Researchers are uncovering how circular bits of DNA found in some cancer cells can help tumors evolve and kill.

Best known as a cell cycle regulator, p53 signaling mediates pro and anti-cancer immune responses as well

The Harvard Medical School researcher’s work on the genetic basis of protein coding and production led him to make groundbreaking discoveries in immunology, molecular biology, and cancer genetics.

The agency gave personal genomics company 23andMe the green light to screen samples for breast cancer–related genetic mutations.

When transplanted into mice, tumor genomes evolve differently than they do in patients, study finds.

Instructor, Department of Systems Biology, University of Texas MD Anderson Cancer Center. Age: 38

The transcriptional regulator dampens the immune system’s ability to elicit an antitumor response, a study shows.

Chris Marshall, who pieced together a critical signaling pathway involved in cancer, has passed away at age 66.

The same microRNAs can have opposing roles in cancer.

The tale of p53, a widely studied tumor suppressor gene, illustrates the inventiveness of researchers who turn mishaps into discoveries.

Charles Sawyers, who began his research career just as the genetic details of human oncogenes were emerging, codeveloped Gleevec, the quintessential targeted cancer therapy.

If one out of three people develops cancer, that means two others don’t. Understanding why could lead to insights relevant to prevention and treatment.

In Chapter 12, "Of Mice and Men," author Sue Armstrong recounts the point at which researchers moved from working with p53 in tissue culture to studying the gene in animal models.

Researchers reconstruct the formation of the giant neochromosomes that contribute to some cancers.

Mutations known to increase the risk of developing ovarian and breast cancer may also make carriers susceptible to heart failure.

Some of the highlights from this year’s American Society for Cell Biology meeting, held earlier this week