Media Coverage (Cell Dynamics)

Researchers from ISB’s Wei and Heath labs show that cancer cells can quickly reprogram themselves in response to treatment, using epigenetic changes to survive drugs — revealing that resistance may begin much earlier than previously understood.

ISB’s Dr. Wei Wei contributed to research showing that certain lung cancers can shift identity and exist in hybrid states, helping explain treatment resistance and suggesting new approaches to diagnosis and therapy for these aggressive, often underdiagnosed tumors.

ISB’s Cory Funk is a guest on the Optispan podcast, and sifts through why hundreds of Alzheimer’s drugs have missed the mark – and what actually moves the needle – turning hard lessons into practical takeaways for patients, clinicians, and researchers.

In this hour-long video interview, Sui Huang discusses his paradigm-changing ideas for how we understand cancer and how they can influence how the disease is treated.

Research from the Heath and Wei labs has uncovered the rapid cellular mechanisms that melanoma cells employ to develop resistance to the cancer drug vemurafenib. By closely examining the initial hours and days after drug exposure, the study reveals how cancer cells activate a backup communication system to bypass the drug’s effects, suggesting potential new combination treatment strategies to overcome this resistance.

Work out of the Heath and Wei labs identified a survival mechanism that allows melanoma cells to quickly evade BRAF inhibitor treatments, and a reversible adaptation that can occur within hours of the first treatment and does not rely on reactivating the BRAF-ERK pathway.

The Wei and Heath labs and collaborators from MIT have uncovered a stealth survival strategy that melanoma cells use to evade targeted therapy, offering a promising new approach to improving treatment outcomes.

Sui Huang challenges the prevailing view of cancer as purely genetic. Huang and colleagues argue that many cancers lack identifiable driver mutations, suggesting non-genetic factors and disrupted gene regulatory networks may play crucial roles in cancer development.