B Vogelstein

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. pmc Digital PCR
    B Vogelstein
    The Howard Hughes Medical Institute and The Johns Hopkins Oncology Center, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 96:9236-41. 1999
  2. pmc Targeted deletion of Smad4 shows it is required for transforming growth factor beta and activin signaling in colorectal cancer cells
    S Zhou
    The Howard Hughes Medical Institute at Johns Hopkins University, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 95:2412-6. 1998
  3. ncbi request reprint Identification of c-MYC as a target of the APC pathway
    T C He
    Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA
    Science 281:1509-12. 1998
  4. pmc PAK1, a gene that can regulate p53 activity in yeast
    S Thiagalingam
    Johns Hopkins Oncology Center, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 92:6062-6. 1995
  5. ncbi request reprint A phosphatase associated with metastasis of colorectal cancer
    S Saha
    Howard Hughes Medical Institute, The Oncology Center, Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Science 294:1343-6. 2001
  6. ncbi request reprint CDX2 is mutated in a colorectal cancer with normal APC/beta-catenin signaling
    L T da Costa
    Program in Human Genetics and Molecular Biology, The Johns Hopkins University, Baltimore, Maryland, MD 21231, USA
    Oncogene 18:5010-4. 1999
  7. ncbi request reprint The beta-catenin binding domain of adenomatous polyposis coli is sufficient for tumor suppression
    I M Shih
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 60:1671-6. 2000
  8. ncbi request reprint Analysis of the 5' region of PMS2 reveals heterogeneous transcripts and a novel overlapping gene
    N C Nicolaides
    Howard Hughes Medical Institute, Baltimore, Maryland 21231, USA
    Genomics 29:329-34. 1995
  9. ncbi request reprint Characterization of MAD2B and other mitotic spindle checkpoint genes
    D P Cahill
    Program in Human Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21231, USA
    Genomics 58:181-7. 1999
  10. ncbi request reprint PUMA induces the rapid apoptosis of colorectal cancer cells
    J Yu
    The Johns Hopkins Oncology Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Mol Cell 7:673-82. 2001

Collaborators

Detail Information

Publications62

  1. pmc Digital PCR
    B Vogelstein
    The Howard Hughes Medical Institute and The Johns Hopkins Oncology Center, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 96:9236-41. 1999
    ..The process provides a reliable and quantitative measure of the proportion of variant sequences within a DNA sample...
  2. pmc Targeted deletion of Smad4 shows it is required for transforming growth factor beta and activin signaling in colorectal cancer cells
    S Zhou
    The Howard Hughes Medical Institute at Johns Hopkins University, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 95:2412-6. 1998
    ..These results provide unequivocal evidence that mutational inactivation of Smad4 causes TGF-beta unresponsiveness and provide a basis for understanding the physiologic role of this gene in tumorigenesis...
  3. ncbi request reprint Identification of c-MYC as a target of the APC pathway
    T C He
    Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA
    Science 281:1509-12. 1998
    ..These results provide a molecular framework for understanding the previously enigmatic overexpression of c-MYC in colorectal cancers...
  4. pmc PAK1, a gene that can regulate p53 activity in yeast
    S Thiagalingam
    Johns Hopkins Oncology Center, Johns Hopkins School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 92:6062-6. 1995
    ..Thus, PAK1 is the prototype for a class of genes that can regulate the activity of p53 in vivo, and the system described here should be useful in identifying other genes in this class...
  5. ncbi request reprint A phosphatase associated with metastasis of colorectal cancer
    S Saha
    Howard Hughes Medical Institute, The Oncology Center, Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Science 294:1343-6. 2001
    ..3. These data suggest that the PRL-3 gene is important for colorectal cancer metastasis and provide a new therapeutic target for these intractable lesions...
  6. ncbi request reprint CDX2 is mutated in a colorectal cancer with normal APC/beta-catenin signaling
    L T da Costa
    Program in Human Genetics and Molecular Biology, The Johns Hopkins University, Baltimore, Maryland, MD 21231, USA
    Oncogene 18:5010-4. 1999
    ..Expression of CDX2 was found to be induced by restoring expression of wild type APC in a colorectal cancer cell line. These findings raise the intriguing possibility that CDX2 contributes to APC's tumor suppressive effects...
  7. ncbi request reprint The beta-catenin binding domain of adenomatous polyposis coli is sufficient for tumor suppression
    I M Shih
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 60:1671-6. 2000
    ..These effects were attenuated in lines with wild-type APC but with mutated beta-catenin. These findings suggest that the beta-catenin-binding domain in the central third of APC is sufficient for its tumor suppressor activity...
