Guillermina (Gigi) Lozano, Ph.D., chair of Genetics at The University of Texas MD Anderson Cancer Center, has been elected to the 2021 class of Fellows of the American Association for Cancer Research (AACR) Academy in recognition of her pioneering work to describe the p53 tumor suppressor pathway, which is undermined in many cancers.
Johns Hopkins Kimmel Cancer Center study co-author Bert Vogelstein, M.D., will present the related talk “Targeting genetic alterations in cancers with immunotherapeutic agents” at 11 a.m., March 1, at the Advances in Genome Biology and Technology (AGBT) conference. More information can be found at: https://www.agbt.org/events/general-meeting/agenda/. NOTE: AGBT provides complimentary press registration to staff and working freelance journalists who wish to cover the meeting. https://www.agbt.org/media/guidelines/
An antioxidant found in green tea may increase levels of p53, a natural anti-cancer protein, known as the “guardian of the genome” for its ability to repair DNA damage or destroy cancerous cells.
A new study describes how cellular survival after radiation exposure depends on behavior of the protein p53 over time. In vulnerable tissues, p53 levels go up and remain high, leading to cell death. In tissues that tend to survive radiation damage, p53 levels oscillate up and down.
Scientists have identified two drugs that are potent against acute myeloid leukemia (AML) when combined, but only weakly effective when used alone. The researchers were able to significantly enhance cancer cell death by jointly administering the drugs that are only partially effective when used as single-agent therapies.
DALLAS – Oct. 29, 2020 – About half of all tumors have mutations of the gene p53, normally responsible for warding off cancer. Now, UT Southwestern scientists have discovered a new role for p53 in its fight against tumors: preventing retrotransposons, or “jumping genes,” from hopping around the human genome. In cells with missing or mutated p53, the team found, retrotransposons move and multiply more than usual. The finding could lead to new ways of detecting or treating cancers with p53 mutations.
In a new article published in the journal Nature Communications, Moffitt Cancer Center researchers describe how the protein TAp63 controls levels of RNA molecules, which subsequently connects the activities of p53 and AKT to promote disease progression.
Research from investigators at Rutgers Cancer Institute of New Jersey shows that a cellular process known as autophagy promotes survival in mouse models by suppressing oxidative stress and a tumor suppressor known as p53.