As an oncologist of three decades, I am still shaken when I hear a patient carries the diagnosis.

I dodged a bullet in 2015 when a large pituitary tumor, likely induced by radiation therapy, turned out not to be a brain cancer.

I am not talking about the usual pituitary tumor; I have had four surgeries for mine.

I was thrilled to see hints that a new approach offers promise in this context.

The innovative approach led to remarkable responses in three individuals with recurrent glioblastoma. Still, all died within about six months.

Glioblastoma Is A Dreadful Cancer

Before we discuss a possible treatment breakthrough, I want to provide some basics about glioblastoma multiforme.

Glioblastoma multiforme (GBM) is a cancer that starts as a growth of cells in the brain or spinal cord. The malignancy grows quickly and can invade and destroy surrounding healthy tissue.

GBM forms from astrocyte cells that support nerves.

Glioblastoma Demographics

Glioblastoma can happen at any age.

However, it tends to occur more often in older adults and more often in men.

Glioblastoma symptoms include headaches that keep getting worse, nausea and vomiting, blurred or double vision, drowsiness, personality change, and seizures.

Glioblastoma Is Lethal

Treatments might slow cancer growth and reduce symptoms.

There’s no cure for glioblastoma multiforme.

Despite treatments such as surgery, radiation therapy, chemotherapy, and electromagnetic field therapy, GBM has a poor prognosis.

While treatment can extend the life of someone with glioblastoma multiforme, there is no cure.

Into the Future: Cancer Management

Cancer treatment used to be all about surgery, chemotherapy, and radiation. But now, a whole new world of treatments is making a huge impact.

One type is targeted therapy. These drugs, like Gleevec and Herceptin, go straight for specific changes in cancer cells and kill them. Loads of people with cancer are benefiting from these treatments.

Then there’s immunotherapy, which boosts your immune system to fight cancer.

Some of these drugs have been incredible at shrinking tumors or even making them vanish in people with advanced cancer. And in some lucky cases, these effects can stick around for years.

You might have heard of immune checkpoint inhibitors, which are already helping lots of people with cancers like melanoma, lung, breast, and bladder cancer.

But there’s also another kind of immunotherapy called CAR T-cell therapy. It’s not as common as the others, but it’s doing amazing things for tough leukemias and lymphomas, often keeping the cancer at bay for a long time.

How CAR T-cell Therapy Works

CAR T-cell therapy, or chimeric antigen receptor T-cell therapy, is a type of immunotherapy that harnesses the power of the body’s immune system to fight cancer.

Here’s how it works:

1. Collection of T-cells: First, doctors collect a type of white blood cell called T-cells from the patient’s blood. T-cells are a crucial part of the immune system for identifying and attacking foreign or abnormal cells, including cancer cells.
2. Genetic Engineering: T-cells are genetically engineered in the laboratory to produce chimeric antigen receptors (CARs) on their surface. These CARs are artificial receptors that empower T-cells to identify and attach to particular proteins, known as antigens, located on the surface of cancer cells.
3. CAR T-cell expansion: The modified T-cells, now equipped with CARs, are multiplied or expanded to create a larger population of CAR T-cells.
4. Infusion into the Patient: The CAR T-cells are introduced into the patient’s bloodstream after expansion. Within the body, these modified CAR T-cells actively search for and specifically attach to cancer cells that exhibit the designated antigen.
5. Attack on Cancer Cells: When a CAR T-cell connects with a cancer cell, it builds a strong immune reaction against the cancer. This reaction can lead to the CAR T-cells directly destroying the cancer cells and calling in other immune cells to help fight against the cancer.
6. Persistence and Memory: Certain CAR T-cells can remain in the body for long, monitoring for any signs of cancer returning. Memory CAR T-cells can also be produced, swiftly reacting if cancer cells reappear.

Overall, CAR T-cell therapy represents a groundbreaking approach to cancer treatment. It leverages the body’s immune system to target and destroy cancer cells specifically.

