By identifying a protein that disrupts the interplay between two key genetic drivers of pancreatic cancer, researchers from the University of Texas MD Anderson Cancer Center significantly dampened metastasis in preclinical studies with cell lines, genetic mouse models, and human pancreatic tumor tissue. According to results presented during the annual meeting of the American Association for Cancer Research (AACR), held April 10-15, the research team found that by targeting and inhibiting transcription factor CREB1 (cyclic AMP-responsive element binding protein1), they could decouple oncogenic KRAS from mutant tumor suppressor p53—driver genes mutated in most pancreatic cancer patients. “Through such decoupling of mutant KRAS and p53, we can start to ‘divide and conquer’ signaling pathways responsible for tumor maintenance and from those that promote metastasis,” said Michael Kim, MD, Assistant Professor in the Department of Surgical Oncology at MD Anderson.
Radiation Oncologists Met With Congressional Leaders to Reverse CMS Cuts and Provide Equal Access to Care
Radiation oncologists met with Congress to urge leaders to consider how the Medicare and Medicaid Services (CMS) proposal to make significant cuts to radiation oncology facilities could be detrimental to the survival of patients with Read more…
FDA Approves Neoadjuvant Pembrolizumab Combination for Early TNBC Indication
The FDA granted approval to the supplemental biologics license application (sBLA) for pembrolizumab (Keytruda) as neoadjuvant therapy for patients with high-risk early-stage triple-negative breast cancer (TNBC) when given in combination with chemotherapy followed by single-agent Read more…
Recommended TVUS Screening Thresholds May Miss Endometrial Cancer in Black Women
Adherence to current clinical guidelines for the evaluation of postmenopausal bleeding may result in systematic underdiagnosis of endometrial cancer (EC) in Black women, according to a study published online July 15 in JAMA Oncology. Kemi M. Read more…