#Rutgers office for mac mac
The authors note these findings strongly implicate FILIP1L as an essential regulator of MAC tumor development.
These defects mirror the same characteristics that are seen in the aggressive form of MAC. This breakdown results in abnormal stabilization of PFDN1 leading to elevated mucin secretion and defects in cell division in colon cancer cells. They also demonstrated that FILIP1L stimulates degradation of a molecular chaperone protein known as PFDN1. Using mouse models, investigators in this study demonstrated that loss of a tumor suppressor protein known as FILIP1L induces colonic epithelial hyperplasia and mucin secretion. What drives the formation of MAC tumors is currently unknown and underexplored. It is characterized by the excess secretion of the protein known as mucin and has an entirely different molecular signature – or biological behavior – than classic CRC. MAC is a distinct and aggressive form of CRC, accounting for 10 to 15 percent of patients ( Nat Rev Clin Oncol, June 2016). New Brunswick, N.J., August 25, 2021 – Researchers from Rutgers Cancer Institute of New Jersey, the state’s only National Cancer Institute-designated Comprehensive Cancer Center, recently discovered a mechanism to explain what drives the formation of mucinous colorectal adenocarcinoma (MAC), a rare subtype of colorectal cancer (CRC), and has also identified the genes responsible for the regulation of this mechanism. The OnlineFirst version of this work was published August 20 in Cancer Research (DOI: 10.1158/0008-5472.CAN-21-0897).Īccording to the American Cancer Society, colorectal cancer (CRC) is the third leading cause of cancer-related death in men and women in the United States.
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