Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287 | From the Division of Personalised Oncology, Walter and ...
KOL Resume for Bert Vogelstein (disease, polyp, rectal, rectal polyp)
Bloomberg-Kimmel Institute for Cancer Immunotherapy, Sidney Kimmel Comprehensive Cancer Center, Baltimore, MD 21287
From the Division of Personalised Oncology, Walter and Eliza Hall Institute of Medical Research (J.T., R.W., M.L., B.L., P.G.), the Department of Medical Oncology, Peter MacCallum Cancer Centre (J.T., B.L.), the Department of Medical Oncology, Western Health (J.T., S.K., M.L., P.G.), the Faculty of Medicine, Dentistry, and Health Sciences, University of Melbourne (J.T., P.G.), the Department of Medical Oncology, Eastern Health (R.W., M.L.), the Eastern Health Clinical School, Faculty of Medicine, Nursing, and Health Sciences, Monash University (R.W., M.L.), the Department of Medical Oncology, Cabrini Health (J.S.), the Department of Medical Oncology, Monash Health (M.H.), the Department of Medical Oncology, St. Vincent's Hospital (S.-A.M.), and the Department of Medical Oncology, Northern Health (B.L.), Melbourne, VIC, the Research and Biostatistics Group, Melanoma Institute Australia, and the Faculty of Medicine and Health, University of Sydney, Sydney (S.N.L.), the Department of Medical Oncology, Bendigo Health, Bendigo, VIC (S.H.), the Department of Medical Oncology, Fiona Stanley Hospital, and Edith Cowan University, Perth, WA (A.K.), the Department of Medical Oncology, Royal Brisbane and Women's Hospital, and the University of Queensland, Brisbane, QLD (M.B.), Newcastle Private Hospital (J.L.), and the Department of Medical Oncology, Calvary Mater Newcastle Hospital (F.D.), Newcastle, NSW, the Department of Medical Oncology, Royal Hobart Hospital, Hobart, TAS (L.N.), and South West Healthcare, Warrnambool, VIC (T.H.) - all in Australia; the Ludwig Center for Cancer Genetics and Therapeutics (J.D.C., Y.W., J.P., N.S., L.D., M.P., N.P., K.W.K., B.V.), the Division of Biostatistics and Bioinformatics (K.L., C.T.), Department of Oncology, Sidney Kimmel Comprehensive Cancer Center (J.D.C., Y.W., J.P., N.S., L.D., M.P., R.H., A.M.L., N.P., K.W.K., B.V.), the Sol Goldman Pancreatic Cancer Research Center (J.D.C., Y.W., J.P., N.S., L.D., M.P., R.H., A.M.L., N.P., K.W.K., B.V.), and the Departments of Pathology (R.H.) and Medicine (A.M.L.), Johns Hopkins University School of Medicine, the Howard Hughes Medical Institute (J.P., N.S., B.V.), the Department of Biomedical Engineering, Johns Hopkins University (J.D.C.), and the Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health (C.T.) - all in Baltimore; and the Institute for Research and Medical Consultations, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia (S.N.L.).
Ludwig Center for Cancer Genetics and Therapeutics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
HHMI, The Johns Hopkins University School of Medicine, Baltimore, MD 21205
Ludwig Center & Howard Hughes Medical Institute, Johns Hopkins Kimmel Cancer Center, Baltimore, United States
Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
Sidney Kimmel Comprehensive Cancer Center
Howard Hughes Medical Institute, Johns Hopkins Medical Institutions
The Ludwig Center, Johns Hopkins University School of Medicine, 733 N. Broadway, Baltimore, MD 21205, USA.
Sidney Kimmel Comprehensive Cancer Center, School of Medicine, Johns Hopkins University, 21287 Baltimore, USA
Ludwig Center and the Howard Hughes Medical Institute at the Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins School of Medicine, 1650 Orleans St., CRB1, Room 520, Baltimore, MD 21128, USA.
4 Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD.
Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Johns Hopkins Kimmel Cancer Center
Prominent publications by Bert Vogelstein
BACKGROUND: Colorectal cancer occurs in approximately 150,000 people each year in the United States. Prognostic assessment influences the treatment of patients with colorectal cancer, including decisions about adjuvant therapy. We evaluated chromosome 18q allelic loss, a genetic event associated with tumor progression, as a prognostic marker for this disease.
METHODS: We developed procedures to examine the status of chromosome 18q with microsatellite markers and DNA from formalin-fixed, ...
|Known for Allelic Loss | Chromosome 18q | Colorectal Cancer | Patients Stage Disease | Human Pair|
Progression of colorectal cancer is associated with multiple tumor suppressor gene defects but inhibition of tumorigenicity is accomplished by correction of any single defect via chromosome transfer.
