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This Week in Cell: Feb 8, 2017

A Massachusetts Institute of Technology-led team catalog essential genes in more than a dozen human acute myeloid leukemia (AML) cell lines. With the help of genome-wide CRISPR-based screening, the researchers tallied gene essentiality in 14 AML lines, defining essential genes, genes that were required only in the lines with mutant Ras oncogene activity, and genes with overlapping biological functions that could not be inactivated at the same time. "It should be possible to apply the approaches we describe to systematically map functional gene networks in mammalian cells and identify targetable liabilities in human cancers," they write.

Small insertions and deletion (indel) hotspots tend to turn up in genes with lineage-specific functions in several human cancer types, according to a paper by researchers from Weill Cornell Medicine, Harvard Medical School, and elsewhere. Starting with whole-genome sequence data for dozens of lung adenocarcinoma samples, the team uncovered indel hotspots in and around genes such as SFTPA1 that code for surfactant proteins. Likewise, data from other solid tumor types, including liver, stomach, or thyroid carcinomas, led to indel hotspots near genes related to secretory protein production in each tissue or lineage type.

A Stanford University team describes differences in the ability of the human apolipoprotein E isoforms ApoE2, ApoE3, and ApoE4 in activating a non-canonical MAP kinase signaling cascade that leads to an uptick in amyloid-beta precursor transcription and synthesis of amyloid-beta protein. Based on their findings in human neurons derived from embryonic stem cells and other experimental systems, the researchers found that the ApoE4 isoform, implicated in Alzheimer's disease risk, stimulated this pathway more effectively than the neutral risk isoform ApoE3 or the protective isoform ApoE2.