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institutionsInstitution
Massachusetts General Hospital Cancer Center
Harvard's largest hospital; leaders in lung cancer targeted therapy, proton therapy, and ctDNA research.
Overview
Massachusetts General Hospital Cancer Center in Boston is Harvard's largest hospital cancer programme, NCI-designated as comprehensive and sixteenth in the Newsweek/Statista oncology ranking, and it matters most for lung cancer targeted therapy. Its Termeer Center for targeted therapies is the home of its ALK, ROS1 and EGFR resistance research, its Francis H. Burr Proton Center anchors a proton therapy programme, and it holds a Broad Institute affiliation for circulating tumour DNA work. OnCo links it to CAR-T for glioma, to the Sybil lung risk and Mirai breast risk models developed with MIT, to Temel's early palliative care paper, and to the losartan pancreatic cancer idea. The brain as a barrier and sanctuary is the bottleneck its neuro-oncology work confronts. Daniel A. Haber, Keith T. Flaherty, Lecia V. Sequist and Ryan B. Corcoran are among the people listed here.
Location
Boston, US
Type
hospital · Harvard University
Newsweek 2026 oncology rank
#16
NCI designation
comprehensive
OnCo score
#12 · 127 points (44 Newsweek + 15 NCI + 68 from 34 linked objects) · ranking
Research output
From OpenAlex, oncology works in the last five years (2022 to 2026, current year in progress); counted on 2026-09-24.
Matched to Massachusetts General Hospital, including child institutions. 3,584 works · 55,693 citations · 66% open access · 11% clinical trials · 2% reviews.
Oncology works per year
8232022
8552023
7652024
7182025
4232026
Most works
- Marcela V. Maus145 works
- Matthew J. Frigault130 works
- Ryan J. Sullivan115 works
- Genevieve Marie Boland95 works
- Kerry Lynn Reynolds94 works
- Areej R El-Jawahri89 works
- Aditya Bardia78 works
- Yevgeniy R. Semenov70 works
- Aparna R. Parikh68 works
- Theodore S. Hong64 works
Most cited
- Targeted therapy (lung)
- Proton therapy
- Neuro-oncology
Anthony L. Zietman
Jenot and William Shipley Professor of Radiation Oncology, Massachusetts General Hospital and Harvard Medical School
Prostate radiotherapyProton therapyDose escalation
Led the proton dose-escalation trial in prostate cancer and the comparative-effectiveness debate over proton therapy.
Constance D. Lehman
Professor of Radiology, Harvard Medical School; Co-Director, Breast Imaging Research Center, Massachusetts General Hospital
Breast imagingAI risk predictionScreening MRI
Breast radiologist who co-developed the Mirai AI model that predicts breast cancer risk from a mammogram.
Daniel A. Haber
Director, Mass General Cancer Center; HHMI Investigator
Circulating tumour cellsEGFR mutationsCancer genetics
Co-discovered EGFR mutations in lung cancer and pioneered circulating tumour cell technology.
Howard L. Kaufman
Surgical Oncologist, Massachusetts General Hospital; Chief Medical Officer, Ankyra Therapeutics
Oncolytic virus therapyMelanomaIntratumoural immunotherapy
Led OPTiM, the trial that made talimogene laherparepvec the first approved oncolytic virus therapy.
Jennifer S. Temel
Clinical Director of Thoracic Oncology and Co-Director, Cancer Outcomes Research and Education Program, Massachusetts General Hospital Cancer Center
Palliative care integrationThoracic oncologyPatient-reported outcomes
Showed that early palliative care helps lung cancer patients live better and longer, changing oncology guidelines worldwide.
Justin F. Gainor
Director, Center for Thoracic Cancers
ALK and ROS1 lung cancerImmunotherapy in oncogene-driven NSCLCRET
Showed that oncogene-driven lung cancers respond poorly to immunotherapy and led the pivotal RET and ALK inhibitor studies.
Keith T. Flaherty
Director of Clinical Research, Mass General Cancer Center
MelanomaBRAF and MEK inhibitorsPrecision oncology trials
Led the first trials of BRAF inhibition in melanoma and chairs the NCI-MATCH precision medicine trial.
Lecia V. Sequist
Director, Center for Innovation in Early Cancer Detection; Landry Family Professor of Medicine
Lung cancerEGFR resistanceEarly detection
Defined EGFR resistance mechanisms in lung cancer and now leads early-detection research including the Sybil AI lung-risk model.
Leif W. Ellisen
Program Director, Breast Medical Oncology
Breast cancer geneticsp53 family and p63Cancer predisposition
Runs breast medical oncology at MGH and studies the tumour-suppressor biology behind hereditary and triple-negative breast cancer.