[ PUBLICATION ]
Carcinogenesis is a multistage process that has been characterized both by the activation of cellular oncogenes and by the loss of function of tumor suppressor genes. Colorectal cancer has been associated with the activation of ras oncogenes and with the deletion of multiple chromosomal regions including chromosomes 5q, 17p, and 18q. Such chromosome loss is often suggestive of the deletion or loss of function of tumor suppressor genes. The candidate tumor suppressor genes from these ...
|Known for Colorectal Cancer | Tumor Suppressor | Chromosome Transfer | Human Pair | Neoplasm Genes|
Circulating Tumor DNA Analyses as Markers of Recurrence Risk and Benefit of Adjuvant Therapy for Stage III Colon Cancer
[ PUBLICATION ]
Importance: Adjuvant chemotherapy in patients with stage III colon cancer prevents recurrence by eradicating minimal residual disease. However, which patients remain at high risk of recurrence after completing standard adjuvant treatment cannot currently be determined. Postsurgical circulating tumor DNA (ctDNA) analysis can detect minimal residual disease and is associated with recurrence in colorectal cancers.
Objective: To determine whether serial postsurgical and postchemotherapy ...
|Known for Recurrence Risk | Circulating Tumor | Colon Cancer | Adjuvant Therapy | Stage Iii|
Activating Mutations of the Noonan Syndrome-Associated SHP2/PTPN11 Gene in Human Solid Tumors and Adult Acute Myelogenous Leukemia
[ PUBLICATION ]
The SH2 domain-containing protein-tyrosine phosphatase PTPN11 (Shp2) is required for normal development and is an essential component of signaling pathways initiated by growth factors, cytokines, and extracellular matrix. In many of these pathways, Shp2 acts upstream of Ras. About 50% of patients with Noonan syndrome have germ-line PTPN11 gain of function mutations. Associations between Noonan syndrome and an increased risk of some malignancies, notably leukemia and neuroblastoma, have ...
|Known for Noonan Syndrome | Activating Mutations | Ptpn11 Shp2 | Proteins Leukemia | Neoplastic Genes|
BACKGROUND: Preventive programs for individuals who have high lifetime risks of colorectal cancer may reduce disease morbidity and mortality. Thus, it is important to identify the factors that are associated with hereditary colorectal cancer and to monitor the effects of tailored surveillance. In particular, patients with Lynch syndrome, hereditary nonpolyposis colorectal cancer (HNPCC), have an increased risk to develop colorectal cancer at an early age. The syndrome is explained by ...
|Known for Colorectal Cancer | Lynch Syndrome | Hereditary Nonpolyposis | Mutations Patients | Mmr Genes|
BACKGROUND: Familial adenomatous polyposis (FAP) is caused by germline mutation of the adenomatous polyposis coli (APC) gene on chromosome 5q.
AIMS: This study assessed genotype-phenotype correlations for extraintestinal lesions in FAP.
METHODS: Mutations of the APC gene were compared with the occurrence of seven extraintestinal manifestations in 475 FAP patients from 51 families. The frequency of manifestations was adjusted for different ages of patients using person years of exposure. ...
|Known for Apc Gene | Mutations Codons | Extraintestinal Manifestations | Familial Adenomatous | Fap Patients|
Detection of somatic mutations and HPV in the saliva and plasma of patients with head and neck squamous cell carcinomas
[ PUBLICATION ]
To explore the potential of tumor-specific DNA as a biomarker for head and neck squamous cell carcinomas (HNSCC), we queried DNA from saliva or plasma of 93 HNSCC patients. We searched for somatic mutations or human papillomavirus genes, collectively referred to as tumor DNA. When both plasma and saliva were tested, tumor DNA was detected in 96% of 47 patients. The fractions of patients with detectable tumor DNA in early- and late-stage disease were 100% (n = 10) and 95% (n = 37), ...
|Known for Somatic Mutations | Plasma Patients | Tumor Dna | Squamous Cell | Oral Cavity|
Accumulated Clonal Genetic Alterations in Familial and Sporadic Colorectal Carcinomas with Widespread Instability in Microsatellite Sequences
[ PUBLICATION ]
A subset of hereditary and sporadic colorectal carcinomas is defined by microsatellite instability (MSI), but the spectra of gene mutations have not been characterized extensively. Thirty-nine hereditary nonpolyposis colorectal cancer syndrome carcinomas (HNPCCa) and 57 sporadic right-sided colonic carcinomas (SRSCCa) were evaluated. Of HNPCCa, 95% (37/39) were MSI-positive as contrasted with 31% (18/57) of SRSCCa (P < 0.000001), but instability tended to be more widespread in SRSCCa (P ...
|Known for Sporadic Colorectal | Microsatellite Sequences | Genetic Alterations | Human Pair | Hmsh2 Mutation|
Frequent ATRX, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas
[ PUBLICATION ]
Mutations in the critical chromatin modifier ATRX and mutations in CIC and FUBP1, which are potent regulators of cell growth, have been discovered in specific subtypes of gliomas, the most common type of primary malignant brain tumors. However, the frequency of these mutations in many subtypes of gliomas, and their association with clinical features of the patients, is poorly understood. Here we analyzed these loci in 363 brain tumors. ATRX is frequently mutated in grade II-III ...
