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Archive - Feb 2020

Date

February 2nd

Laura van’t Veer, Inventor of Agendia’s MammaPrint Breast Cancer Assay, Honored with Luminary Award at Precision Medicine World Conference (PMWC 2020)

Laura van ‘t Veer (photo here, also see more photos at end), PhD, Co-Founder of Agendia Inc. and developer of MammaPrint, the 70-gene risk of recurrence assay for breast cancer patients, was recognized by the Precision Medicine World Conference (PMWC) with the PMWC Luminary Award on January 21, 2020. This award recognizes individuals who have made significant contributions to accelerate personalized medicine within the clinical setting. As a Professor of Laboratory Medicine and Director of Applied Genomics at the University California San Francisco (UCSF) Helen Diller Family Comprehensive Cancer Center, Dr. van ‘t Veer is committed to translational medicine that aims to leverage the genomic makeup of patient tumors and improve their clinical outcomes. Dr. van ‘t Veer has authored more than 280 peer-reviewed scientific articles and is a co-inventor on 6 patents. In 2007, she received the European Society of Medical Oncology (ESMO) life-time achievement award for translational research in breast cancer, in 2014 the European Union Women Innovator Award, and in 2015 the EPO European Inventor award. In 2019, she was recognized by 24/7 Wall Street as one of “32 Amazing Women Inventors.” Currently, Dr. van ‘t Veer serves as the Biomarker Committee Chair for the Quantum Leap Healthcare Collaborative (QLHC)-sponsored I-SPY 2 adaptive clinical trial. By using genomic information obtained from participating patients, this trial seeks to elucidate how different tumors will respond to novel drug regimens, thus improving patient outcomes. At the PMWC Awards Reception, Dr. van’t Veer was introduced by Agendia CEO Mark Straley. Tal Bahar Co-Founder and President, PMWC commented, “We are delighted to have Dr.

February 2nd

Recurrent Mutations in Splicing Factor (SRSF2) Gene Cause Excessive Nonsense-Mediated Decay (NMD) and May Cause Many Different Blood Cancers

A genetic mutation that disrupts how DNA sends messages to the rest of a cell has been linked to a large number of blood cancers. Thanks to a collaboration between biologists at Cold Spring Harbor Laboratory (CSHL) and an oncologist at Memorial Sloan Kettering Cancer Center (MSKCC), we now know how the mutation triggers a chain of biological events that lead to most leukemias. The deadly chain of events begins with RNA splicing, a process that converts messages from DNA into instructions for making proteins in a cell. Errors in RNA splicing can result in poorly formed proteins that are unable to do their job. The CSHL-MSKCC team found that in blood cancers, a process associated with splicing called nonsense-mediated mRNA decay (NMD) is excessively active. After splicing converts DNA messages, the NMD process normally serves as "quality control," destroying messages that contain mistakes before a broken protein is made. The laboratory of Adrian Kraimer (photo), PhD, at CSHL determined that when the gene called SRSF2 is mutated, NMD destroys many more messages, including some that have not been likely targets of NMD before. Messages that are important for healthy blood cell production are one of these new targets. The result of excessively active NMD is less healthy blood cells and more sickly or immature cells--a hallmark of blood cancer. "RNA splicing factor mutations are seen in virtually all forms of leukemia, both chronic as well as acute myeloid leukemias and also even chronic lymphocytic leukemia," said Omar Abdel-Wahab, MD, at MSKCC. "I'm a hematological oncologist--I think a lot about blood cancer--so this caught my attention right away." Scientists have seen other cancers manipulate NMD into protecting solid tumors.

