The Broad Institute is the genomics powerhouse behind DepMap, cBioPortal co-development, and the Cancer Cell Line Encyclopedia.
The Broad Institute of MIT and Harvard in Cambridge, Massachusetts, is the genomics research institute behind DepMap, the Cancer Cell Line Encyclopedia, PRISM drug screening and the co-development of cBioPortal; its Cancer Program under Getz and Matthew Meyerson, with Zhang's CRISPR technology, makes it the reference source for functional genomics in cancer. OnCo links it to CRISPR functional genomics and synthetic lethality, to the Cancer Dependency Map and TCGA Pan-Cancer Atlas papers, and to people including Todd R. Golub and Francisca Vazquez. It bears on bottlenecks about preclinical models that do not predict people and undruggable drivers, and on the idea of an open foundation model of the cancer cell trained on perturbation data. Whether cell-line dependencies translate to patients is the open question. The Koch Institute and Wellcome Sanger Institute are its linked partners.
From OpenAlex, oncology works in the last five years (2022 to 2026, current year in progress); counted on 2026-09-17.
Matched to Broad Institute, including child institutions. 690 works · 15,885 citations · 77% open access · 5% clinical trials · 3% reviews.
Uses organoids and functional genomics to find what pancreatic cancers depend on beyond KRAS.
Bradley Bernstein mapped the chromatin landscapes that let cancer cells switch identities and resist drugs.
Led the first personalised neoantigen peptide vaccine trial in melanoma and mapped how CLL evolves under treatment.
Eli and Edythe Broad gave $100 million in 2004 to start the Broad Institute and kept giving until their total passed $700 million in 2013; the genomics it produced underpins much of precision oncology.
Built UNI and CONCH, the pathology foundation models that let AI read whole-slide images across cancer types.
Pioneer of CRISPR-Cas9 genome editing in human cells, the tool behind cancer dependency screens and edited cell therapies.
Francisca Vazquez leads DepMap, the public map of which genes each cancer cell line cannot live without.
Wrote the algorithms (MuTect, MutSig, ABSOLUTE) that most cancer genome studies use to find mutations.
Co-discovered EGFR mutations in lung cancer and linked Fusobacterium to colorectal cancer.
Showed that gene expression could classify cancers, then built the Broad into the engine of cancer genomics.
Engineer who showed low-pass sequencing of blood can replace tumour biopsies and built ultra-sensitive MRD tests.
Together with COMPASS it made sequencing at diagnosis of advanced disease a standard expectation, and it found the BRAF-deletion class that a hotspot test misses.
Cancers are defined as much by the tissue they come from as by the mutations they carry, which is why the same drug can work in one organ and fail in another with the same mutation. TCGA is the shared public dataset behind most modern biomarkers and target discovery.
DepMap is the lookup table drug hunters use to ask: which cancers would die if we blocked this gene, and how would we recognise them? It generated targets such as WRN and PRMT5-MTAP now in clinical trials, and it is public.
It is the reference multi-platform dataset and the reason a KRAS wild-type report is treated as a search for another driver rather than as an absence.
It is the empirical basis for treating the two histologies as separate diseases for targeted therapy and as one disease for immunotherapy, which is exactly how they are treated.
It is the argument that immune biology matters across the whole disease rather than only in the mismatch repair deficient sixth, and the reason microsatellite-stable tumours with high neoantigen load are still being pursued for immunotherapy.
It is the reference table the field still argues against, and it made two practical points that outlived it: a tumour with no driver on a standard panel usually has one that the panel did not look for, and pathway activity measured on protein does not follow from the mutation list.
Many older people carry blood clones one or two steps from leukaemia, and those clones also drive heart disease through inflammation. CHIP is why blood-based cancer tests must filter out mutations from blood cells, and it opens a route to preventing both leukaemia and cardiovascular events in carriers.
Shares Break up the liquid droplets where oncogenic transcription happens, Catherine J. Wu, Let patients themselves donate their records and samples for ultra-rare cancers, Genomic correlates of immune-cell infiltrates in colorectal carcinoma.
Shares Gad Getz, Pool every multi-sample tumour genome into one open evolution atlas, Catherine J. Wu, Let patients themselves donate their records and samples for ultra-rare cancers.
Shares An open-science consortium on the undruggable drivers, open until a candidate, DepMap (Cancer Dependency Map), CRISPR functional genomics, Preclinical results do not reproduce.
Shares Break up the liquid droplets where oncogenic transcription happens, An open map of which cancer proteins any drug can stick to, Attack the backup copy when a tumour has lost the original gene, The undruggable drivers.
Shares Boltz-1 / Boltz-2 (MIT, open), An open map of which cancer proteins any drug can stick to, Score every model system on how well it predicted real trial results, An open foundation model of the cancer cell trained on perturbation data.
Shares Pick the laboratory model that matches the patient, not the one to hand, Score every model system on how well it predicted real trial results, An open model of every cancer cell state, built from perturbation atlases, Andrew J. Aguirre.
Shares DepMap (Cancer Dependency Map), CRISPR functional genomics, Preclinical results do not reproduce, Lab models that fail to predict what happens in patients.
Shares Boltz-1 / Boltz-2 (MIT, open), DepMap (Cancer Dependency Map), Synthetic lethality approaches, CRISPR functional genomics.
Open-source projects that this organisation maintains, from OnCo's own catalogue: licence and last activity as the repository reported them on the day of the fetch. Listing is not endorsement; check the licence before reuse and the validation before clinical use.
The Broad Institute's Genome Analysis Toolkit: variant discovery for germline and somatic DNA, including the Mutect2 somatic caller and copy-number tools most cancer pipelines start from.
Infers large-scale copy-number variation from single-cell RNA-seq to tell tumour cells from normal, from the Trinity CTAT project.
Fusion transcript detection from RNA-seq using STAR chimeric alignments, part of the Trinity CTAT toolkit.
Estimates tumour fraction in cell-free DNA from ultra-low-pass whole-genome sequencing, a workhorse of liquid biopsy research.
The pipelines that process the sequencing behind each DepMap release.
The code behind the Cancer Dependency Map portal, where CRISPR screens and drug sensitivities across cancer cell lines are explored openly.