  8. ncbi request reprint Analysis of the 5' region of PMS2 reveals heterogeneous transcripts and a novel overlapping gene
    N C Nicolaides
    Howard Hughes Medical Institute, Baltimore, Maryland 21231, USA
    Genomics 29:329-34. 1995
    ..In addition, a novel gene encoding a 34.5-kDa polypeptide was found to initiate transcriptionally within PMS2 from the opposite strand...
  9. ncbi request reprint Characterization of MAD2B and other mitotic spindle checkpoint genes
    D P Cahill
    Program in Human Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland, 21231, USA
    Genomics 58:181-7. 1999
    ..No new mutations were identified, suggesting that genes yet to be discovered are responsible for most of the checkpoint defects observed in aneuploid cancers...
  10. ncbi request reprint PUMA induces the rapid apoptosis of colorectal cancer cells
    J Yu
    The Johns Hopkins Oncology Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Mol Cell 7:673-82. 2001
    ..Based on its unique expression patterns, p53 dependence, and biochemical properties, PUMA may be a direct mediator of p53-associated apoptosis...
  11. ncbi request reprint Identification of a gene located at chromosome 5q21 that is mutated in colorectal cancers
    K W Kinzler
    Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231
    Science 251:1366-70. 1991
    ..Further studies will be required to determine whether the gene is mutated in other sporadic tumors or in the germ line of patients with an inherited predisposition to colonic tumorigenesis...
  12. ncbi request reprint Secreted and cell surface genes expressed in benign and malignant colorectal tumors
    P Buckhaults
    Howard Hughes Medical Institute, Johns Hopkins Medical Institution, Baltimore, Maryland 21231, USA
    Cancer Res 61:6996-7001. 2001
    ..This study extends knowledge of the differences in gene expression that underlie various stages of neoplasia and suggests specific diagnostic approaches that may be useful for the early detection of colorectal neoplasia...
  13. ncbi request reprint 14-3-3Sigma is required to prevent mitotic catastrophe after DNA damage
    T A Chan
    The Johns Hopkins Oncology Center, Program in Human Genetics, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Nature 401:616-20. 1999
    ..These results may indicate a mechanism for maintaining the G2 checkpoint and preventing mitotic death...
  14. ncbi request reprint Characterization of human FAST-1, a TGF beta and activin signal transducer
    S Zhou
    Howard Hughes Medical Institute, Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Mol Cell 2:121-7. 1998
    ..These data suggest that responses to TGF beta family members may be mediated by a DNA-binding complex formed by hFAST-1, hSmad2, and hSmad4...
  15. pmc Apoptosis and APC in colorectal tumorigenesis
    P J Morin
    The Howard Hughes Medical Institute, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 93:7950-4. 1996
    ..Further evaluation demonstrated that this was due to the induction of cell death through apoptosis. These results suggest that apoptosis plays a role not only in advanced tumors but also at the very earliest stages of neoplasia...
  16. pmc PPARdelta is an APC-regulated target of nonsteroidal anti-inflammatory drugs
    T C He
    Johns Hopkins Oncology Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
    Cell 99:335-45. 1999
    ..These findings suggest that NSAIDs inhibit tumorigenesis through inhibition of PPARdelta, the gene for which is normally regulated by APC...
  17. pmc A simplified system for generating recombinant adenoviruses
    T C He
    The Howard Hughes Medical Institute, 424 North Bond Street, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 95:2509-14. 1998
    ..Homogeneous viruses can be obtained from this procedure without plaque purification. This system should expedite the process of generating and testing recombinant adenoviruses for a variety of purposes...
  18. ncbi request reprint Human Smad3 and Smad4 are sequence-specific transcription activators
    L Zawel
    Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Mol Cell 1:611-7. 1998
    ..These results define a novel biochemical property of Smad proteins that is likely to play a direct role in the biologic responses to TGF beta and related ligands...
  19. ncbi request reprint Cell surface tumor endothelial markers are conserved in mice and humans
    E B Carson-Walter
    The Howard Hughes Medical Institute, Baltimore, Maryland 21231, USA
    Cancer Res 61:6649-55. 2001
    ..The coordinate expression of TEM1, TEM5, and TEM8 on tumor endothelium in humans and mice makes these genes attractive targets for the development of antiangiogenic therapies...
  20. pmc Ferredoxin reductase affects p53-dependent, 5-fluorouracil-induced apoptosis in colorectal cancer cells
    P M Hwang
    Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Nat Med 7:1111-7. 2001
    ..These data, coupled with the effects of pharmacologic inhibitors of reactive oxygen species, indicate that FR contributes to p53-mediated apoptosis through the generation of oxidative stress in mitochondria...
