Cancer

Scientists have applied a new method of analyzing cell states to identify a gene required for breast stem cells to differentiate. This gene, RUNX1, is deregulated or mutated in some leukemias and breast cancers. The novel approach, known as PEACS, could also be used to screen for drugs that activate or inhibit the expression regulators of stem cell differentiation.

A novel approach that allows real-time imaging of the immune system’s response to the presence of tumors—without the need for blood draws or invasive biopsies—offers a potential breakthrough both in diagnostics and in the ability to monitor efficacy of cancer therapies.

Biologists at Whitehead Institute and MIT have discovered a vulnerability of brain cancer cells that could be exploited to develop more-effective drugs against brain tumors.

A widely conserved family of RNA-binding proteins known to be expressed in neural stem cells and other stem cell types has now been shown to play a role in controlling both the state and behavior of breast cancer cells.

Long known for its ability to help organisms successfully adapt to environmentally stressful conditions, the highly conserved molecular chaperone heat-shock protein 90 (HSP90) also enables estrogen receptor-positive (ER+) breast cancers to develop resistance to hormonal therapy.  

Metastatic cancer cells, which can migrate from primary tumors to seed new malignancies, have thus far been resistant to the current arsenal of anticancer drugs. Now, however, researchers at Whitehead Institute have identified a critical weakness that actually exploits one of these cells’ apparent strengths—their ability to move and invade tissues. Their research could inform novel approaches to screening tumors for personalized therapy or to drugs that specifically target these cells.

Whitehead Institute scientists have identified a genetic cause of a facial disorder known as hemifacial microsomia (HFM). The researchers find that duplication of the gene OTX2 induces HFM, the second-most common facial anomaly after cleft lip and palate.

Scientists at Whitehead Institute have pinpointed a major mitochondrial pathway that imbues cancer cells with the ability to survive in low-glucose environments. By identifying cancer cells with defects in this pathway or with impaired glucose utilization, the scientists can predict which tumors will be sensitive to these anti-diabetic drugs known to inhibit this pathway.

Having recently discovered a set of powerful gene regulators that control cell identity in a few mouse and human cell types, Whitehead Institute scientists are now showing that these regulators—which they named “super-enhancers”—act across a vast array of human cell types and are enriched in mutated regions of the genome that are closely associated with a broad spectrum of diseases.

Protein production or translation is tightly coupled to a highly conserved stress response—the heat shock response and its primary regulator, heat shock factor 1 (HSF1)—that cancer cells rely on for survival and proliferation, according to Whitehead Institute researchers. In mouse models of cancer, therapeutic inhibition of translation interrupts HSF1’s activity, dramatically slowing tumor growth and potentially rendering drug-resistant tumors responsive to other therapies.