Broad Institute of MIT and Harvard

02/09/2026

A genetic test from Broad Clinical Labs (BCL) and the US Department of Veterans Affairs is enabling a large, nationwide clinical trial on prostate cancer. Developed by Jason Vassy, Niall Lennon, Tyler Seibert (UCSD), and others, the low-cost test uses BCL’s clinical blended genome-exome method to measure both rare and common genetic risk factors. The trial, led by VA researchers, is enrolling 5,000 veterans nationally to explore whether the test can help men at high risk get diagnosed earlier and help those at low risk avoid unnecessary biopsies.

The low-cost method, from Broad Clinical Labs and VA scientists, could potentially identify men at high risk who may benefit from earlier prostate cancer screening.

02/03/2026

Please note: the Broad Discovery Center will be closed on Thursday, February 5 for a special event.

01/29/2026

Physician scientist Anna Greka, a core institute member at the Broad Institute, is on a mission to find and cure genetic diseases that collectively impact millions of people in the U.S. Shared drug targets, called "nodes," underlie many of these genetic disorders. Hear from her on how targeting these nodes unlocks the potential to treat multiple genetic diseases with the same drug, and how her patients motivate her every day.

01/28/2026

Our genetics play a role in determining the microbial community living in our mouths, according to a new study that analyzed over 12,500 oral microbiome profiles. The work led by Broad and Mass General Brigham scientists uncovers 11 regions of the human genome associated with different levels of bacteria species in the mouth — including a link between a genetic variation and the microbial community that is tied to dental health.

Given how strong of an effect genetics has on our resident bacteria, the researchers hope their work leads to more discoveries about our DNA’s connection to the microbiome.

Analysis of the now largest collection of oral microbiome profiles reveals interactions between human and bacterial DNA.

01/26/2026

After training an AI model on sections of DNA that regulate gene expression, researchers at Broad and Mass General Brigham found that the new model, called DNA-Diffusion, successfully created short DNA sequences that can turn genes on or off in specific cells.

To test the technology’s therapeutic potential, the researchers targeted a gene that protects against chronic lymphocytic leukemia that is often turned off in patients with the disease. They found that many of the AI generated sequences effectively switched on the gene, even more so than their natural counterparts.

The generative AI model designed sequences that successfully reactivated a protective gene in leukemia cell lines.

01/16/2026

Over the last decade, Broad researchers have identified a variant of the CARD9 gene as protective in inflammatory bowel disease (IBD) and discovered its mechanism. Now, they have developed small-molecule drug candidates that mimic the effects of this rare gene variant and could potentially treat IBD. This human genetics-to-therapeutics pipeline can be applied to other challenging drug targets and diseases.

The molecules mimic a gene variant that protects against Crohn’s, demonstrating a roadmap for using genetics to develop therapies for inflammatory bowel disease and other chronic inflammatory disorders.

01/12/2026

New research from Broad and has uncovered a key biological pathway behind fibrosis, or tissue scarring, in inflammatory bowel disease (IBD). When inflammation goes unchecked, it can trigger scarring that leads to organ dysfunction—or even failure—yet patients currently have few treatment options.

Now, scientists have identified the molecular roots of fibrosis. They discovered a specific “crosstalk” between specific types of cells that leads to tissue scarring. The team also identified GLIS3 as the “master regulator” of this messaging.

The study points to possible new therapeutic strategies, such as targeting the GLIS3 pathway.

01/08/2026

Please note: the Broad Discovery Center will be closed on Saturday, January 10, 2026 due to building maintenance.

01/07/2026

Fibrosis, or damaging tissue scarring, occurs in many inflammatory diseases and can lead to organ dysfunction or failure. Ramnik Xavier, Dan Graham, and colleagues characterized the crosstalk between immune cells and fibroblasts that leads to fibrosis in inflammatory bowel disease. They identified a master regulator, the transcription factor GLIS3, that mediates the cell-to-cell communication. Interrupting this cellular pathway could help prevent or reduce fibrosis in patients with IBD or other diseases of chronic inflammation.

New study finds a biological pathway responsible for dangerous scarring, which could possibly be targeted by new treatments.

12/17/2025

Our immune system loses its ability to fight infection with age. To try to overcome this decline, Feng Zhang and colleagues have found a way to temporarily program cells in the liver to produce specific molecules that improve T-cell function. They used mRNA to deliver three key factors to the liver that promote T-cell survival. Treated animals showed much larger and more diverse T cell populations in response to vaccination, and also responded better to cancer immunotherapy treatments.

Stimulating the liver to produce some of the signals of the thymus can reverse age-related declines in T-cell populations and enhance response to vaccination.

12/10/2025

Friedreich’s ataxia, a rare but devastating genetic disorder, occurs due to loss of the key mitochondrial protein, frataxin. Now, scientists at Broad and Mass General Brigham, with support from the Friedreich’s Ataxia Research Alliance, have used the power of worm genetics to discover a new potential drug target for FA, suggesting a path for developing new medicines. They found that certain mutations in the mitochondrial gene FDX2 could bypass the cell’s need for frataxin. They then showed that the FDX2/frataxin balance is important, and when frataxin levels are low, simultaneously reducing FDX2 can help restore production of crucial iron-sulfur clusters. Future work could reveal the precise balance necessary and how it is regulated in humans, and whether this could be a viable therapeutic approach.

Researchers from Mass General Brigham and the Broad Institute have discovered a potential drug target for the mitochondrial disorder Friedreich’s ataxia, suggesting a path for the development of new medicines