Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Emi Ota Machida"'
Autor:
Kornel E. Schuebel, Stephen B. Baylin, Yang Y. Yu, Steven A. Belinsky, Christine A. Stidley, Mathewos Tessema, Emi Ota Machida
Publikováno v:
Carcinogenesis. 30:1132-1138
Aberrant promoter hypermethylation is one of the major mechanisms in carcinogenesis and some critical growth regulatory genes have shown commonality in methylation across solid tumors. Twenty-six genes, 14 identified through methylation in colon and
Autor:
D. Neil Watkins, Leander Van Neste, Stephen B. Baylin, Hariharan Easwaran, Mingzhou Guo, Sabine C. Glöckner, James G. Herman, Wei Zhang, Kornel E. Schuebel, Nita Ahuja, David H. Wang, Emi Ota Machida
Publikováno v:
Cancer Research. 68:2764-2772
SRY-box containing gene 17 (Sox17) is a member of the high mobility group (HMG) transcription factor superfamily, which plays critical roles in the regulation of development and stem/precursor cell function, at least partly through repression of Wnt
Autor:
Marco A. Riojas, Sabine C. Glöckner, Emi Ota Machida, Nita Ahuja, Stephen B. Baylin, Mingzhou Guo
Publikováno v:
Cancer Biology & Therapy. 6:1710-1716
The hypermethylation of tumor-suppressor gene promoter regions has been shown to result in the epigenetic inactivation of many genes. ASC/TMS1 is a pro-apoptotic gene that has been shown to be methylated in many different human neoplasms. The methyla
Autor:
Randy Willink, Malcolm V. Brock, Steven A. Belinsky, Stephen B. Baylin, Mathewos Tessema, Wayne Yu, Leander Van Neste, Emi Ota Machida, Christine A. Stidley, Kieu Do, Yang Y. Yu
Publikováno v:
Cancer research. 68(6)
Chromosomal aberrations associated with lung cancer are frequently observed in the long arm of chromosome 6. A candidate susceptibility locus at 6q23-25 for lung cancer was recently identified; however, no tumor suppressor genes inactivated by mutati
Autor:
William H. Westra, James G. Herman, Emi Ota Machida, Stephen B. Baylin, Julien D.F. Licchesi, Craig M. Hooker
Publikováno v:
Carcinogenesis. 29(5)
Background: Atypical adenomatous hyperplasia (AAH) is now recognized as a precursor lesion from which lung adenocarcinomas arise and thus represents an ideal target for studying the early genetic and epigenetic alterations associated with lung tumori