S B Baylin

Summary

Affiliation: Johns Hopkins University
Country: USA

Publications

  1. ncbi request reprint Methylation-specific PCR
    J G Herman
    The Johns Hopkins Oncology Center, Baltimore, Maryland, USA
    Curr Protoc Hum Genet . 2001
  2. ncbi request reprint DNA hypermethylation in tumorigenesis: epigenetics joins genetics
    S B Baylin
    The Johns Hopkins Oncology Center, 1650 East Orleans Street, Baltimore, MD 21231, USA
    Trends Genet 16:168-74. 2000
  3. ncbi request reprint Tying it all together: epigenetics, genetics, cell cycle, and cancer
    S B Baylin
    Johns Hopkins Comprehensive Cancer Center and the Department of Medicine, Baltimore, MD 21231, USA
    Science 277:1948-9. 1997
  4. pmc Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands
    J G Herman
    Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 93:9821-6. 1996
  5. ncbi request reprint Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer
    S B Baylin
    The Johns Hopkins Comprehensive Cancer Center and Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Hum Mol Genet 10:687-92. 2001
  6. ncbi request reprint A gene hypermethylation profile of human cancer
    M Esteller
    The Johns Hopkins Comprehensive Cancer Center, 1650 Orleans Street, Baltimore, MD 21231, USA
    Cancer Res 61:3225-9. 2001
  7. ncbi request reprint Promoter hypermethylation of the DNA repair gene O(6)-methylguanine-DNA methyltransferase is associated with the presence of G:C to A:T transition mutations in p53 in human colorectal tumorigenesis
    M Esteller
    Tumor Biology, The Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 61:4689-92. 2001
  8. ncbi request reprint DNA methylation, chromatin inheritance, and cancer
    M R Rountree
    The Johns Hopkins Oncology Center, Tumor Biology Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland, MD 21231, USA
    Oncogene 20:3156-65. 2001
  9. ncbi request reprint Sequence-specific DNA binding activity of RNA helicase A to the p16INK4a promoter
    S Myöhänen
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    J Biol Chem 276:1634-42. 2001
  10. ncbi request reprint p14ARF silencing by promoter hypermethylation mediates abnormal intracellular localization of MDM2
    M Esteller
    Department of Oncology, The Johns Hopkins Comprehensive Cancer Center, Baltimore, Maryland 21231, USA
    Cancer Res 61:2816-21. 2001

