Time: 2024-11-14
research_worker at the National Institutes of Health ( NIH ) have make a groundbreaking discovery in understanding how RAS gene, commonly mutate in cancer, drive tumor growth. The survey, print in Nature Cancer on Nov. 11, 2024, uncover that mutant RAS protein play a crucial function in transport particular nuclear protein, lead to uncontrolled tumor growth. RAS gene are know to be the second most frequently mutate gene in cancer, drive some of the deadly cancer such as pancreatic, colorectal, and lung cancers.
The survey, light-emitting_diode by Dr. Douglas Lowy, the deputy director of NIH's National Cancer Institute ( NCI ), shed light on a new nerve_pathway through which mutant RAS gene promote cancer growth. By let_go_of a nuclear protein name EZH2 from a complex that is transport from the nucleus to the cytoplasm, mutant RAS protein facilitate the dislocation of a tumor suppressor protein know as DLC1. blocking mutant RAS can prevent EZH2 from being let_go_of, thereby restore the activity of DLC1.
The research_worker found that combining RAS inhibitor with target cancer drug that reactivate DLC1's tumor suppressor activity have a potent consequence on cancer cell, more so than RAS inhibitor alone. This discovery open up new possibility for development treatment combination that target the extra function of mutant RAS protein in drive tumor growth. The survey also propose that this mechanism may be a park feature in cancer with mutate RAS gene, supply new penetration into potential treatment scheme for different cancer types.
The findings of this survey rich_person excite deduction for better cancer treatment result. The research_worker are now research how this new function of RAS protein can be use to development effective treatment for RAS-drive cancer, particularly in pancreatic cancer where treatment option are express. By understanding the intricate mechanism through which Mutant protein lend to tumor growth, new avenue for target therapy and personalize medicine may be develop to combat the lay_waste_to effects of neoplasms.