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Cultured human cells are the foundation for disease and drug research. Now Whitehead Institute researchers have designed a growth medium that more closely resembles the cells’ environment in the body—and demonstrated that, relative to decades-old recipes that have remained the workhorses of cell culture studies, it significantly alters the cells’ inner workings.

Using red blood cells modified to carry disease-specific antigens, a team of scientists from Whitehead Institute and Boston Children’s Hospital have prevented and alleviated two autoimmune diseases—multiple sclerosis (MS) and type 1 diabetes—in early stage mouse models.  This research is an exciting step toward therapeutics for autoimmune diseases, which affect an estimated 23 million Americans.

Investigators at Whitehead Institute and the Broad Institute have succeeded in identifying the set of essential genes—those required for cellular proliferation and survival—in each of 14 human acute myeloid leukemia (AML) cell lines that had previously been characterized by genome sequencing. By combining their “gene essentiality map” with the existing genomic information, their study revealed liabilities in genetically defined subset of cancers that could be exploited for new therapies.

Parkinson’s disease (PD) and other “synucleinopathies” are known to be linked to the misfolding of alpha-synuclein protein in neurons. Less clear is how this misfolding relates to the growing number of genes implicated in PD through analysis of human genetics. Two new studies from researchers affiliated with Whitehead Institute and Massachusetts Institute of Technology explain how they used a suite of novel biological and computational methods to shed light on the question.

The use of proteasome inhibitors to treat cancer has been greatly limited by the ability of cancer cells to develop resistance to these drugs. But Whitehead Institute researchers have found a mechanism underlying this resistance--a mechanism that naturally occurs in many diverse cancer types and that may expose vulnerabilities to drugs that spur the natural cell-death process.