The Car T-cell approach offers hope for patients with certain types of advanced or treatment-resistant cancers.

Harvard’s New Study

Massachusetts General Hospital researchers recently took a new approach to CAR-T treatment.

MGH researchers engineered CAR-TEAM cells to treat mixed cell populations in tumors.

Collaborating with Mass General neurosurgeons, the team tried the approach in an early (phase 1) clinical trial of patients with recurrent glioblastoma.

Exciting News

Here are the exciting results:

The first three patients in the trial showed dramatic responses within days.

“We were shocked. These results exceeded our expectations,” offered Stephen J. Bagley, MD, MSCE, section chief of neuro-oncology at Penn Medicine.

But did this translate to extraordinary clinical results? In a word, no.

News Headlines Versus Reality

Using a new delivery system and dual-targeting, the novel approach translated to a rapid response.

Let’s look at the clinic outcomes for the four patients:

• Patient #1 maintained tumor regression for 33 days.
• Patient #2 died (not from treatment but from hydrocephalus (for which the patient declined treatment). This patient had two months of stable disease before the hydrocephalus.
• Patient #3 is at seven months of no progression.
• Patient #4 had three months of tumor stability.
• Patients #5 and #6 had one month of stability at the time of the report.

The dual-targeting and a new delivery system produced rapid results.

But There Were Side Effects

All patients had some side effects (neurotoxicity) within 72 hours of treatment.

Moderate side effects included fatigue, skin ulceration, anorexia, lower oxygen levels, muscle weakness, and drops in some blood counts (lymphocytes, a type of white blood cell).

Into the Future

Researchers are looking to enroll 18 patients in a new trial.

They will examine response length and how that affects survival length.
In addition, the researchers will try to understand why CAR-T works better in some patients than others.

The ability to serially pull out spinal fluid allows for rapid analysis of biomarkers.

My Take

I hope this pilot study improves the management of aggressive brain tumors.

If ongoing studies improve outcomes, researchers may consider using the CAR-T cell approach earlier in the disease process.

Targeting multiple cellular targets with local delivery may help us manage other solid tumors.

The post Breakthrough: New Treatment Sparks Remarkable, Swift Reversal of Brain Cancer in Early Clinical Trials appeared first on Medika Life.

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.

This third installment highlights recent advances in treating multiple myeloma. The first in the series lays the foundation for understanding how CAR T works, while the second outlines its uses for B cell cancers.

Multiple myeloma is a relatively uncommon yet serious disease estimated to impact more than 30,000 US citizens this year. Although several treatment options exist, the illness is considered incurable as most treatments do not resolve the condition permanently—including the most recent advancements with CAR T cells. Here, we describe an approach using a different variant of CAR T cells for multiple myeloma that holds promise for those with treatment-resistant forms of the disease.

What is Multiple Myeloma?

Multiple myeloma (MM) or myeloma is a cancer of the plasma B cells found in the bone marrow. Although these white blood cells typically produce antibodies, for people with multiple myeloma, the plasma cells multiply faster than the body can handle, produce abnormal antibodies, and set the body out of balance. The illness can spread to other organs through the bloodstream, and masses of plasma cells may form in the bone marrow or soft tissues, as well.

The illness usually occurs to people 60 years and older, and is unlikely to develop in individuals under 40 years of age. The symptoms can be widely varying—some even report having no symptoms at all—but most with this disease experience bone pain and fatigue. Other common complications include anemia, kidney problems, or thickened blood.

Without treatment, the prognosis is poor. However, with the advent of chemotherapy and more advanced medicines, survival is usually four to five years. If diagnosed early, the five-year survival rate exceeds 77%.

Patients with active myeloma first receive a combination of drugs to target the abnormal cells. Another alternative is chemotherapy. For example, I contributed to the creation of Velcade, a chemotherapy medicine which slows or stops the growth of myeloma cells. Stem cell transplants, steroids and even CAR T therapy—a newer medical technology which alters patient cells in the lab and infuses them back into the body to fight the cancer—may be tried as other potential options. Unfortunately, once a therapy fails, the body typically becomes resistant to its reintroduction and thus loses efficacy.

