Loading
Bert Vogelstein is the most-cited scientist in cancer genetics: he mapped how colorectal cancer develops and founded the field of cancer genome sequencing and blood-based detection.
Bert Vogelstein is Clayton Professor of Oncology, Co-Director of the Ludwig Center and an HHMI Investigator at Johns Hopkins Hospital and the Sidney Kimmel Comprehensive Cancer Center. He is the most-cited scientist in cancer genetics, having mapped with Kenneth Kinzler how colorectal cancer develops through the adenoma-carcinoma sequence, discovered the tumour-suppressor role of p53 and sequenced the first cancer genomes. His selected papers survey cancer genome landscapes and describe detection and localisation of surgically resectable cancers with a multi-analyte blood test. That test, CancerSEEK, is the basis of multi-cancer early detection, and his laboratory continues to work on liquid biopsy and blood-based screening.
For stage II colon cancer, where most patients are cured by surgery alone, a blood test can identify the minority who benefit from chemotherapy and spare everyone else its side effects. It does not yet prove that treating ctDNA-positive patients improves survival compared with not treating them.
A blood test can find early, treatable cancers in people who feel well, including cancers for which no screening exists. It is not a replacement for mammography or colonoscopy but a possible addition. Larger randomised trials are needed to show benefit outweighs harm.
The proof of principle for multi-cancer blood tests that include pancreas; the sensitivity figures come from known cancers, not from screening.
It quantifies how little DNA an operable pancreatic cancer sheds and why every serious early detection panel pairs DNA with proteins.
Encouraging for targeted therapy: unlike some cancers, the drivers do not differ between deposits, so one biopsy is enough to choose a RAS or repair-directed drug.
Minimal residual disease became measurable in solid tumours, and the DYNAMIC and CIRCULATE trials that followed turned the measurement into a treatment decision.
The evidence that molecular cyst-fluid testing can spare operations, now part of specialist practice although not a universal standard.
This small trial explained why colorectal cancer had seemed immune-resistant (most is MMR-proficient) and established the principle that a genomic feature, not the tissue of origin, can predict immunotherapy response. It led directly to the 2017 tissue-agnostic approval of pembrolizumab and to routine MMR/MSI testing of many cancers. Every patient with advanced dMMR cancer should now be considered for checkpoint blockade.
Shares Genetic instability in colorectal cancers, Distant metastasis occurs late during the genetic evolution of pancreatic cancer, Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability, Whole-exome sequencing of neoplastic cysts of the pancreas reveals recurrent mutations in components of ubiquitin-dependent pathways.
Shares Combined circulating tumor DNA and protein biomarker-based liquid biopsy for the earlier detection of pancreatic cancers, Detection and localization of surgically resectable cancers with a multi-analyte blood test, Core signaling pathways in human pancreatic cancers revealed by global genomic analyses, DETECT-A: a blood test plus PET-CT to screen 10,006 women with no symptoms.
Shares Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia, Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development, Core signaling pathways in human pancreatic cancers revealed by global genomic analyses, Intraductal papillary mucinous neoplasm and other pancreatic cystic precursors.
Shares Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development, A combination of molecular markers and clinical features improve the classification of pancreatic cysts, The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers, Le 2015: PD-1 blockade works in tumours with mismatch-repair deficiency, whatever the organ.
Shares Combined circulating tumor DNA and protein biomarker-based liquid biopsy for the earlier detection of pancreatic cancers, Detection and localization of surgically resectable cancers with a multi-analyte blood test, DETECT-A: a blood test plus PET-CT to screen 10,006 women with no symptoms, The molecular evolution of acquired resistance to targeted EGFR blockade in colorectal cancers.
Shares El-Deiry 1993: WAF1, the gene through which p53 stops cell division, Hollstein 1991: p53 mutations in human cancers, Vogelstein, Lane and Levine 2000: surfing the p53 network, Somatic mutation theory of cancer.
Shares Presence of somatic mutations in most early-stage pancreatic intraepithelial neoplasia, Recurrent GNAS mutations define an unexpected pathway for pancreatic cyst development, A combination of molecular markers and clinical features improve the classification of pancreatic cysts, Pancreatic ductal adenocarcinoma.
Shares Le 2015: PD-1 blockade works in tumours with mismatch-repair deficiency, whatever the organ, Mismatch repair deficient (MSI-high) pancreatic ductal adenocarcinoma, Johns Hopkins Hospital / Sidney Kimmel Comprehensive Cancer Center, Colorectal cancer roadmap: from the adenoma-carcinoma sequence and the first screening trials to total mesorectal excision, oxaliplatin, RAS testing, immunotherapy for mismatch repair-deficient disease, ctDNA-guided treatment and organ preservation.