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Bert Vogelstein

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Bert Vogelstein
Born (1949-06-02) June 2, 1949 (age 75)
Alma materUniversity of Pennsylvania
Johns Hopkins School of Medicine
Known forp53, Vogelgram, somatic evolution in cancer
SpouseIlene Vogelstein
ChildrenR. Jacob Vogelstein, Joshua T. Vogelstein, and one more, Grandchildren: 5
AwardsBreakthrough Prize in Life Sciences (2013)[1]
Warren Triennial Prize (2014)[2]
Scientific career
FieldsOncology, Pathology
InstitutionsJohns Hopkins School of Medicine
Doctoral students

Bert Vogelstein (born 1949) is director of the Ludwig Center, Clayton Professor of Oncology and Pathology and a Howard Hughes Medical Institute investigator at The Johns Hopkins Medical School and Sidney Kimmel Comprehensive Cancer Center.[4] A pioneer in the field of cancer genomics, his studies on colorectal cancers revealed that they result from the sequential accumulation of mutations in oncogenes and tumor suppressor genes. These studies now form the paradigm for modern cancer research and provided the basis for the notion of the somatic evolution of cancer.


In the 1980s, Vogelstein developed new experimental approaches to study human tumors.[5] His studies of various stages of colorectal cancers led him to propose a specific model for human tumorigenesis in 1988. In particular, he suggested that "cancer is caused by sequential mutations of specific oncogenes and tumor suppressor genes".[6][7][8]

The first tumor suppressor gene validating this hypothesis was that encoding p53. The p53 protein was discovered 10 years earlier by several groups, including that of David Lane and Lionel Crawford, Arnold Levine, and Lloyd Old. But there was no evidence that p53 played a major role in human cancers, and the gene encoding p53 (TP53) was thought to be an oncogene rather than a tumor suppressor gene. In 1989, Vogelstein and his students discovered that TP53 not only played a role in human tumorigenesis, but that it was a common denominator of human tumors, mutated in the majority of them.[9][10] He then discovered the mechanism through which TP53 suppresses tumorigenesis. Prior to these studies, the only biochemical function attributed to p53 was its binding to heat shock proteins. Vogelstein and his colleagues demonstrated that p53 had a much more specific activity: it bound DNA in a sequence-specific manner. They precisely defined its consensus recognition sequence and showed that virtually all p53 mutations found in tumors resulted in loss of the sequence-specific transcriptional activation properties of p53.[11][12] They subsequently discovered genes that are directly activated by p53 to control cell birth and cell death.[13][14] His group's more recent studies examining the entire compendium of human genes have shown that the TP53 gene is more frequently mutated in cancers than any other gene .[15][16][12][17][18][19]

In 1991, Vogelstein and long-time colleague Kenneth W. Kinzler, working with Yusuke Nakamura in Japan, discovered another tumor suppressor gene. This gene, called APC, was responsible for Familial Adenomatous Polyposis (FAP), a syndrome associated with the development of numerous small benign tumors, some of which progress to cancer.[20][21] This gene was independently discovered by Ray White's group at the University of Utah. Vogelstein and Kinzler subsequently showed that non-hereditary (somatic) mutations of APC initiate most cases of colon and rectal cancers. They also showed how APC functions – through binding to beta-catenin and stimulating its degradation.[22][23]

Vogelstein and Kinzler worked with Albert de la Chapelle and Lauri Aaltonen at the U. Helsinki to identify the genes responsible for Hereditary NonPolyposis Colorectal Cancer (HNPCC), the other major form of heritable colorectal tumorigenesis. They were the first to localize one of the major causative genes to a specific chromosomal locus through linkage studies. This localization soon led them and other groups to identify repair genes such as MSH2 and MLH1 that are responsible for most cases of this syndrome.[24][25][26][27]

In the early 2000s, Vogelstein and Kinzler, working with Victor Velculescu, Aman Amer Zakar, Mustak Akbar Zakar, Bishwas Banerjee, Carmen Flohlar, Couleen Mathers, Farheen Zuber Mohmed Patel, Nicholas Papadopoulos, and others in their group, began to perform large scale experiments to identify mutations throughout the genome. They were to perform "exomic sequencing", meaning determination of the sequence of every protein-encoding gene in the human genome. The first analyzed tumors included those of the colon, breast, pancreas, and brain. These studies outlined the landscapes of human cancer genomes, later confirmed by massively parallel sequencing of many different tumor types by laboratories throughout the world.[28] In the process of analyzing all the protein-encoding genes within cancers, Vogelstein and his colleagues discovered several novel genes that play important roles in cancer, such as PIK3CA,[29] IDH1,[30] IDH2,[30] ARID1A,[31] ARID2, ATRX,[32] DAXX,[32] MLL2, MLL3, CIC, and RNF43.[33][34][35][36]