The Current Reality of CAR T Therapy 

CAR T therapy has recently been approved to treat multiple myeloma, but it is only considered after four or more refractory lines of treatment—in other words, when other four or more options fail to achieve lasting remission. The two existing CAR T therapies on the market target B cell maturation antigen (BCMA), an antigen expressed on the surface of malignant plasma cells; in this piece, the antigen will be referred to as Target 1.

A Chimeric Antigen Receptor T cell derives its name from the synthetic combination of T cell and antibody properties. Patient T cells are taken from the body and modified to detect Target 1 through an antibody-based fusion receptor (scFv). The lysing process relies on signaling from the T cell. As seen in Figure 1, when the CAR T antigen receptor binds with Target 1 on the cancer cell, the CAR T cell releases chemicals to trigger the cancer cell’s death.

Clinical trials have confirmed these CAR T therapies as safe to use and capable of producing results. A study of Ide-cel found 73% of participants had a decrease in their cancer. Even more successfully, a study of Cilta-cel saw a 98% response rate, with 78% of patients showing no signs of cancer in their bone marrow. The outstanding issue with both treatments, however, is that relapse does eventually occur—around 8.8 months later for Ide-cel, and 22 months later with Cilta-cel.

With relapse and treatment resistance a prevailing concern for multiple myeloma treatments—not just CAR T—researchers are seeking new ways to sustain longer remission and increase survivability when other alternatives are exhausted.  One possible method is to enhance current CAR T protocols with a new therapeutic target.

Methods 

In their study, Mailankody et al. consider the safety of an alternative antigen target. The target is known as G protein-coupled receptor, class C, group 5, member D (GPRC5D), but shall be referred to as Target 2 for simplicity. Despite its unknown function in tissues, it poses as a promising CAR T antigen target due to its presence in several myeloma cell lines and in bone marrow plasma cells.

The team chose a second generation CAR T design for their product. Second generation CAR T cells contain a single costimulatory domain (shown in blue in Figure 2) inside the T cell to extend the life of the cell once in the body. The chimeric antigen receptor in this study is tailored to find cancer cells that express Target 2 (denoted in green in Figure 2).

As depicted in Figure 3, the researchers first collected patient T cells through leukapheresis. They modified the T cells, expanded them to large numbers, and then infused the CAR T cells back into the body after completing preparatory chemotherapy. The patients received an escalating dose of the trial CAR T infusion, totalling to four doses.

Results 

A total of 17 participants received CAR T therapy, all who have previously tried five different kinds of multiple myeloma treatment. The majority of participants developed cancer resistance to their last line of treatment; this includes a group of individuals who previously received Target 1 CAR T therapy.

On the whole, this study successfully confirms Target 2 CAR T therapy as safe and effective, particularly for individuals who have already received Target 1 CAR T cell therapy or have run through several other therapeutic options. Around 78% of patients had a partial response or better, and 59% had a very good partial response or better. The therapy was effective even ten months after infusion for some individuals.

Common CAR T therapy side effects include cytokine release syndrome and immune effector cell-associated neurotoxicity (ICANS). While both conditions can be reversed with prompt treatment, the severity of both side effects can range from mild to life-threatening. Most participants experienced milder cytokine release, with the exception of one patient who experienced life-threatening side effects. All with side effects were treated.

Future Directions

Mailankody et al. demonstrate that Target 2 CAR T therapy can effectively treat multiple myeloma. If Target 1 CAR T therapy fails, Target 2 appears to be a viable alternative. The results also suggest that using Target 1 and Target 2 CAR T therapies in succession could lead to positive outcomes. A third alternative is to enhance the T cell design further to allow for tandem targeting; an ideal synergy could be attained if T cells were fitted with both Target 1 and Target 2 receptors, hopefully resulting in longer remission periods and increased survival.