  21. ncbi request reprint Counting alleles reveals a connection between chromosome 18q loss and vascular invasion
    W Zhou
    Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD 21231, USA
    Nat Biotechnol 19:78-81. 2001
    ..This approach imparts a rigorous statistical basis to LOH analyses, and should be able to provide more reliable information than heretofore possible in LOH studies of diverse tumor types...
  22. pmc Converting cancer genes into killer genes
    L T da Costa
    Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 93:4192-6. 1996
    ..The strategy may be generally applicable to neoplastic diseases in which the underlying patterns of genetic alterations or abnormal gene expression are known...
  23. ncbi request reprint Requirement for p53 and p21 to sustain G2 arrest after DNA damage
    F Bunz
    The Howard Hughes Medical Institute and The Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA
    Science 282:1497-501. 1998
    ..Thus, p53 and p21 appear to be essential for maintaining the G2 checkpoint in human cells...
  24. ncbi request reprint 14-3-3 sigma is a p53-regulated inhibitor of G2/M progression
    H Hermeking
    Johns Hopkins Oncology Center, Baltimore, Maryland, USA
    Mol Cell 1:3-11. 1997
    ..As the fission yeast 14-3-3 homologs rad24 and rad25 mediate similar checkpoint effects, these results document a molecular mechanism for G2/M control that is conserved throughout eukaryotic evolution and regulated in human cells by p53...
  25. ncbi request reprint Mad-related genes in the human
    G J Riggins
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Nat Genet 13:347-9. 1996
    ..These data suggest that this gene family may prove to be important in the suppression of neoplasia, imparting the growth inhibitory effects of TGF-beta-like ligands...
  26. ncbi request reprint Evidence that genetic instability occurs at an early stage of colorectal tumorigenesis
    I M Shih
    Johns Hopkins Oncology Center, Department of Pathology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Cancer Res 61:818-22. 2001
    ..These findings demonstrate that AI is a common event, even in very small tumors, and suggest that chromosomal instability occurs very early during colorectal neoplasia...
  27. ncbi request reprint Short mononucleotide repeat sequence variability in mismatch repair-deficient cancers
    L Zhang
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 61:3801-5. 2001
    ..In particular, (G)(8) tracts were considerably more prone to mutation than (A)(8) tracts, and the sequences or chromatin structures surrounding the mononucleotide tracts seemed to affect their mutability significantly...
  28. pmc Identification and classification of p53-regulated genes
    J Yu
    Graduate Program in Human Genetics, The Johns Hopkins University, Baltimore, MD 21205, USA
    Proc Natl Acad Sci U S A 96:14517-22. 1999
    ..The results revealed substantial heterogeneity in the transcriptional responses to p53, even in cells derived from a single epithelial cell type, and pave the way to a deeper understanding of p53 tumor suppressor action...
  29. ncbi request reprint Suppression of human colorectal carcinoma cell growth by wild-type p53
    S J Baker
    Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 249:912-5. 1990
    ....
  30. ncbi request reprint Genomic organization of the human PMS2 gene family
    N C Nicolaides
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Genomics 30:195-206. 1995
    ..The similarity and number of these genes made specific amplification of hPMS2 problematic, but knowledge of them aided the successful design of oligonucleotides for this purpose...
  31. pmc Genetic disruption of PPARdelta decreases the tumorigenicity of human colon cancer cells
    B H Park
    Johns Hopkins Oncology Center and Howard Hughes Medical Institute, 1650 Orleans Street, Room 590, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 98:2598-603. 2001
    ..These data suggest that suppression of PPARdelta expression contributes to the growth-inhibitory effects of the APC tumor suppressor...
  32. ncbi request reprint Genes expressed in human tumor endothelium
    B St Croix
    Johns Hopkins Oncology Center, Howard Hughes Medical Institute, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Science 289:1197-202. 2000
    ..These studies demonstrate that tumor and normal endothelium are distinct at the molecular level, a finding that may have significant implications for the development of anti-angiogenic therapies...
  33. ncbi request reprint Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC
    P J Morin
    Howard Hughes Medical Institute and Johns Hopkins Oncology Center, 424 North Bond Street, Baltimore, MD 21231, USA
    Science 275:1787-90. 1997
    ..These results indicate that regulation of beta-catenin is critical to APC's tumor suppressive effect and that this regulation can be circumvented by mutations in either APC or beta-catenin...
  34. ncbi request reprint Role of BAX in the apoptotic response to anticancer agents
    L Zhang
    Howard Hughes Medical Institute, Oncology Center, and Program in Human Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Science 290:989-92. 2000
    ..These results establish an unambiguous role for BAX in apoptotic processes in human epithelial cancers and may have implications for cancer chemoprevention strategies...
