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Making cancer less cancerous

"This master regulator is normally turned off in adult cells, but it is very active during embryonic development and in all highly aggressive tumors studied to date," says Linda Resar, M.D., an associate professor of medicine, oncology and pediatrics, and affiliate in the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. "Our work shows for the first time that switching this gene off in aggressive cancer cells dramatically changes their appearance and behavior." A description of the experiments appears in the May 2 issue of the journal PLOS ONE…

New target for personalized cancer therapy

The research team has pinpointed the cancer abnormality to a mutation in a gene called PIK3CA that results in a mutant protein, which may be an early cancer switch. By disrupting the mutated signaling pathway, the Case Western Reserve team, led by John Wang, PhD, inhibited the growth of cancer cells, opening the possibility to new cancer therapies. Their findings, "Gain of interaction with IRS1 by p110 helical domain mutants is crucial for their oncogenic functions," was published on May 2 in the journal Cancer Cell. Cancer arises from a single cell, which has mutated in a small number of genes because of random errors in the DNA replication process…