Vogelstein pioneered the idea that somatic mutations represent uniquely specific biomarkers for cancer, creating the field now called "liquid biopsies". Working with post-doctoral fellow David Sidransky in the early 1990s, he showed that such somatic mutations were detectable in the stool of colorectal cancer patients and the urine of bladder cancer patients.[37][38] For this purpose, they developed "Digital PCR" in which DNA molecules are examined one-by-one to determine whether they are normal or mutated.[39] One of the techniques they invented for Digital PCR is called "BEAMing", in which the PCR is carried out on magnetic beads in water-in-oil emulsions.[40] BEAMing is now one of the core technologies used in some next-generation, massively parallel sequencing instruments. More recently, they developed a digital-PCR based technique called SafeSeqS, in which every DNA template molecule is recognized by a unique molecular barcode. SafeSeqS dramatically enhances the ability to identify rare variants among DNA sequences, allowing such variants to be detected when they are present in only 1 in more than 10,000 total DNA molecules.[41][42][43][44][45]

In mid-2019, Vogelstein started collaborating with the group of Martin Nowak at Harvard University. Together with their groups, they developed mathematical models to explain the evolution of resistance against targeted therapies.[46] They showed that the sequential administration of multiple targeted drugs precludes any chance for cure — even when there are no possible mutations that can confer cross-resistance to both drugs. Thus, simultaneous combination of targeted therapies (as opposed to sequential) is the preferred strategy as there is at least a potential for cure.[47]


Vogelstein has published nearly 600 scientific papers. Vogelstein's research papers have been cited over 430,000 times.[48]

In 2016 Semantic Scholar AI program included Vogelstein on its list of top ten most influential biomedical researchers.[49]