  35. pmc Mechanisms underlying losses of heterozygosity in human colorectal cancers
    S Thiagalingam
    Oncology Center, Program in Molecular Biology, Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 98:2698-702. 2001
    ....
  36. ncbi request reprint Mutations of mitotic checkpoint genes in human cancers
    D P Cahill
    The Johns Hopkins Oncology Center, Program in Human Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Nature 392:300-3. 1998
    ..The normal mitotic checkpoints of cells displaying microsatellite instability become defective upon transfer of mutant hBUB1 alleles from either of two CIN cancers...
  37. ncbi request reprint Detecting colorectal cancer in stool with the use of multiple genetic targets
    S M Dong
    Division of Head and Neck Cancer Research, Department of Otolaryngology-Head and Neck Surgery, The Johns Hopkins Medical School, The Johns Hopkins University, Baltimore, MD, USA
    J Natl Cancer Inst 93:858-65. 2001
    ..Additional work is needed to determine the specificity of these genetic tests for detecting colorectal neoplasia in asymptomatic patients and to more precisely estimate the prevalence of the mutations and sensitivity of the assay...
  38. ncbi request reprint Association of the APC tumor suppressor protein with catenins
    L K Su
    Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 262:1734-7. 1993
    ..A 27-residue fragment of APC containing a 15-amino acid repeat was sufficient for the interaction with the catenins. These results suggest an important link between tumor initiation and cell adhesion...
  39. pmc A naturally occurring hPMS2 mutation can confer a dominant negative mutator phenotype
    N C Nicolaides
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Mol Cell Biol 18:1635-41. 1998
    ..These results have significant implications for understanding the relationship between mutagenesis and carcinogenesis and the ability to generate mammalian cells with mutator phenotypes...
  40. ncbi request reprint Conversion of diploidy to haploidy
    H Yan
    Howard Hughes Medical Institute, The Oncology Center, Department of Mathematical Sciences, The Johns Hopkins University, Baltimore, Maryland 21231, USA
    Nature 403:723-4. 2000
  41. ncbi request reprint Going mad with Smads
    S Zhou
    Johns Hopkins Oncology Center, Baltimore, MD 21231, USA
    N Engl J Med 341:1144-6. 1999
  42. pmc Top-down morphogenesis of colorectal tumors
    I M Shih
    The Howard Hughes Medical Institute, Johns Hopkins Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 98:2640-5. 2001
    ..Genetically altered cells in the superficial portions of the mucosae spread laterally and downward to form new crypts that first connect to preexisting normal crypts and eventually replace them...
  43. ncbi request reprint Sulindac suppresses tumorigenesis in the Min mouse
    Y Beazer-Barclay
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Carcinogenesis 17:1757-60. 1996
    ..The conservation of sulindac activity in the Min mouse provides an opportunity to explore the mechanism of sulindac suppression as well as to test other potential chemopreventive agents...
  44. ncbi request reprint Characterization of the yeast transcriptome
    V E Velculescu
    Program in Human Genetics and Molecular Biology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cell 88:243-51. 1997
    ..These studies provide insight into global patterns of gene expression in yeast and demonstrate the feasibility of genome-wide expression studies in eukaryotes...
  45. ncbi request reprint Chromosome 17 deletions and p53 gene mutations in colorectal carcinomas
    S J Baker
    Oncology Center, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 244:217-21. 1989
    ..The data suggest that p53 gene mutations may be involved in colorectal neoplasia, perhaps through inactivation of a tumor suppressor function of the wild-type p53 gene...
  46. ncbi request reprint Securin is required for chromosomal stability in human cells
    P V Jallepalli
    The Johns Hopkins Oncology Center, 1650 Orleans Street, Baltimore, MD 21231, USA
    Cell 105:445-57. 2001
    ..These results illuminate the function of mammalian securin and show that it is essential for the maintenance of euploidy...
  47. ncbi request reprint Use of isogenic human cancer cells for high-throughput screening and drug discovery
    C J Torrance
    The Howard Hughes Medical Institute, 1650 Orleans Street, Baltimore, MD 21231, USA
    Nat Biotechnol 19:940-5. 2001
    ..The present data demonstrate a broadly applicable approach for mining therapeutic agents targeted to the specific genetic alterations responsible for cancer development...
  48. ncbi request reprint Monoallelic mutation analysis (MAMA) for identifying germline mutations
    N Papadopoulos
    Howard Hughes Medical Institute, Baltimore, Maryland, USA
    Nat Genet 11:99-102. 1995
    ....