The post CAR T Therapy For Drug Resistant Multiple Myeloma appeared first on Medika Life.

Date of Release: Dec. 5, 2020 

WASHINGTON /PRNewswire/ — Three studies being presented during the 62nd American Society of Hematology (ASH) Annual Meeting and Exposition report promising results in the use of cutting-edge genome editing and cellular therapies for hard-to-treat blood disorders and cancers.

In the first study, researchers used CRISPR/Cas9 to treat two inherited blood disorders, beta thalassemia and sickle cell disease (SCD). The trial, which demonstrated remarkable improvements in all seven participants, is the first time this revolutionary approach has been used successfully in these patient populations.

“Given that the only FDA-approved cure for sickle cell disease, a bone marrow transplant, is not widely accessible, having another curative option would be life-changing for a large number of the sickle cell disease population,” said press briefing moderator Catherine Bollard, MD, of Children’s National Research Institute and George Washington University. “While longer follow-up data are needed, this study is extremely exciting for the field.”

The second two studies point to new opportunities to reach a broader patient population with chimeric antigen receptor T-cell (CAR-T) therapy. While this cellular immunotherapy has dramatically improved outcomes for patients with some blood cancers, it does not work in all patients. One of the new studies offers an explanation as to why some patients do not respond to CD19-CAR-T therapy and suggest a way to overcome this resistance. The other study suggests CD19-CAR-T may be a viable option for some patients with high-risk non-Hodgkin lymphoma who have not responded to standard treatments.

“Getting more data on CD19-CAR-T therapy in the high-risk non-Hodgkin lymphoma population is very important,” said Dr. Bollard. “We know that CD19-CAR-T therapy does not work for some patients, so these studies underscore the need to better understand the immune evasion mechanisms T cells might be susceptible to and not just focus on their role as a vehicle for the CAR. Doing so may improve our capacity to administer effective T-cell immunotherapies.”

This press briefing will take place on Saturday, December 5, at 9:30 a.m. Pacific time on the ASH annual meeting virtual platform.

CRISPR-based Gene Editing Shows Early Promise in First Clinical Trials
4: Safety and Efficacy of CTX001 in Patients with Transfusion-Dependent β- Thalassemia and Sickle Cell Disease: Early Results from the Climb THAL-111 and Climb SCD-121 Studies of Autologous CRISPR-CAS9–Modified CD34+ Hematopoietic Stem and Progenitor Cells

Investigators from across the globe report promising interim safety and efficacy data from 10 patients who received an investigational gene-editing based therapy, CTX001. The trials are the first to test a CRISPR-Cas9 gene editing therapy in humans for a genetic disease, researchers reported.

Sickle cell disease (SCD) can cause a variety of health problems including episodes of severe pain, called vaso-occlusive crises, as well as organ damage and strokes. Patients with transfusion-dependent thalassemia are dependent on blood transfusions from early childhood. The only available cure for both diseases is a bone marrow transplant from a closely related donor, an option that is not available for the vast majority of patients because of difficulty locating matched donors, the cost, and the risk of complications.

In the studies, the researchers’ goal is to functionally cure the blood disorders using CRISPR/Cas9 gene-editing by increasing the production of fetal hemoglobin, which produces normal, healthy red blood cells as opposed to the misshapen cells produced by faulty hemoglobin in the bodies of individuals with the disorders.

The clinical trials involve collecting stem cells from the patients. Researchers edit the stem cells using CRISPR-Cas9 and infuse the gene-modified cells into the patients. Patients remain in the hospital for approximately one month following the infusion.

Prior to receiving their modified cells, the seven patients with beta thalassemia required blood transfusions approximately every three to four weeks and the three patients with SCD suffered episodes of severe pain roughly every other month. All the individuals with beta thalassemia have been transfusion independent since receiving the treatment, a period ranging between two and 18 months. Similarly, none of the individuals with SCD have experienced vaso-occlusive crises since CTX001 infusion. All patients showed a substantial and sustained increase in the production of fetal hemoglobin.