|Known for Idh1 Mutations | Malignant Gliomas | Cic Fubp1 | Glioma Humans | Alternative Lengthening|
Genetic inactivation of AKT1, AKT2, and PDPK1 in human colorectal cancer cells clarifies their roles in tumor growth regulation
[ PUBLICATION ]
Phosphotidylinositol-3-kinase (PI3K) signaling is altered in the majority of human cancers. To gain insight into the roles of members of this pathway in growth regulation, we inactivated AKT1, AKT2, or PDPK1 genes by targeted homologous recombination in human colon cancer cell lines. Knockout of either AKT1 or AKT2 had minimum effects on cell growth or downstream signaling. In contrast, knockout of both AKT1 and AKT2 resulted in markedly reduced proliferation in vitro when growth factors ...
|Known for Akt1 Akt2 | Knockout Mice | Colorectal Cancer | Glycogen Synthase Kinase | Cell Growth|
Germline mutations of the gene encoding bone morphogenetic protein receptor 1A in juvenile polyposis
[ PUBLICATION ]
Juvenile polyposis (JP; OMIM 174900) is an autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers1,2. Previous studies have demonstrated a locus for JP mapping to 18q21.1 (ref. 3) and germline mutations in the homolog of the gene for mothers against decapentaplegic, Drosophila, (MADH4, also known as SMAD4) in several JP families4. However, mutations in MADH4 are only present in a subset of JP cases5, and ...
|Known for Juvenile Polyposis | Germline Mutations | Protein Receptor | Bone Morphogenetic | Preschool Chromosomes|
DAXX/ATRX, MEN1, and mTOR Pathway Genes Are Frequently Altered in Pancreatic Neuroendocrine Tumors
[ PUBLICATION ]
Pancreatic neuroendocrine tumors (PanNETs) are a rare but clinically important form of pancreatic neoplasia. To explore the genetic basis of PanNETs, we determined the exomic sequences of 10 nonfamilial PanNETs and then screened the most commonly mutated genes in 58 additional PanNETs. The most frequently mutated genes specify proteins implicated in chromatin remodeling: 44% of the tumors had somatic inactivating mutations in MEN1, which encodes menin, a component of a histone ...
|Known for Neuroendocrine Tumors | Mutations Genes | Mtor Pathway | Suppressor Proteins | Daxx Atrx|
Exome Sequencing of Head and Neck Squamous Cell Carcinoma Reveals Inactivating Mutations in NOTCH1
[ PUBLICATION ]
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide. To explore the genetic origins of this cancer, we used whole-exome sequencing and gene copy number analyses to study 32 primary tumors. Tumors from patients with a history of tobacco use had more mutations than did tumors from patients who did not use tobacco, and tumors that were negative for human papillomavirus (HPV) had more mutations than did HPV-positive tumors. Six of the genes that were ...
|Known for Exome Sequencing | Cell Carcinoma | Mutations Notch1 | Neck Squamous | Tumor Suppressor Genes|
Bert Vogelstein: Influence Statistics
|mutational status gnas||#1|
|treeomics theorem benchmarking||#1|
|biomarkers control studies||#1|
|isogenic cell panel||#1|
|pairs lowgrade tumours||#1|
|snrnp antism antisera||#1|
|sporadic colorectal fap||#1|
|serial analysis ctdna||#1|
|ncams nih3t3 cells||#1|
|intestinal polyps mutation||#1|
|abdominal sites mice||#1|
|dna sequences respect||#1|
|apc gene mapc||#1|
|gene dcc chromosome||#1|
|α1ar antagonists mortality||#1|
|mutations early stages||#1|
|mice mice biomarkers||#1|
|c57bl polymorphism human||#1|
|chromosome 17p mutation||#1|
|cells 1433σ cells||#1|
|biomarkers tumor circulating||#1|
|mutations muts homolog||#1|
|tem7 alternative splicing||#1|
|apc crc cells||#1|
|active compounds docking||#1|
|abnormal telomeres tumors||#1|
|interspecific map regions||#1|
|somatic mutations cck2r||#1|
|influenza virus facs||#1|
|recombinant adenoviral plasmid||#1|
|microsatellite sequences tumors||#1|
|somatic mutations bcorl1||#1|
|chromosome 18q patients||#1|
|neoplasms smad proteins||#1|
|ribosomal regulator humans||#1|
|fecal dna patients||#1|
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Key People For Colorectal Cancer
Bert Vogelstein:Expert Impact
Concepts for whichBert Vogelsteinhas direct influence:Colorectal cancer, Colorectal cancers, Somatic mutations, Tumor dna, Pancreatic cancer, Nuclear matrix, P53 gene, Genetic instability.
Bert Vogelstein:KOL impact
Concepts related to the work of other authors for whichfor which Bert Vogelstein has influence:Colorectal cancer, Gene expression, Cell cycle, Dna damage, Tumor suppressor, Microsatellite instability, Growth factor.
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