  49. pmc Carcinogen-specific induction of genetic instability
    A Bardelli
    The Johns Hopkins Oncology Center, Howard Hughes Medical Institute, and Graduate Program in Human Genetics and Molecular Biology, 1650 Orleans Street, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 98:5770-5. 2001
    ..These data demonstrate that exposure to specific carcinogens can indeed select for tumor cells with distinct forms of genetic instability and vice versa...
  50. ncbi request reprint Mutation screening of the TNFRSF11A gene encoding receptor activator of NF kappa B (RANK) in familial and sporadic Paget's disease of bone and osteosarcoma
    A B Sparks
    Molecular Genetics Laboratory, Johns Hopkins Oncology Center, Baltimore, MD, USA
    Calcif Tissue Int 68:151-5. 2001
    ..These data indicate that TNFRSF11A mutations contribute neither to the vast majority of cases of sporadic or familial PDB, nor to the development of osteosarcoma...
  51. ncbi request reprint Identification of FAP locus genes from chromosome 5q21
    K W Kinzler
    Molecular Genetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 253:661-5. 1991
    ..Both genes were also expressed in a wide variety of tissues. Further studies of MCC and APC and their potential interaction should prove useful for understanding colorectal neoplasia...
  52. ncbi request reprint Genetic instabilities in human cancers
    C Lengauer
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Nature 396:643-9. 1998
    ..Recognition and comparison of these instabilities are leading to new insights into tumour pathogenesis...
  53. ncbi request reprint Molecular cloning of the N-terminus of GTBP
    N C Nicolaides
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Genomics 31:395-7. 1996
    ..Here, we describe the isolation of its 5' terminus, allowing definition of the entire coding region. Several polymorphisms within the 5' end were identified and are presented...
  54. ncbi request reprint APC binds to the novel protein EB1
    L K Su
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 55:2972-7. 1995
    ..This conservation suggests an essential function for EB1 that might provide clues to the mechanism through which APC suppresses colonic neoplasia...
  55. ncbi request reprint A model for p53-induced apoptosis
    K Polyak
    The Howard Hughes Medical Institute, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
    Nature 389:300-5. 1997
    ....
  56. ncbi request reprint Specific p53 mutations detected in plasma and tumors of hepatocellular carcinoma patients by electrospray ionization mass spectrometry
    P E Jackson
    Department of Environmental Health Sciences, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
    Cancer Res 61:33-5. 2001
    ..Ten plasma samples from healthy individuals were all negative. This molecular diagnostic technique has implications for prevention trials and for the early diagnosis of HCC...
  57. pmc Combination bacteriolytic therapy for the treatment of experimental tumors
    L H Dang
    The Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, The Johns Hopkins School of Medicine, and the Johns Hopkins Oncology Center, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 98:15155-60. 2001
    ..This strategy, called combination bacteriolytic therapy (COBALT), has the potential to add a new dimension to the treatment of cancer...
  58. ncbi request reprint Assessing tumors in living animals through measurement of urinary beta-human chorionic gonadotropin
    I M Shih
    The Johns Hopkins Oncology Center, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Nat Med 6:711-4. 2000
  59. ncbi request reprint Serial analysis of gene expression
    V E Velculescu
    Oncology Center, Johns Hopkins University, Baltimore, MD 21231, USA
    Science 270:484-7. 1995
    ..SAGE should provide a broadly applicable means for the quantitative cataloging and comparison of expressed genes in a variety of normal, developmental, and disease states...
  60. pmc Identification of CDK4 as a target of c-MYC
    H Hermeking
    Howard Hughes Medical Institute, The Johns Hopkins Oncology Center, The Johns Hopkins University School of Medicine, 424 North Bond Street, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 97:2229-34. 2000
    ..Ectopic expression of CDK4 in these cells partially alleviated the growth defect. Thus, CDK4 provides a direct link between the oncogenic effects of c-MYC and cell-cycle regulation...
  61. ncbi request reprint Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene
    L K Su
    Molecular Genetics Laboratory, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 256:668-70. 1992
    ..Sequence comparison of mApc between normal and Min-affected mice identified a nonsense mutation, which cosegregated with the Min phenotype. This mutation is analogous to those found in FAP kindreds and in sporadic colorectal cancers...
  62. ncbi request reprint Identification of p53 as a sequence-specific DNA-binding protein
    S E Kern
    Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21231
    Science 252:1708-11. 1991
    ..These data suggest that a function of p53 may be mediated by its ability to bind to specific DNA sequences in the human genome, and that this activity is altered by mutations that occur in human tumors...