In the United States, the incarcerated population is aging. About 15% of incarcerated adults, or approximately 175,000 people, are now 55 years or older. As the incarcerated population ages, cancer has become one of the greatest threats to their health. And despite the growing prevalence, cancer outcomes among those incarcerated are worse than for those with no history of incarceration. 

In a new study, Yale researchers investigated the quality of cancer care received by people diagnosed with cancer during and immediately after incarceration — and whether differences in access to care might explain some of the mortality gaps. They found that people who had a cancer diagnosed during a period of incarceration, or shortly after their release, were less likely to receive prompt, guideline-recommended cancer care.

The findings are published in the journal JAMA Network Open. 

Metastatic melanoma cells that have spread to lymph nodes survive by relying on a protein called ferroptosis suppressor protein 1 (FSP1)—a surprising metabolic dependency that could open the door to a new class of cancer treatments, according to a new study led by Harvard T.H. Chan School of Public Health. The researchers say the study not only highlights the therapeutic potential of drugs that inhibit FSP1, but also offers new ways to understand cancer and its vulnerabilities.

Blocking the action in cancer cells of a key protein reduced by up to 80% tumor growth in mice with a common type of lung cancer.

New prostate cancer research from an international team led by the Center for Genetic Epidemiology at the Keck School of Medicine of USC has yielded discoveries that could improve screening and treatment for patients of African ancestry. The scientists identified variants of five genes —ATM, BRCA2, CHEK2, HOXB13 and PALB2—linked in this population to aggressive disease or to cancer that spreads, or metastasizes, to other organs. The study also found a wide range of risk among participants. By combining data on the five specific genes with the polygenic risk score for prostate cancer and information about family history of prostate cancer, the researchers introduced a method that could help identify those most likely to face deadlier forms of the disease.  The research included data and samples from more than 12,000 Black men from North America and Africa. This included over 7,000 prostate cancer cases and a control group of nearly 5,000. Study participants carrying disease-causing variants of these genes were up to six times as likely to develop prostate cancer compared to those without them. Carriers of dangerous genetic variants who also had prostate cancer in their families and polygenic risk scores in the top 10% faced the highest risk of potentially life-threatening disease. Compared to those at average risk, they were seven times more likely to develop prostate cancer, 18 times more likely to have aggressive disease, and 34 times more likely to get metastatic cancer.

 

The gene p53 acts as a tumor suppressor and often is called the ‘guardian of the genome.’ But when p53 mutates, it can flip from protector to promoter of cancer. Gene p53 is mutated in about 50% of human cancers, yet, despite its central role in cancer biology, it has remained unclear whether specific p53 mutations could be used to guide cancer treatment strategies. Bringing new insights into this topic, researchers at Baylor College of Medicine have discovered that certain p53 mutants could be exploited to help fight cancer.

Cancer Research UK and Wellcome Trust-funded scientists at The Institute for Cancer Research, London, find the key point determining how bowel cancer will grow. “Big Bang” moment occurs when bowel cancer cells successfully hide themselves from the immune system. Further research could find which people with bowel cancer will respond to immunotherapies and bowel cancer vaccines in future.