A new multicenter study by researchers at the Icahn School of Medicine at Mount Sinai, in collaboration with the Clinical Proteomic Tumor Analysis Consortium (CPTAC) and colleagues around the world, has discovered that the genes we are born with—known as germline genetic variants—play a powerful, underappreciated role in how cancer develops and behaves.

Published in the April 14 online issue of Cell, the study, “Precision Proteogenomics Reveals Pan-Cancer Impact of Germline Variants,” is the first to detail how millions of inherited genetic differences influence the activity of thousands of proteins within tumors.

Drawing on data from more than 1,000 patients across 10 different cancer types, the research illustrates how a person’s unique genetic makeup can shape the biology of their cancer.

Cells use many complex genetic repair backup systems to fix DNA damage and remain healthy throughout their lives.

A team of CiRA researchers has uncovered the crucial role of EIF3D—a protein translational regulator—in primed pluripotency. The research is published in the journal Science Advances.

According to the central dogma of molecular biology, information flows from DNA to RNA to protein. While much is known about pluripotency —the ability to differentiate into any other cell type in the body and to divide indefinitely—in terms of transcriptional and epigenetic regulation, as well as signal transduction, how protein translation ties these control mechanisms together remains largely underexplored.

To identify genes important for maintaining primed pluripotency—a state poised for differentiating into various cell types in the body, the research team, led by Associate Professor Kazutoshi Takahashi and Assistant Professor Chikako Okubo, began with a genome-wide genetic screen based on CRISPR interference (CRISPRi) that systemically reduces the expression of every single gene in the genome of a pluripotent stem cell (PSC) line.