Researchers report that the safety of CTX001 infusion was generally consistent with the chemotherapy regimen received prior to cell infusion. Four serious adverse events related or possibly related to CTX001 were reported in one patient with thalassemia: headache, haemophagocytic lymphohistiocytosis (HLH), acute respiratory distress syndrome, and idiopathic pneumonia syndrome. The patients have now recovered.

“There is a great need to find new therapies for beta thalassemia and sickle cell disease,” said Haydar Frangoul, MD, Medical Director of Pediatric Hematology and Oncology at Sarah Cannon Research Institute, HCA Healthcare’s TriStar Centennial Medical Center. “What we have been able to do through this study is a tremendous achievement. By gene editing the patient’s own stem cells we may have the potential to make this therapy an option for many patients facing these blood diseases.”

Because of the precise way CRISPR-Cas9 gene editing works, Dr. Frangoul suggested the technique could potentially cure or ameliorate a variety of diseases that have genetic origins. 

The trial was sponsored by CRISPR Therapeutics and Vertex Pharmaceuticals.

Haydar Frangoul, MD, The Children’s Hospital at TriStar Centennial and Sarah Cannon Research Institute, will present this study in a plenary presentation on Sunday, December 6, at 7:00a.m. Pacific time on the ASH annual meeting virtual platform. The study will be simultaneously published in the New England Journal of Medicine at the time of the press briefing presentation.

CAR T-Cell Therapy Shows Promise Against High-Risk Non-Hodgkin Lymphoma
700: Primary Analysis of Zuma-5: A Phase 2 Study of Axicabtagene Ciloleucel (Axi-Cel) in Patients with Relapsed/Refractory (R/R) Indolent Non-Hodgkin Lymphoma (iNHL)

The cellular immunotherapy axicabtagene ciloleucel (axi-cel) has dramatically improved the outlook for patients with large B cell lymphoma. In a phase II clinical trial, this therapy brought considerable benefits to patients with non-Hodgkin lymphomas, reducing cancer cells to undetectable levels in nearly 80% of study participants. While non-Hodgkin lymphomas are generally slower growing and less aggressive than large B cell lymphoma, the results suggest axi-cel may be a promising option for patients who have a history of relapse or a lack of response to available therapies. 

“We were very impressed with the magnitude of the responses, and also the durability,” said senior study author Caron Jacobson, MD, of Dana-Farber Cancer Institute. “This treatment has meaningfully affected high-risk patients with these diseases. I was also struck early on by how favorable the safety profile was compared to what we’ve been seeing in the fast-growing lymphomas such as large B cell lymphoma.”

When undergoing axi-cel therapy, a patient’s T cells are removed and genetically altered to express a receptor that seeks and destroys cancer cells. The engineered cells, called chimeric antigen receptor T cells (CAR T cells), are then re-infused into the patient. In previous trials for large B cell lymphoma, the therapy has been shown to reduce cancer cells below detectable levels, described as a complete response, in a substantial portion of patients.

To test the therapy for treating indolent B-cell non-Hodgkin lymphoma, the researchers administered axi-cel to 146 patients with either follicular lymphoma (FL) or marginal zone lymphoma (MZL) at multiple U.S. medical centers. Before the trial, the patients all had continuing lymphoma despite undergoing multiple previous treatments.

Researchers tracked patients for a median of nearly 18 months and analyzed efficacy outcomes among the 84 patients with FL who had at least 12 months of follow-up, and the 20 patients with MZL who had at least one month of follow-up. Overall, 92% of participants achieved an objective response to the treatment and 78% achieved a complete response. By 12 months after their infusion, 72% were still in response. After 17.5 months, 64% were still in response.

All 146 treated patients were analyzed for safety. Almost all patients experienced adverse events, with 86% experiencing adverse events of grade 3 or higher. Seven percent experienced grade 3 or higher cytokine release syndrome, and 19% experienced grade 3 or higher neurologic events. Response rates were slightly higher, and rates of adverse events were slightly lower among patients with FL compared to those with MZL, trends that Dr. Jacobson said may be further illuminated after data become available for a larger number of patients with MZL.