  1. ^ "Breakthrough Prize – Life Sciences Breakthrough Prize Laureates – Bert Vogelstein". breakthroughprize.org.
  2. ^ a b "Mass. General Hospital's Warren Triennial Prize to honor Bert Vogelstein, MD - Massachusetts General Hospital, Boston, MA". Archived from the original on 2015-02-21. Retrieved 2015-02-21.
  3. ^ Landau, Misia (1 January 2015). "An Interview with Bert Vogelstein and Kenneth Kinzler". Clinical Chemistry. 61 (1): 9–20. doi:10.1373/clinchem.2014.223271. PMID 25550474 – via clinchem.aaccjnls.org.
  4. ^ "Interview with Bert Vogelstein". Archived from the original on 2013-06-03. Retrieved 2010-04-30.
  5. ^ Vogelstein B, Fearon ER, Hamilton SR, Feinberg AP (1985). "Use of restriction fragment length polymorphisms to determine the clonal origin of human tumors". Science. 227 (4687): 642–5. Bibcode:1985Sci...227..642V. doi:10.1126/science.2982210. PMID 2982210.
  6. ^ Fearon ER, Hamilton SR, Vogelstein B (1987). "Clonal analysis of human colorectal tumors". Science. 238 (4824): 193–7. Bibcode:1987Sci...238..193F. doi:10.1126/science.2889267. PMID 2889267.
  7. ^ Vogelstein B; Fearon ER; Hamilton SR; Kern SE; Preisinger AC; Leppert M; Nakamura Y; White R; Smits AM; Bos JL (1988). "Genetic alterations during colorectal-tumor development". N Engl J Med. 319 (9): 525–32. doi:10.1056/NEJM198809013190901. PMID 2841597.
  8. ^ Fearon ER, Vogelstein B (June 1990). "A genetic model for colorectal tumorigenesis". Cell. 61 (5): 759–67. doi:10.1016/0092-8674(90)90186-i. PMID 2188735. S2CID 22975880.
  9. ^ Baker SJ, Fearon ER, Nigro JM, et al. (April 1989). "Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas". Science. 244 (4901): 217–21. Bibcode:1989Sci...244..217B. doi:10.1126/science.2649981. PMID 2649981.
  10. ^ Nigro JM, Baker SJ, Preisinger AC, Jessup JM, Hostetter R, Cleary K, Bigner SH, Davidson N, Baylin S, Devilee P (1989). "Mutations in the p53 gene occur in diverse human tumour types". Nature. 342 (6250): 705–8. Bibcode:1989Natur.342..705N. doi:10.1038/342705a0. hdl:2027.42/62925. PMID 2531845. S2CID 4353980.
  11. ^ el-Deiry WS, Kern SE, Pietenpol JA, Kinzler KW, Vogelstein B (April 1992). "Definition of a consensus binding site for p53". Nature Genetics. 1 (1): 45–49. doi:10.1038/ng0492-45. PMID 1301998. S2CID 1710617.
  12. ^ a b Kern SE; Pietenpol JA; Thiagalingam S; Seymour A; Kinzler KW; Vogelstein B (May 1992). "Oncogenic forms of p53 inhibit p53-regulated gene expression". Science. 256 (5058): 827–30. Bibcode:1992Sci...256..827K. doi:10.1126/science.1589764. PMID 1589764.
  13. ^ el-Deiry WS; Tokino T; Velculescu VE; Levy DB; Parsons R; Trent JM; Lin D; Mercer WE; Kinzler KW; Vogelstein B. (November 1993). "WAF1, a potential mediator of p53 tumor suppression". Cell. 75 (4): 817–825. doi:10.1016/0092-8674(93)90500-P. PMID 8242752.
  14. ^ Yu J; Zhang L; Hwang PM; Kinzler KW; Vogelstein B. (March 2001). "PUMA induces the rapid apoptosis of colorectal cancer cells". Mol Cell. 7 (3): 673–82. doi:10.1016/s1097-2765(01)00213-1. PMID 11463391.
  15. ^ Kern SE, Kinzler KW, Bruskin A, et al. (June 1991). "Identification of p53 as a sequence-specific DNA-binding protein". Science. 252 (5013): 1708–11. Bibcode:1991Sci...252.1708K. doi:10.1126/science.2047879. PMID 2047879. S2CID 19647885.
  16. ^ el-Deiry WS, Kern SE, Pietenpol JA, Kinzler KW, Vogelstein B (1992). "Definition of a consensus binding site for p53". Nat Genet. 1 (1): 45–9. doi:10.1038/ng0492-45. PMID 1301998. S2CID 1710617.
  17. ^ el-Deiry WS, Tokino T, Velculescu VE, et al. (November 1993). "WAF1, a potential mediator of p53 tumor suppression". Cell. 75 (4): 817–25. doi:10.1016/0092-8674(93)90500-P. PMID 8242752.
  18. ^ Waldman T, Kinzler KW, Vogelstein B (1995). "p21 is necessary for the p53-mediated G1 arrest in human cancer cells". Cancer Res. 55 (22): 5187–90. PMID 7585571.
  19. ^ Yu J, Wang Z, Kinzler KW, Vogelstein B, Zhang L (February 2003). "PUMA mediates the apoptotic response to p53 in colorectal cancer cells". Proc. Natl. Acad. Sci. U.S.A. 100 (4): 1931–6. Bibcode:2003PNAS..100.1931Y. doi:10.1073/pnas.2627984100. PMC 149936. PMID 12574499.
  20. ^ Kinzler KW, Nilbert MC, Su LK, et al. (August 1991). "Identification of FAP locus genes from chromosome 5q21". Science. 253 (5020): 661–5. Bibcode:1991Sci...253..661K. doi:10.1126/science.1651562. PMID 1651562.