Lori J. Wirth
Medical Director, Center for Head and Neck Cancers, Massachusetts General Hospital Cancer Center
Thyroid cancerRET-targeted therapyHead and neck cancer
Led LIBRETTO-001 in thyroid cancer, which made selpercatinib the first RET-selective drug approved for RET-driven tumours.
Marcela V. Maus
Director, Cellular Immunotherapy Program, Massachusetts General Hospital Cancer Center; Professor, Harvard Medical School
CAR T-cell therapySolid tumour cell therapyGlioblastoma
Cell therapy engineer whose CAR-TEAM cells produced rapid regressions of recurrent glioblastoma.
Matthew R. Smith
Director, Genitourinary Malignancies Program, Massachusetts General Hospital Cancer Center
Prostate cancerAndrogen receptor inhibitorsBone health
Led ARASENS and SPARTAN, trials that established darolutamide triplet therapy and apalutamide for prostate cancer.
Noopur Raje
Director, Center for Multiple Myeloma, Massachusetts General Hospital Cancer Center
Multiple myelomaCAR T-cell therapyBone disease
Led the first-in-human trial of BCMA CAR-T (bb2121) in myeloma and studies of bone disease treatment.
Robert L. Martuza
Neurosurgeon and researcher, Department of Neurosurgery, Massachusetts General Hospital and Harvard Medical School; Molecular Neurosurgery Laboratory and Brain Tumor Research Center
NeurosurgeryOncolytic herpes simplex virusGlioma
Robert Martuza built the first genetically engineered virus designed to treat a cancer, a herpes virus crippled so that it could only replicate in dividing tumour cells.
Ryan B. Corcoran
Director, Gastrointestinal Cancer Center; Scientific Director, Termeer Center for Targeted Therapy
Colorectal cancerBRAF and KRAS resistanceLiquid biopsy
Worked out why BRAF inhibitors fail in colorectal cancer and how to combine drugs to overcome it.
Ryan J. Sullivan
Associate Director, Melanoma Program
MelanomaImmune-related adverse eventsTargeted and immune therapy sequencing
Ryan Sullivan is a melanoma trialist and a leading voice on managing immunotherapy side effects.
Scott R. Plotkin
Neuro-oncologist and Director of the Family Center for Neurofibromatosis, Massachusetts General Hospital
Neurofibromatosis type 2SchwannomasNeuro-oncology trials
Boston neuro-oncologist who showed that bevacizumab can shrink vestibular schwannomas and restore hearing in people with neurofibromatosis type 2.
Theodore S. Hong
Director, Gastrointestinal Radiation Oncology
Proton therapyLiver and pancreatic cancer radiationTotal neoadjuvant therapy
Showed how radiation, including proton therapy, can be used in liver and pancreatic cancers previously considered unsuitable.
rctInternational Journal of Radiation Oncology, Biology, Physics 2024
PARTIQoL: phase 3 randomised trial of proton therapy versus IMRT for localised prostate cancer (ASTRO 2024 late-breaking abstract)
For men with low- or intermediate-risk prostate cancer, protons and modern IMRT give the same excellent quality of life and cancer control, so the choice can rest on access, cost and convenience rather than on an expected sparing of bowel or bladder. The result removes prostate cancer from the list of adult indications where a proton advantage was assumed but untested.
observationalJournal of Thoracic Oncology 2022357 citations
Diminished efficacy of programmed death-(ligand)1 inhibition in STK11- and KEAP1-mutant lung adenocarcinoma is affected by KRAS mutation status
It corrected a widely repeated simplification. An STK11 or KEAP1 mutation is not by itself a reason to expect immunotherapy to fail; it is a reason to expect it in a KRAS-mutant tumour, which is how the result should be read on a report.
rctJournal of Clinical Oncology 2019changed practice313 citations
ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancer
It turned the laboratory prediction into a clinical rule: after a second-generation ALK inhibitor, genotype the tumour, and treat the absence of an ALK mutation as evidence that the cancer has stopped depending on ALK.
observationalJournal of Clinical Oncology 2019423 citations
EGFR-mutant adenocarcinomas that transform to small-cell lung cancer and other neuroendocrine carcinomas: clinical outcomes
It is the practical guide to what to do after transformation: treat it as small-cell lung cancer with platinum and etoposide, expect central nervous system disease, and do not expect a checkpoint inhibitor to help.