Collaborators

Detail Information

Publications35

  1. ncbi request reprint Methylation-specific PCR
    J G Herman
    The Johns Hopkins Oncology Center, Baltimore, Maryland, USA
    Curr Protoc Hum Genet . 2001
    ..Methylation-specific PCR can be used to investigate imprinted genes, to assess human tumors for clonality by studying genes inactivated on the X chromosome, and to examine abnormally methylated CpG islands in neoplasia...
  2. ncbi request reprint DNA hypermethylation in tumorigenesis: epigenetics joins genetics
    S B Baylin
    The Johns Hopkins Oncology Center, 1650 East Orleans Street, Baltimore, MD 21231, USA
    Trends Genet 16:168-74. 2000
    ..Methylation changes constitute potentially sensitive molecular markers to define risk states, monitor prevention strategies, achieve early diagnosis, and track the prognosis of cancer...
  3. ncbi request reprint Tying it all together: epigenetics, genetics, cell cycle, and cancer
    S B Baylin
    Johns Hopkins Comprehensive Cancer Center and the Department of Medicine, Baltimore, MD 21231, USA
    Science 277:1948-9. 1997
  4. pmc Methylation-specific PCR: a novel PCR assay for methylation status of CpG islands
    J G Herman
    Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 93:9821-6. 1996
    ....
  5. ncbi request reprint Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancer
    S B Baylin
    The Johns Hopkins Comprehensive Cancer Center and Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Hum Mol Genet 10:687-92. 2001
    ..In the translational arena, the promoter hypermethylation changes hold great promise as DNA tumor markers and their potentially reversible state creates a target for cancer therapeutic strategies involving gene reactivation...
  6. ncbi request reprint A gene hypermethylation profile of human cancer
    M Esteller
    The Johns Hopkins Comprehensive Cancer Center, 1650 Orleans Street, Baltimore, MD 21231, USA
    Cancer Res 61:3225-9. 2001
    ....
  7. ncbi request reprint Promoter hypermethylation of the DNA repair gene O(6)-methylguanine-DNA methyltransferase is associated with the presence of G:C to A:T transition mutations in p53 in human colorectal tumorigenesis
    M Esteller
    Tumor Biology, The Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 61:4689-92. 2001
    ..008). Our data suggest that epigenetic silencing of MGMT by promoter hypermethylation may lead to G:C to A:T transition mutations in p53...
  8. ncbi request reprint DNA methylation, chromatin inheritance, and cancer
    M R Rountree
    The Johns Hopkins Oncology Center, Tumor Biology Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland, MD 21231, USA
    Oncogene 20:3156-65. 2001
    ....
  9. ncbi request reprint Sequence-specific DNA binding activity of RNA helicase A to the p16INK4a promoter
    S Myöhänen
    Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    J Biol Chem 276:1634-42. 2001
    ..This interaction is decreased in cancer cells, where this gene is aberrantly transcriptionally silent...
  10. ncbi request reprint p14ARF silencing by promoter hypermethylation mediates abnormal intracellular localization of MDM2
    M Esteller
    Department of Oncology, The Johns Hopkins Comprehensive Cancer Center, Baltimore, Maryland 21231, USA
    Cancer Res 61:2816-21. 2001
    ..Taken together, these data support that epigenetic silencing of p14ARF by promoter hypermethylation is a key mechanism in the disturbance of the MDM2 nuclear localization in human cancer...
  11. ncbi request reprint Dnmt3a and Dnmt3b are transcriptional repressors that exhibit unique localization properties to heterochromatin
    K E Bachman
    The Johns Hopkins Oncology Center, Tumor Biology Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    J Biol Chem 276:32282-7. 2001
    ....
  12. ncbi request reprint Methylation patterns of the E-cadherin 5' CpG island are unstable and reflect the dynamic, heterogeneous loss of E-cadherin expression during metastatic progression
    J R Graff
    Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
    J Biol Chem 275:2727-32. 2000
    ....
  13. pmc Transcriptional regulation of Wnt inhibitory factor-1 by Miz-1/c-Myc
    J D F Licchesi
    Cancer Biology Program, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, MD 21231, USA
    Oncogene 29:5923-34. 2010
    ..Our data reveal novel insights into c-Myc-mediated DNA methylation-dependent transcriptional silencing, a mechanism that might contribute to the dysregulation of Wnt signaling in cancer...
  14. pmc Roles of trk family neurotrophin receptors in medullary thyroid carcinoma development and progression
    L M McGregor
    Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
    Proc Natl Acad Sci U S A 96:4540-5. 1999
    ..These results suggest that trk family receptor genes participate in MTC development and progression, and, in particular, that trkB may limit MTC tumor growth by inhibition of angiogenesis...
  15. pmc Loss of a single Hic1 allele accelerates polyp formation in Apc(Δ716) mice
    H P Mohammad
    The Sidney Kimmel Comprehensive Cancer Institute at Johns Hopkins, Johns Hopkins University, Baltimore, MD, USA
    Oncogene 30:2659-69. 2011
    ....
  16. ncbi request reprint Cell-substratum interactions mediate oncogene-induced phenotype of lung cancer cells
    L F Barr
    Department of Medicine, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA
    Cell Growth Differ 7:1149-56. 1996
    ..However, forced suspension of such cells restores the expression of neuroendocrine SCLC features. These studies indicate that cell environment, as much as gene expression events, profoundly affects aspects of the SCLC cell phenotype...
  17. ncbi request reprint Notch signaling induces cell cycle arrest in small cell lung cancer cells
    V Sriuranpong
    Oncology Center, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231, USA
    Cancer Res 61:3200-5. 2001
    ..Notch activation, in the setting of a highly proliferative hASH1-dependent NE neoplasm, can be associated with growth arrest and apparent reduction in neoplastic potential...
  18. ncbi request reprint DNMT1 binds HDAC2 and a new co-repressor, DMAP1, to form a complex at replication foci
    M R Rountree
    The Johns Hopkins Oncology Center, Tumor Biology Laboratory, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
    Nat Genet 25:269-77. 2000
    ..Thus, DNMT1 not only maintains DNA methylation, but also may directly target, in a heritable manner, transcriptionally repressive chromatin to the genome during DNA replication...
  19. pmc A potential tumor suppressor role for Hic1 in breast cancer through transcriptional repression of ephrin-A1
    W Zhang
