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Drug resistance is one of the greatest obstacles to effective cancer therapy. Research has shown that cancer cells can use any number of genes and strategies to achieve or acquire resistance to particular therapies. Until recently, scientists have taken a piecemeal approach to understanding the problem of resistance—unraveling individual mechanisms without reaching any kind of overarching theme.

One of the primary limitations to the effectiveness of cancer therapeutics is . This month , Ó³»­´«Ã½ researchers Rick Wilson, Levi Garraway, and colleagues describe their work unraveling drug resistance mechanisms for ALK tyrosine kinase inhibitors in ALK-dependent non-small cell lung cancers. They screened nearly 16,000 corresponding to over 12,000 genes, identifying a range of known mechanisms able to confer resistance to ALK inhibitors, along with new ones including purinergic P2Y receptors (G-protein coupled receptors) acting through Protein Kinase C signaling.

The Ó³»­´«Ã½ of MIT and Harvard has entered into a partnership with Calico around the biology and genetics of aging and early-stage drug discovery. The partnership will support several efforts at the Ó³»­´«Ã½ to advance the understanding of age-related diseases and to propel the translation of these findings into new therapeutics.

Scientists studying the human gut microbiome often analyze stool to measure what’s living in the gut. However, they were uncertain how well those samples represented the microbial make-up of the intestine. Reporting in , a team led by Curtis Huttenhower and Xochitl Morgan of the Ó³»­´«Ã½ and Harvard T. H. Chan School of Public Health used 16S sequencing to compare the microbial composition in stool with that found in the intestines of rhesus macaques. The team discovered that microbial communities found in feces correlated highly with those found in the large intestines and moderately with those of the small intestines, supporting the use of stool in microbiome studies.