translationalCancer Discovery 2016changed practice946 citations
Molecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancer
It made repeat biopsy and genotyping at progression the standard in ALK-positive lung cancer, because after a second-generation inhibitor the presence or absence of an ALK mutation is what separates patients who should receive a third-generation inhibitor from those who should not.
translationalNew England Journal of Medicine 2016398 citations
Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F
It is the cleanest demonstration in oncology that resistance is a property of a particular drug bound to a particular protein rather than a property of the tumour, and that genotyping at every progression can reopen an option that looked closed.
translationalJournal of Clinical Oncology 2012changed practice1,173 citations
ROS1 rearrangements define a unique molecular class of lung cancers
It defined a class of lung cancer by a rearrangement and a clinical phenotype at the same time, and it is the reason ROS1 testing is recommended for every patient with adenocarcinoma rather than only for those with an obvious risk profile.
translationalScience Translational Medicine 2011changed practice2,775 citations
Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors
The case for re-biopsy at progression, for treating resistance as a diagnosis rather than an endpoint, and for the idea of a drug holiday. It is also the origin of resistance-directed sequencing: what you give next should depend on what the tumour became.
4 more, oldest last
Anaplastic lymphoma kinase inhibition in non-small-cell lung cancerTemel: early palliative care alongside chemotherapy improved quality of life, mood and survival in lung cancerMET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signalingActivating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib
Similar pages
- JournalScience Translational Medicine
Shares Constance D. Lehman, Marcela V. Maus, Lecia V. Sequist, Genotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitors.
- PersonAlice T. Shaw
Shares ROS1 rearrangements define a unique molecular class of lung cancers, Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F, ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancer, Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer.
- CancerVestibular schwannoma (acoustic neuroma)
Shares Scott R. Plotkin, INTUITT-NF2, Gamma Knife, Stereotactic radiosurgery (Gamma Knife, CyberKnife, linac SRS).
- TreatmentCrizotinib
Shares ROS1 rearrangements define a unique molecular class of lung cancers, Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F, ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancer, Molecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancer.
- PathwayResistance routes: how a blocked pathway comes back
Shares Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F, MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling, ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancer, EGFR-mutant adenocarcinomas that transform to small-cell lung cancer and other neuroendocrine carcinomas: clinical outcomes.
- BiomarkerALK kinase-domain resistance mutation (G1202R and the rest)
Shares Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F, ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancer, Molecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancer, Small-molecule kinase inhibitors.
- TreatmentLorlatinib
Shares Justin F. Gainor, Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198F, ALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancer, Molecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancer.
- TermLinear energy transfer (LET)
Shares PARTIQoL: phase 3 randomised trial of proton therapy versus IMRT for localised prostate cancer (ASTRO 2024 late-breaking abstract), PARTIQoL, Radiotherapy roadmap: X-rays → shaped beams → fewer fractions, particles and FLASH, Proton therapy.
cancers
technologies
CAR-T for glioma (IL13Rα2, GD2, EGFRvIII, multi-target)Gamma KnifeMirai (MIT breast cancer risk from mammograms)Proton therapyProton therapy machines: cyclotrons, synchrotrons and single-room systemsSmall-molecule kinase inhibitorsStereotactic radiosurgery (Gamma Knife, CyberKnife, linac SRS)Sybil (MIT/MGH lung cancer risk from CT)
companies
institutions
pathways
trials
roadmaps
ideas
people
bottlenecks
key papers
Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinibALK resistance mutations and efficacy of lorlatinib in advanced anaplastic lymphoma kinase-positive non-small-cell lung cancerAnaplastic lymphoma kinase inhibition in non-small-cell lung cancerDiminished efficacy of programmed death-(ligand)1 inhibition in STK11- and KEAP1-mutant lung adenocarcinoma is affected by KRAS mutation statusEGFR-mutant adenocarcinomas that transform to small-cell lung cancer and other neuroendocrine carcinomas: clinical outcomesGenotypic and histological evolution of lung cancers acquiring resistance to EGFR inhibitorsMET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signalingMolecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancerPARTIQoL: phase 3 randomised trial of proton therapy versus IMRT for localised prostate cancer (ASTRO 2024 late-breaking abstract)Resensitization to crizotinib by the lorlatinib ALK resistance mutation L1198FROS1 rearrangements define a unique molecular class of lung cancersTemel: early palliative care alongside chemotherapy improved quality of life, mood and survival in lung cancer
Open-source projects
All open source in oncology →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 reference open implementation of radiomic feature extraction, standardised against the Image Biomarker Standardisation Initiative.
A self-supervised CT foundation model for lesion characterisation and prognosis, with code and weights.
A whole-body CT foundation model trained on 148,000 scans, released with weights.