PNAS: scientists are expected to successfully block cancer progression

February 2, 2020 news / Biovalley BIOON / -- myc is a protein family composed of three related proteins, which will be overexpressed in cancer, and about 100000 people die of cancer every year in the United States; in recent years, researchers have not succeeded in blocking Myc, but fortunately, these proteins have a disadvantage, namely, the chromosome binding cofactor named wdr5 Photo source: National Institutes of health understands the mechanism of Myc, wdr5 and other cofactors or can help develop new drugs to effectively block myc's function and cancer progress Recently, an international journal Proceedings of the National Academy of Sciences was published entitled "interaction of the oncoprotein transcription factor myc with its chromium." In the Research Report of cofactor wdr5 is essential for more maintenance, scientists from Vanderbilt University and other institutions found that interfering with the interaction between myc and wdr5 in the process of cancer growth can promote the rapid and comprehensive decline of tumor Tansey said that if the interaction between myc and wdr5 can be an effective treatment, we may need to know whether destroying the interaction between myc and wdr5 in a cancer model can affect tumor growth Using a laboratory grown model of Burkitt's lymphoma, a non-Hodgkin's lymphoma or immune cell cancer, the researchers found that breaking the link between myc and wdr5 might promote the disappearance of the tumor In 2015, researchers revealed the crystal structure of interaction between myc and wdr5 through joint research Based on the results of this study, later researchers will develop new drugs that can target myc through wdr5 through joint research Original source: Lance R Thomas, Clare M Adams, Jing Wang, et al Interaction of the oncoprotein transcription factor myc with its chromium cofactor wdr5 is essential for more maintenance, Proceedings of the National Academy of Sciences (2019) Doi: 10.1073/pnas.1910391116