New Discoveries and Honors

The University of Texas MD Anderson Cancer Center, where former Damon Runyon Clinical Investigator Cassian Yee, MD, runs his lab, is home to the Moon Shots program, a cancer research initiative inspired by America's drive toward space in the 1960s. Recently, Dr. Yee and his colleagues announced a project that combines these two ambitions: sending T cells into space to inform the development of new cancer treatments.

Lung cancer is the leading cause of cancer death in the United States, and nearly a third of these cancers are driven by mutations in the KRAS gene. Long considered an “undruggable” cancer target, mutant KRAS proteins are known to rewire alveolar type II progenitor (AT2) cells, which line the lung surface and are responsible for repairing lung tissue after injury.

Although many childhood cancers are now curable with chemotherapy, these lifesaving treatments often carry serious long-term side effects. Studies have shown, for example, that childhood cancer survivors are fifteen times more likely than the general population to suffer from congestive heart failure.  For patients and pediatric oncologists, the toxicity of chemotherapy drugs is tolerated only because there are no better options—in the United States, that is.

In cancer treatment, “targeted therapies” refer to drugs that identify and attack specific proteins in cancer cells that help them survive and grow, while leaving normal cells alone. Due to their specificity, targeted therapies tend to be less toxic than chemotherapy or radiation therapies. Often, they take the form of small molecule inhibitors, which bind to the cancer-promoting proteins and disable them. Unfortunately, however, small molecule inhibitors only work for a subset of cancers.

Few scientific studies meet with more controversy than those that suggest a substance may cause or prevent cancer. As a leading epidemiologist of colorectal cancer, former Damon Runyon Clinical Investigator Andrew T. Chan, MD, MPH, is no stranger to this rollercoaster.

Adoptive T cell therapies, in which a patient’s own immune cells are genetically engineered to target their cancer cells, have been remarkably effective in treating certain blood cancers. Unfortunately, this success has not translated to solid tumors, where T cells face unique challenges in the tumor environment that limit their persistence and function.

Some cancer cells, such as those in lung tumors, change drastically in appearance and behavior when they develop resistance to targeted therapies. The result of these changes, collectively known as histological transformation (HT), is a more aggressive tumor type. HT necessitates a new therapeutic strategy, since the original oncogene is no longer driving the tumor’s spread.

Blood stem cells, like all living things, lose their regenerative capacity with age. Because blood stem cells generate not only blood but all the cells in our immune system, age-related dysfunction can lead to a plethora of systemic issues in older adults, including blood cancer. There is, of course, no stopping time. But according to a new study from researchers at the Columbia Stem Cell Initiative, including Damon Runyon Fellow James Swann, VetMB, DPhil, there may be a way to slow down the clock.

One in eight women in the U.S. will develop breast cancer during their lifetime, and for many, the best treatment option is surgical removal of the tumor, known as a lumpectomy. Unfortunately, the surgical tools currently in use do not always accurately identify the extent of the tumor, necessitating a second surgery for up to a third of patients.

Prostate cancer is a disease with many subtypes, some of which are more difficult to treat than others. While most prostate cancer cells rely on androgen hormones to grow—allowing androgen blockers to emerge as an effective therapy—15 to 20 percent of prostate cancers evolve to be “androgen-independent.” One such subtype is known as castration-resistant neuroendocrine prostate cancer (CRPC-NE), for which chemotherapy is the primary treatment strategy.

A tissue biopsy, in which a section of skin is surgically removed for microscopic evaluation, has long been the most effective means of diagnosing skin cancer. But biopsies are invasive and time-consuming procedures, with patients often waiting days for results, developing scars, or forgoing biopsy altogether and opting to “wait and see.” Given that one in five Americans will develop skin cancer in their lifetime, this is a dilemma many of us have experienced firsthand.

Immunotherapies to treat pancreatic cancer—a disease with a nearly 90 percent mortality rate—have been the subject of intensive research efforts in recent years, largely because they have succeeded where other treatment approaches have failed. New developments in mRNA vaccines, immune-enhancing therapies, and combination immunotherapy-chemotherapy regimens have marked a new era in pancreatic cancer treatment. But still, for many patients, nothing seems to work.

Just as the study of a growing plant or animal must take into account its environment, cancer researchers must look beyond a tumor to understand how the surrounding tissue impacts its development. In the case of gliomas, the most common and aggressive type of brain tumor, this means looking at neurons—what signals they emit, and how these signals may play a role in brain tumor progression.  

Renal cell carcinoma ranks among the top ten most common cancers globally, with the clear cell subtype (ccRCC) accounting for the majority of metastatic cases. While some ccRCC tumors respond to immunotherapy treatment, it is often difficult to predict which patients will benefit.

Only about one percent of the human genome contains what we recognize as protein-coding genes: DNA sequences that are transcribed into RNA sequences and then translated into proteins. Much of the intervening space between genes consists of mobile DNA sequences, known as transposable elements, which have the ability to “copy and paste” themselves throughout the genome.

Metastatic pancreatic cancer is often resistant to chemotherapy-based treatments, and clinicians do not currently have a good way to predict whether a patient’s cancer will respond or not. At the Abramson Cancer Center of the University of Pennsylvania, former Damon Runyon-Rachleff Innovator Gregory L. Beatty, MD, PhD, and his colleagues are seeking to uncover the factors that determine response so that patients and clinicians can make better informed treatment decisions.