    The Sidney Kimmel Comprehensive Cancer Center and Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Oncogene 29:2467-76. 2010
    ....
  20. pmc The NuRD complex cooperates with DNMTs to maintain silencing of key colorectal tumor suppressor genes
    Y Cai
    Department of Oncology and The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins University, Baltimore, MD, USA
    Oncogene 33:2157-68. 2014
    ..Since CHD4 has ATPase activity, our data identify CHD4 as a potentially novel drug target in cancer. ..
  21. doi request reprint Role of nuclear architecture in epigenetic alterations in cancer
    H P Easwaran
    The Sidney Kimmel Cancer Research Center at Johns Hopkins University, Bunting Blaustein Cancer Research Building, Baltimore, Maryland 21231 1000, USA
    Cold Spring Harb Symp Quant Biol 75:507-15. 2010
    ..We emphasize the need for further studies to elucidate the direct relationship between nuclear structure alterations and aberrant epigenetic patterns in cancers...
  22. ncbi request reprint Aberrant gene silencing in tumor progression: implications for control of cancer
    S B Baylin
    The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland 21231, USA
    Cold Spring Harb Symp Quant Biol 70:427-33. 2005
    ..This hypothesis has potential impact on means to prevent and control cancer and for the use of epigenetic markers for cancer risk assessment and early diagnosis...
  23. ncbi request reprint DNA methylation patterns in hereditary human cancers mimic sporadic tumorigenesis
    M Esteller
    The Johns Hopkins Oncology Center, 1650 Orleans Street, Baltimore, MD 21231, USA
    Hum Mol Genet 10:3001-7. 2001
    ..This study demonstrates that hereditary cancers "mimic" the DNA methylation patterns present in the sporadic tumors...
  24. ncbi request reprint Abrogation of the Rb/p16 tumor-suppressive pathway in virtually all pancreatic carcinomas
    M Schutte
    Department of Oncology, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21205, USA
    Cancer Res 57:3126-30. 1997
    ..Similar results were obtained in an independently analyzed series of 19 pancreatic carcinomas. These data demonstrate the central role of the Rb/p16 pathway in the development of pancreatic carcinoma...
  25. ncbi request reprint Methylation of the HIC-1 candidate tumor suppressor gene in human breast cancer
    H Fujii
    The Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA
    Oncogene 16:2159-64. 1998
    ..Furthermore, the HIC-1 gene is densely methylated in approximately one-half of the alleles in normal breast epithelium, which may predispose this tissue to inactivation of this gene by loss of heterozygosity...
  26. ncbi request reprint Inactivation of CACNA1G, a T-type calcium channel gene, by aberrant methylation of its 5' CpG island in human tumors
    M Toyota
    The Johns Hopkins Oncology Center, Baltimore, Maryland 21231, USA
    Cancer Res 59:4535-41. 1999
    ..Inactivation of CACNA1G may play a role in cancer development by modulating calcium signaling, which potentially affects cell proliferation and apoptosis...
  27. ncbi request reprint Cloning and chromosomal localization of the human BARX2 homeobox protein gene
    A Krasner
    Department of Oncology, John Hopkins University School of Medicine, Baltimore, MD 21231, USA
    Gene 250:171-80. 2000
    ..This chromosomal location, along with the reported expression of murine barx2 in craniofacial development, suggests that BARX2 may be causally involved in the craniofacial abnormalities in Jacobsen syndrome...
  28. ncbi request reprint Mice deficient in the candidate tumor suppressor gene Hic1 exhibit developmental defects of structures affected in the Miller-Dieker syndrome
    M G Carter
    Graduate Program in Human Genetics and Molecular Biology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
    Hum Mol Genet 9:413-9. 2000
    ..These findings demonstrate a role for Hic1 in the development of structures affected in the Miller-Dieker syndrome, and provide functional evidence to strengthen its candidacy as a gene involved in this disorder...
  29. ncbi request reprint p53 activates expression of HIC-1, a new candidate tumour suppressor gene on 17p13.3
    M M Wales
    Human Genetics Graduate Program, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Nat Med 1:570-7. 1995
    ..3...
  30. ncbi request reprint New 5' regions of the murine and human genes for DNA (cytosine-5)-methyltransferase
    J A Yoder
    Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, New York, New York 10032, USA
    J Biol Chem 271:31092-7. 1996
    ..Tanigawa, G., and Szyf, M. (1992) J. Biol. Chem. 267, 7368-7377) actually lies in an intron that is more than 5 kilobases downstream of the transcription start sites...
  31. pmc Frequent aberrant methylation of p16INK4a in primary rat lung tumors
    D S Swafford
    Inhalation Toxicology Research Institute, Albuquerque, New Mexico 87185, USA
    Mol Cell Biol 17:1366-74. 1997
    ..Furthermore, rat lung cancer appears to be an excellent model in which to investigate the mechanisms of de novo gene methylation and the role of p16 dysfunction in the progression of neoplasia...
  32. ncbi request reprint An achaete-scute homologue essential for neuroendocrine differentiation in the lung
    M Borges
    The Oncology Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
    Nature 386:852-5. 1997
    ....
  33. pmc Frequent epigenetic inactivation of Wnt antagonist genes in breast cancer
    H Suzuki
    First Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan
    Br J Cancer 98:1147-56. 2008
    ..Our results confirm the frequent methylation and silencing of Wnt antagonist genes in breast cancer, and suggest that their loss of function contributes to activation of Wnt signalling in breast carcinogenesis...
  34. ncbi request reprint Frequent epigenetic silencing of the bone morphogenetic protein 2 gene through methylation in gastric carcinomas
    X Z Wen
    Department of Molecular Oncology, Graduate School of Medicine and Dentistry, Tokyo Medical and Dental University, Bunkyo ku, Tokyo, Japan
    Oncogene 25:2666-73. 2006
    ..7%) than in intestinal type (25%) gastric carcinomas (P = 0.007). Thus, aberrant BMP-2 methylation and the resultant loss of BMP-2 expression may be related to gastric carcinogenesis, particularly in the diffuse type...
  35. pmc Isolation and characterization of the cDNA encoding human DNA methyltransferase
    R W Yen
    Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231
    Nucleic Acids Res 20:2287-91. 1992
    ..Isolation of the cDNA for human DNA MTase will allow further study of the regulation of DNA MTase expression, and of the role of this enzyme in establishing DNA methylation patterns in both normal and neoplastic cells...