TY - JOUR
T1 - Molecular Mechanisms in Barrett's Metaplasia and Its Progression
AU - Izzo, Julie G.
AU - Luthra, Rajyalakshmi
AU - Wu, Tseung Teh
AU - Correa, Arlene M.
AU - Luthra, Madan
AU - Anandasabapathy, Sharmila
AU - Chao, K. S.Clifford
AU - Hung, Mien Chie
AU - Aggarwal, Bharat
AU - Hittelman, Walter N.
AU - Ajani, Jaffer A.
N1 - Funding Information:
Supported in part by National Institutes of Health grant nos. NIH-NCI RO1 DE13157-04 (to W.N.H.), NIH-NCI EDRN CA 86390 (to M.R.S.), and the University of Texas M. D. Anderson Esophageal Multidisciplinary Research Project Grant, Riverkreek Foundation, and the Dallas, Cantu, Smith, and Park Families.
PY - 2007/4
Y1 - 2007/4
N2 - The dramatic increase in the incidence and poor overall survival rates of esophageal/gastroesophageal junction adenocarcinoma underscore the necessity to discover molecular markers that can be used for risk assessment, early diagnosis, and targeted therapeutic intervention. Barrett's esophagus (BE) is proposed to represent a precursor of esophageal/gastroesophageal junction adenocarcinoma. BE progression to invasive cancer is defined by a metaplasia-dysplasia-carcinoma progression characterized by an increasing accumulation of genetic changes associated with alterations in molecular gatekeepers of cell circuitries and tissue homeostasis. Using a combination of in situ tissue-based and high-throughput analyses, we investigated alterations of cell-cycle regulators and inflammation-associated molecular effectors. Our data suggest a potential synergistic effect of these alterations for the BE progression to cancer, and underscore the potential use of these markers: (1) in molecular panels assessing cancer risk in BE patients; and (2) as potential therapeutic targets for chemopreventive interventions and to enhance response to anti-neoplastic therapies.
AB - The dramatic increase in the incidence and poor overall survival rates of esophageal/gastroesophageal junction adenocarcinoma underscore the necessity to discover molecular markers that can be used for risk assessment, early diagnosis, and targeted therapeutic intervention. Barrett's esophagus (BE) is proposed to represent a precursor of esophageal/gastroesophageal junction adenocarcinoma. BE progression to invasive cancer is defined by a metaplasia-dysplasia-carcinoma progression characterized by an increasing accumulation of genetic changes associated with alterations in molecular gatekeepers of cell circuitries and tissue homeostasis. Using a combination of in situ tissue-based and high-throughput analyses, we investigated alterations of cell-cycle regulators and inflammation-associated molecular effectors. Our data suggest a potential synergistic effect of these alterations for the BE progression to cancer, and underscore the potential use of these markers: (1) in molecular panels assessing cancer risk in BE patients; and (2) as potential therapeutic targets for chemopreventive interventions and to enhance response to anti-neoplastic therapies.
UR - https://www.scopus.com/pages/publications/34247134563
U2 - 10.1053/j.seminoncol.2007.01.005
DO - 10.1053/j.seminoncol.2007.01.005
M3 - Article
C2 - 17449347
AN - SCOPUS:34247134563
SN - 0093-7754
VL - 34
SP - S2-S6
JO - Seminars in Oncology
JF - Seminars in Oncology
IS - SUPPL. 1
ER -