February 1st

Penn Doctor Chases Cure for His Own Rare Disease (Castleman Disease); One in Ten Have a Rare Diseae (Over 7,000 Rare Diseases), But for 95% of These Diseases, There Is Not a Single FDA-Approved Drug

In the introduction to his memoir “Chasing My Cure: A Doctor’s Race to Turn Hope Into Action (https://chasingmycure.com/), Dr. David Fajgenbaum discussed how he learned that “hope cannot be a passive concept.” “It’s a choice and a force,” he wrote. “Hoping for something takes more than casting out a wish to the universe and waiting for it to occur. Hope should inspire action. And when it does inspire action in medicine and science, that hope can become a reality, beyond your wildest dreams.” Hope is something Dr. Fajgenbaum, 34, an Assistant Professor of Medicine at The Perelman School Of Medicine at the University of Pennsylvania, knows Intimately. He’s been in hospital rooms as a patient and a doctor — seeing both sides of what it’s like to diagnose and be diagnosed with a deadly disease. He knows what it’s like to experience radical ups and downs in his own health and see others go through the same thing. His life changed in 2010 while he was a third-year medical student at the same university where he now works. He began noticing strange, sudden shifts in his health — from night sweats to fatigue. Within several weeks, his organs were failing, and in November of that year, he was read his last rites. What was wrong? Dr. Fajgenbaum received a very rare diagnosis: Castleman disease (https://www.healthline.com/health/castleman-disease), an immune disorder that results in an overgrowth of cells in the lymph nodes. While not a form of cancer, the condition is often initially confused with a cancer diagnosis. The lymph nodes generally tied to the condition are those found in the neck, underarm, groin, and collarbone. For Dr.

Researchers Identify Possible New Combination Treatment for Advanced Melanoma

A study by researchers at the UCLA Jonsson Comprehensive Cancer Center and coleagues suggests that using an immunotherapy drug called NKTR-214, also known as bempegaldesleukin, in combination with an infusion of anti-tumor immune cells (T cells), may produce a stronger immune response that could help fight advanced melanoma. When tested in mice with melanoma tumors that were unlikely to stimulate an immune response, the approach increased the number of anti-tumor immune cells, and those immune cells lived longer and functioned better than the standard therapy, empowering the cells to destroy the tumor. Adoptive cell therapy is a type of immunotherapy that has had promising results for treating people with advanced cancers. The approach involves extracting and harvesting immune cells from a patient and engineering them in the laboratory to attack specific antigens on the surface of tumors. One challenge is that it requires giving patients interleukin 2, a protein signaling molecule in the immune system, to promote the development and expansion of the infused immune cells. But interleukin 2 can also activate cells to suppress the immune system, and because it is highly toxic, it can have serious adverse side effects. Researchers have been seeking ways to produce large number of immune cells without exposing patients to those negative side effects — including by combining adoptive cell therapy with other treatments. In this study, researchers used mice to test NKTR-214 in combination with adoptive cell therapy. Using bioluminescence imaging, the researchers tracked the movement of T cells in the mice that received the combination therapy. The team observed an expansion of T cells in the spleen, the organ that helps accelerate the activation and expansion of T cells throughout the body.

In Study of IL-1Beta, UCLA Researchers Find Chronic Inflammation Contributes to Cancer Metastasis

A recent study by UCLA researchers has revealed a detailed epigenetic mechanism for how interleukin-1-beta, a common cytokine that helps fight infections during inflammation, plays a critical role in cancer metastasis. The researchers found that chronic exposure to interleukin-1beta can promote lung cancer metastasis through inheritable changes of gene expression without altering DNA sequence. Because of these gene alterations, cancer cells can memorize this phenotype -- known as epithelial-to-mesenchymal transition, an important step during cancer metastasis -- to successfully reach distance organs and subsequently colonize. Lung cancer remains the most lethal cancer type in the United States. The vast majority of people with lung cancer die from tumor reoccurrence or metastasis. Therefore, one of the biggest challenges in treating cancer is stopping it from metastasizing to other parts of the body. Scientists have known that chronic inflammation facilities tumor progression, but how this process leads to the spread of cancer is not well elucidated. Previous research has showed interleukin-1beta is correlated with poor survival in people with non-small cell lung cancer (NSCLC) and exposure of this cytokine prompts the expression of genes that are often involved in invasion during metastasis in multiple cancers. The UCLA team enhanced the understanding of the process by studying the role of chronic interleukin-1beta exposure in the epithelial-to-mesenchymal transition. The researchers investigated the role of interleukin-1beta in lung cancer metastasis by looking at in vitro models of lung cancer to help provide insight into the cells' behaviors. They specifically examined whether interleukin-1beta induced epithelial-to-mesenchymal transition in lung cancer cells.