Caron Jacobson, MD, Dana-Farber Cancer Institute, will present this study in an oral presentation on Monday, December 7, at 1:30 p.m. Pacific time on the ASH annual meeting virtual platform.

Study Suggests Opportunity to Personalize Immunotherapy for Patients with Large B Cell Lymphoma
556: CD58 Aberrations Limit Durable Responses to CD19 CAR in Large B Cell Lymphoma Patients Treated with Axicabtagene Ciloleucel but Can be Overcome through Novel CAR Engineering

While the immunotherapy axi-cel has revolutionized treatment for large B cell lymphoma, it does not work for everyone. In a new study, researchers uncovered a likely explanation for why about one-quarter of patients do not respond well to this therapy. The researchers used this information to create a modified version of the treatment that may overcome the problem and make the therapy effective for more patients. 

Axi-cel achieves a complete and lasting response in about 40-50% of patients treated. The treatment involves removing a patient’s T cells and engineering them to express a certain receptor. These engineered cells, called CAR T cells, are then re-infused into the patient, where they use the receptor to seek and destroy cancer cells.

The new study focuses on the role of a protein called CD58 in this process. Analyzing genetic samples from 51 patients treated with axi-cel, the researchers discovered that the tumors of about 25% of the patients lacked a fully functioning version of this protein. In all but one of these patients, the therapy had no lasting effect. The researchers then created a mouse model that lacked CD58 and tested three different CAR-T therapies in the mice. None worked.

Probing the biological mechanisms further, the researchers determined that CD58 helps activate the engineered T cells and assists with the process of killing cancer cells. Without a functional CD58 protein, CAR T cells are less effective. To overcome this problem, the researchers altered the engineering process by adding another protein, called CD2, to fill the role of CD58. Experiments in mice suggest these modified CAR T cells are capable of functioning well without CD58 present.

The researchers said they believe the approach could lead to clinical trials in the next one to two years. If successful, the modified treatment could significantly expand the pool of patients who are likely to benefit from axi-cel therapy.

“Achieving an uptick of 20-25% in the complete response rate would really bring cures to a large number of additional patients,” said senior study author Robbie G. Majzner, MD, of Stanford University School of Medicine. “Ultimately, we could potentially screen patients for CD58 status and provide a more precision approach to this therapy.”

In addition to leading to a next-generation therapy for large B cell lymphoma, the work could have relevance for immunotherapy research more broadly. “CD58 is an emerging biomarker,” said Dr. Majzner. “Endowing immunotherapeutics with the ability to get around CD58 loss may emerge as important for other cancers, as well.”

Robbie G. Majzner, MD, Stanford University School of Medicine, will present this study in an oral presentation on Monday, December 7, at 7:30 a.m. Pacific time on the ASH annual meeting virtual platform.

Additional press briefings will take place throughout the meeting on health disparities, practice-changing clinical trials, COVID-19, and late-breaking abstracts. For the complete annual meeting program and abstracts, visit www.hematology.org/annual-meeting. Follow ASH and #ASH20 on Twitter, Instagram, LinkedIn, and Facebook for the most up-to-date information about the 2020 ASH Annual Meeting.

The American Society of Hematology (ASH) (www.hematology.org) is the world’s largest professional society of hematologists dedicated to furthering the understanding, diagnosis, treatment, and prevention of disorders affecting the blood. For more than 60 years, the Society has led the development of hematology as a discipline by promoting research, patient care, education, training, and advocacy in hematology. ASH publishes Blood (www.bloodjournal.org), the most cited peer-reviewed publication in the field, and Blood Advances (www.bloodadvances.org), an online, peer-reviewed open-access journal.

SOURCE American Society of Hematology

Related Links

www.hematology.org

The post Genome Editing and Cellular Therapies Show Promise for Treating Blood Disorders, Cancers appeared first on Medika Life.