Chimeric antigen receptor (CAR) T cell therapy, in which a patient’s own immune T cells are genetically engineered to target their cancer cells, is one of the most promising advances in cancer therapy of the past decade. Having demonstrated the effectiveness of CAR T cells against a range of blood cancers, researchers now seek to design CAR T cells that can remain active in the body for longer and more efficiently eliminate tumors, with the goal of reducing costs and bringing CAR T therapy to more patients.

Cell adhesion molecules (CAMs) are proteins found on the cell surface that facilitate interactions between cells. They are responsible for organizing and binding cells within tissue structures, creating circuits between neurons, and chaperoning immune cells to their destinations. Known as “cellular glue” and essential for organ function, CAMs are found throughout the body. And now, a synthetic version of these molecules (synCAMs) can be found in the Cell Design Institute of the University of California, San Francisco, where Damon Runyon Fellow Adam J.

Small-cell lung cancer (SCLC), which accounts for about 15% of lung cancer diagnoses, is a relatively rare but aggressive disease. Most SCLC patients respond to chemotherapy at first, but nearly all experience disease recurrence, and at that point treatment options become scarce. Because SCLC is driven by mutations that knock out “tumor suppressor” genes, rather than activate cancer driver genes, it has been difficult to treat with targeted therapies. (Consider how much harder it is to edit writing that contains no mistakes but has had all its best phrases erased.)

Myeloproliferative neoplasms (MPNs) are cancers that arise when a mutated blood stem cell begins to produce too many mature blood cells. A number of mutations can drive MPNs, and studies have demonstrated that different mutations result in different clinical outcomes.

Thanks to research by Damon Runyon scientists Melody Smith, MD, Elizabeth Hughes, PhD, and many others, the impact of gut bacteria on cancer immunotherapy response is becoming clearer. The presence of certain bacteria, such as Akkermansia muciniphila, in patient stool samples has been shown to correlate with better response to immunotherapies, suggesting that these microbes play a pivotal role in stimulating immune response.

Pancreatic cancers are notoriously resistant to treatment, in part because more than 90% of tumors are driven by mutations in the notorious KRAS gene. Once considered an “undruggable” cancer target, the first KRAS inhibitors are now making their way into clinics, but so far therapies have only been approved for the treatment of lung cancer. In the meantime, the best hope for stopping pancreatic cancer may be to inhibit the signaling pathways activated by mutant KRAS proteins, namely the KRAS–MAPK pathway, which controls cell growth and division.

We are delighted to announce that former Damon Runyon-Illini 4000 Fellow Daniel J. Blair, PhD, of St. Jude Children’s Research Hospital, has been named a 2022 STAT Wunderkind. This award, granted annually to “the best early-career researchers in health and medicine in North America,” recognizes Dr. Blair’s exceptional promise in the field of synthetic chemistry.

In 2018, the Foundation for the National Institutes of Health (FNIH) established the FNIH Trailblazer Prize for Clinician-Scientists to recognize “the outstanding contributions of early career clinician-scientists” whose research “translates basic scientific observations into new paradigm-shifting approaches for diagnosing, preventing, treating or curing disease.” 

Each year, the Damon Runyon-Jake Wetchler Award for Pediatric Innovation is given to a third-year Damon Runyon Fellow whose research has the greatest potential to impact the prevention, diagnosis, or treatment of pediatric cancer. This year, the award recognizes the work of Anand G. Patel, MD, PhD, a Damon Runyon-Sohn Pediatric Cancer Fellow at St. Jude Children's Research Hospital. As a physician-scientist, Dr. Patel both provides care for children with cancer and their families and investigates ways to improve their treatment options.

Chimeric antigen receptor (CAR) T cell therapy, in which a patient’s own immune cells are genetically engineered to target cancer cells, has revolutionized the treatment of certain blood cancers. Unfortunately, CAR T cell therapy is much less effective against solid tumors, such as pancreatic or skin cancer. Part of the problem in these cases is that the genetically altered T cells quickly become dysfunctional; even those that exhibit a strong anti-tumor response at first soon reach a state of exhaustion. At the University of California, Los Angeles, Damon Runyon Clinical Investigator Anusha Kalbasi, MD, and his colleagues are investigating how to make these T cells last longer to better treat melanoma and other deadly solid tumors. Recently, they had a breakthrough.