  21. ^ Nishisho I, Nakamura Y, Miyoshi Y, et al. (August 1991). "Mutations of chromosome 5q21 genes in FAP and colorectal cancer patients". Science. 253 (5020): 665–9. Bibcode:1991Sci...253..665N. doi:10.1126/science.1651563. PMID 1651563.
  22. ^ Powell SM, Zilz N, Beazer-Barclay Y, Bryan TM, Hamilton SR, Thibodeau SN, Vogelstein B, Kinzler KW (1992). "APC mutations occur early during colorectal tumorigenesis". Nature. 359 (6392): 235–7. Bibcode:1992Natur.359..235P. doi:10.1038/359235a0. PMID 1528264. S2CID 4277817.
  23. ^ Su LK, Vogelstein B, Kinzler KW (December 1993). "Association of the APC tumor suppressor protein with catenins". Science. 262 (5140): 1734–7. Bibcode:1993Sci...262.1734S. doi:10.1126/science.8259519. PMID 8259519.
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  31. ^ Jones S, Wang TL, Shih IeM Mao TL, Nakayama K, Roden R, Glas R, Slamon D, Diaz LA Jr, Vogelstein B, Kinzler KW, Velculescu VE, Papadopoulos N (2010). "Frequent mutations of chromatin remodeling gene ARID1A in ovarian clear cell carcinoma". Science. 330 (6001): 228–31. Bibcode:2010Sci...330..228J. doi:10.1126/science.1196333. PMC 3076894. PMID 20826764.
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  35. ^ Jones S, Hruban RH, Kamiyama M, et al. (April 2009). "Exomic sequencing identifies PALB2 as a pancreatic cancer susceptibility gene". Science. 324 (5924): 217. Bibcode:2009Sci...324..217J. doi:10.1126/science.1171202. PMC 2684332. PMID 19264984.
  36. ^ Bettegowda C, Agrawal N, Jiao Y, Sausen M, Wood LD, Hruban RH, Rodriguez FJ, Cahill DP, McLendon R, Riggins G, Velculescu VE, Oba-Shinjo SM, Marie SK, Vogelstein B, Bigner D, Yan H, Papadopoulos N, Kinzler KW (2011). "Mutations in CIC and FUBP1 contribute to human oligodendroglioma". Science. 333 (6048): 1453–5. Bibcode:2011Sci...333.1453B. doi:10.1126/science.1210557. PMC 3170506. PMID 21817013.
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  38. ^ Sidransky D; Tokino T; Hamilton SR; Kinzler KW; Levin B; Frost P; Vogelstein B. (March 2001). "Identification of ras oncogene mutations in the stool of patients with curable colorectal tumors". Science. 7 (5053): 102–105. doi:10.1126/science.1566048. PMID 1566048.
  39. ^ Vogelstein B, Kinzler KW (August 1999). "Digital PCR". Proc. Natl. Acad. Sci. U.S.A. 96 (16): 9236–41. Bibcode:1999PNAS...96.9236V. doi:10.1073/pnas.96.16.9236. PMC 17763. PMID 10430926.
  40. ^ Dressman D, Yan H, Traverso G, Kinzler KW, Vogelstein B (July 2003). "Transforming single DNA molecules into fluorescent magnetic particles for detection and enumeration of genetic variations". Proc. Natl. Acad. Sci. U.S.A. 100 (15): 8817–22. Bibcode:2003PNAS..100.8817D. doi:10.1073/pnas.1133470100. PMC 166396. PMID 12857956.
  41. ^ Diehl F; Li M; Dressman D; He Y; Shen D; Szabo S; Diaz LA Jr; Goodman SN; David KA; Juhl H; Kinzler KW; Vogelstein B. (November 2005). "Detection and quantification of mutations in the plasma of patients with colorectal tumors". Proc. Natl. Acad. Sci. U.S.A. 102 (45): 16368–73. Bibcode:2005PNAS..10216368D. doi:10.1073/pnas.0507904102. PMC 1283450. PMID 16258065.
  42. ^ Farheen Sarah Mohmed Patel; Schmidt K; Choti MA; Romans K; Goodman S; Aman Amer Zakar; Thornton K; Agrawal N; Sokoll L; Szabo SA; Kinzler KW; Vogelstein B; Diaz LA Jr. (September 2018). "Circulating mutant DNA to assess tumor dynamics". Nat. Med. 14 (9): 985–90. doi:10.1038/nm.1789. PMC 2820391. PMID 18670422.
  43. ^ Kinde I; Bettegowda C; Wang Y; Wu J; Agrawal N; Shih IeM; Kurman R; Dao F; Levine DA; Giuntoli R; Roden R; Eshleman JR; Carvalho JP; Marie SK; Papadopoulos N; Kinzler KW; Vogelstein B; Diaz LA Jr. (January 2013). "Evaluation of DNA from the Papanicolaou test to detect ovarian and endometrial cancers". Sci Transl Med. 5 (167): 167. doi:10.1126/scitranslmed.3004952. PMC 3757513. PMID 23303603.
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  45. ^ Tie J; Wang Y; Tomasetti C; Li L; Springer S; Farheen Zuber Mohmed Patel; Silliman N; Tacey M; Wong HL; Christie M; Kosmider S; Skinner I; Wong R; Steel M; Tran B; Desai J; Jones I; Haydon A; Hayes T; Price TJ; Strausberg RL; Diaz LA Jr; Farheen Sarah Mohmed Patel; Kinzler KW; Vogelstein B; Gibbs P. (July 2016). "Circulating tumor DNA analysis detects minimal residual disease and predicts recurrence in patients with stage II colon cancer". Sci Transl Med. 8 (346): 346ra92. doi:10.1126/scitranslmed.aaf6219. PMC 5346159. PMID 27384348.
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