Our Discoveries

A key mechanism that fuels uncontrolled cell growth is uncovered in yeast

Scientists have long wondered how cancer cells use a protein complex, called TOR, to survive and proliferate in nutrient-poor conditions. Now, CCR researchers have discovered how a protein that is targeted by TOR drives this process, which holds important implications for understanding cancer and some genetic disorders.

amplified TNIK contributes to LSCC progression

Potential therapeutic target for lung squamous cell carcinoma identified

CCR researchers have identified the protein TNIK as a therapeutic target for lung squamous cell carcinoma, the second most common type of lung cancer. Using human lung cancer cells transplanted into preclinical models, researchers found that the cells responded to a pharmacological treatment that inhibited TNIK and also resulted in cell death in the transplanted tumor cells.

Fecal microbiota transplants help patients with advanced melanoma respond to immunotherapy

A collaborative study between the National Cancer Institute (NCI) and the UPMC Hillman Cancer Center at the University of Pittsburgh suggests that fecal microbiota transplants can help patients with advanced melanoma respond to immunotherapy. “Our study is one of the first to demonstrate in patients that altering the composition of the gut microbiome can improve the response to immunotherapy,” says study co-leader Giorgio Trinchieri, M.D., Chief of CCR’s Laboratory of Integrative Cancer Immunology.

New way to address chemoresistance linked to the protein SLFN11

CCR researchers have discovered two complementary roles for the protein Schlafen-11 (SLFN11) in determining patient response to chemotherapy. These findings have implications for how to overcome this resistance and provide new treatment options for patients with small cell lung cancer (SCLC) and many other cancers.

Genetics, not just smoking, influence small cell lung cancer risk

People with mutations in DNA repair genes may be more likely than others to develop small cell lung cancer. Identifying these mutations in patients could help guide treatment decisions.

DNA damage during a critical phase in the cell cycle called G1

New findings show how damaged cells survive the cell cycle

As cells divide and replicate, important safety checkpoints are in place to ensure that most faulty cells with damaged DNA do not survive the cell cycle. In a new twist, CCR researchers discovered how some damaged cells use molecular inertia to drive past these safety checkpoints and continue through the cell cycle.

New insights into what fuels an aggressive form of kidney disease

Researchers have uncovered a key mechanism behind an aggressive form of kidney cancer, whereby cells lacking an important enzyme are unable to replicate and maintain healthy mitochondrial DNA. This results in more genetic abnormalities in the cells, fueling the growth and spread of cancer.

New connection between gut microbes and liver cancer uncovered in mice

Researchers have uncovered a mechanism by which gut microbes can influence the immune response against nearby liver tumors in mice. The new findings could potentially explain why some people with liver or gut diseases, such as primary sclerosing cholangitis and colitis, tend to be more susceptible to cholangiocarcinoma.

Analysis of T cells from melanoma patients uncovers characteristics leading to cancer regression

CCR researchers used state-ot-the-art analytic techniques to determine characteristics of cells used in effective adoptive T cell therapy (ACT) in patients with advanced melanoma. This new information opens the door to manufacturing these cells in the laboratory and using them in immunotherapy for common cancers, including liver, breast, prostate, and colon cancer.

Embryonic stem cells have their own strategy for protecting chromosome ends

According to new research from CCR scientists, embryonic stem cells have a unique way of protecting their telomeres, the structures at the ends of chromosomes that shorten with every cell division. Understanding it could help explain how some cancer cells circumvent the growth limits imposed by the natural shortening of telomeres that occurs as we age.

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