the skin to dissolve the top layers of skin cells. Chemical peels may be used to treat actinic keratosis. This type of treatment is also called chemabrasion and chemexfoliation.

Other drug therapy

Retinoids (drugs related to vitamin A) are sometimes used to treat squamous cell carcinoma of the skin. Diclofenac and ingenol are topical drugs used to treat actinic keratosis.

New types of treatment are being tested in clinical trials.

Information about clinical trials is available from the NCI website.

Follow-up tests may be needed.

Some of the tests that were done to diagnose the cancer or to find out the stage of the cancer may be repeated. Some tests will be repeated in order to see how well the treatment is working. Decisions about whether to continue, change, or stop treatment may be based on the results of these tests.

Some of the tests will continue to be done from time to time after treatment has ended. The results of these tests can show if your condition has changed or if the cancer has recurred (come back). These tests are sometimes called follow-up tests or check-ups.

If basal cell carcinoma and squamous cell carcinoma recur (come back), it is usually within 5 years of initial treatment. Talk to your doctor about how often you should have your skin checked for signs of cancer.

Treatment of Squamous Cell Carcinoma of the Skin

Treatment of squamous cell carcinoma that is localized may include the following:

• Simple excision.
• Mohs micrographic surgery.
• Radiation therapy.
• Curettage and electrodesiccation.
• Cryosurgery.
• Photodynamic therapy, for squamous cell carcinoma in situ (stage 0).

Treatment of squamous cell carcinoma that is metastatic or cannot be treated with local therapy may include the following:

• Chemotherapy.
• Retinoid therapy and immunotherapy (interferon).
• A clinical trial of a new treatment.

Treatment of recurrent squamous cell carcinoma that is not metastatic may include the following:

• Simple excision.
• Mohs micrographic surgery.
• Radiation therapy.

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