Genomes and Genes
S B Baylin
Affiliation: Johns Hopkins University
- Methylation-specific PCRJ 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...
- Tying it all together: epigenetics, genetics, cell cycle, and cancerS B Baylin
Johns Hopkins Comprehensive Cancer Center and the Department of Medicine, Baltimore, MD 21231, USA
Science 277:1948-9. 1997
- DNA hypermethylation in tumorigenesis: epigenetics joins geneticsS 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...
- Methylation-specific PCR: a novel PCR assay for methylation status of CpG islandsJ G Herman
Oncology Center, Johns Hopkins Medical Institutions, Baltimore, MD 21231, USA
Proc Natl Acad Sci U S A 93:9821-6. 1996....
- Aberrant patterns of DNA methylation, chromatin formation and gene expression in cancerS 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...
- Sequence-specific DNA binding activity of RNA helicase A to the p16INK4a promoterS 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...
- DNA methylation, chromatin inheritance, and cancerM 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....
- 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 tumorigenesisM 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...
- A gene hypermethylation profile of human cancerM Esteller
The Johns Hopkins Comprehensive Cancer Center, 1650 Orleans Street, Baltimore, MD 21231, USA
Cancer Res 61:3225-9. 2001....
- Transcriptional regulation of Wnt inhibitory factor-1 by Miz-1/c-MycJ 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...
- p14ARF silencing by promoter hypermethylation mediates abnormal intracellular localization of MDM2M 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...
- Methylation patterns of the E-cadherin 5' CpG island are unstable and reflect the dynamic, heterogeneous loss of E-cadherin expression during metastatic progressionJ R Graff
Comprehensive Cancer Center, Johns Hopkins University, Baltimore, Maryland 21231, USA
J Biol Chem 275:2727-32. 2000....
- Dnmt3a and Dnmt3b are transcriptional repressors that exhibit unique localization properties to heterochromatinK 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....
- Roles of trk family neurotrophin receptors in medullary thyroid carcinoma development and progressionL 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...
- Cell-substratum interactions mediate oncogene-induced phenotype of lung cancer cellsL 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...
- Loss of a single Hic1 allele accelerates polyp formation in Apc(Δ716) miceH P Mohammad
The Sidney Kimmel Comprehensive Cancer Institute at Johns Hopkins, Johns Hopkins University, Baltimore, MD, USA
Oncogene 30:2659-69. 2011....
- DNMT1 binds HDAC2 and a new co-repressor, DMAP1, to form a complex at replication fociM 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...
- Notch signaling induces cell cycle arrest in small cell lung cancer cellsV 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...
- A potential tumor suppressor role for Hic1 in breast cancer through transcriptional repression of ephrin-A1W 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....
- DNA methylation patterns in hereditary human cancers mimic sporadic tumorigenesisM 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...
- Aberrant gene silencing in tumor progression: implications for control of cancerS 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...
- Role of nuclear architecture in epigenetic alterations in cancerH 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...
- Abrogation of the Rb/p16 tumor-suppressive pathway in virtually all pancreatic carcinomasM 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...
- Mice deficient in the candidate tumor suppressor gene Hic1 exhibit developmental defects of structures affected in the Miller-Dieker syndromeM 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...
- Inactivation of CACNA1G, a T-type calcium channel gene, by aberrant methylation of its 5' CpG island in human tumorsM 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...
- Methylation of the HIC-1 candidate tumor suppressor gene in human breast cancerH 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...
- Cloning and chromosomal localization of the human BARX2 homeobox protein geneA 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...
- p53 activates expression of HIC-1, a new candidate tumour suppressor gene on 17p13.3M M Wales
Human Genetics Graduate Program, Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
Nat Med 1:570-7. 1995..3...
- New 5' regions of the murine and human genes for DNA (cytosine-5)-methyltransferaseJ 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...
- Frequent aberrant methylation of p16INK4a in primary rat lung tumorsD 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...
- An achaete-scute homologue essential for neuroendocrine differentiation in the lungM Borges
The Oncology Center, The Johns Hopkins Medical Institutions, Baltimore, Maryland 21231, USA
Nature 386:852-5. 1997....
- Frequent epigenetic inactivation of Wnt antagonist genes in breast cancerH 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...
- Frequent epigenetic silencing of the bone morphogenetic protein 2 gene through methylation in gastric carcinomasX 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...
- Isolation and characterization of the cDNA encoding human DNA methyltransferaseR 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...