In the quest to solve cancer’s mysteries, they come in handy when describing tongue-twisting processes and pathways that somehow allow tumors to form and thrive. Two examples are ERK (extracellular-signal-related kinase) and JNK (c-June N-Terminal Kinase), enzymes that may offer unexpected solutions for treating some endometrial and colon cancers.
A study led by Gordon Mills, M.D., Ph.D., professor and chair of Systems Biology at The University of Texas MD Anderson Cancer Center with Lydia Cheung, Ph.D. as the first author, points to cellular mutations in the gene PIK3R1 which activate ERK and JNK, thus allowing tumor growth. Results from the study, were published in this month’s issue of Cancer Cell.
The PIK3R1 gene has been thought to impact the PI3K pathway since its discovery over two decades ago. The PI3K signaling pathway has long been known to play a role in cancer cell proliferation, and targeting why and how PI3K allows tumor cells to grow has been an important area of study and treatment.
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