Molecular pathways: Involvement of Helicobacter pylori-triggered inflammation in the formation of an epigenetic field defect, and its usefulness as cancer risk and exposure markers

Clinical Cancer Research

Volumn 18, Issue 4, 2012, Pages 923-929

  Ushijima, Toshikazu ^a   Hattori, Naoko ^a  

^a NATIONAL CANCER CENTER RESEARCH INSTITUTE   (Japan)

Author keywords

[No Author keywords available]

Indexed keywords

3 DEAZANEPLANOCIN A; 5 AZA 2' DEOXYCYTIDINE; ALCOHOL; AZACITIDINE; NONSTEROID ANTIINFLAMMATORY AGENT; SODIUM CHLORIDE;

CANCER INCIDENCE; CANCER PREVENTION; CANCER RISK; CANCER SCREENING; CELL INFILTRATION; CHRONIC INFLAMMATION; CONCENTRATION (PARAMETERS); DISEASE ASSOCIATION; DNA METHYLATION; ENVIRONMENTAL EXPOSURE; EPIGENETICS; GENE ACTIVATION; GENE EXPRESSION; GENE MUTATION; GENE TARGETING; HELICOBACTER INFECTION; HIGH RISK POPULATION; HUMAN; LIFE HISTORY; MOLECULAR PATHOLOGY; NONHUMAN; PRIORITY JOURNAL; REVIEW; STOMACH CANCER; STOMACH CARCINOGENESIS; TISSUE INJURY; TUMOR SUPPRESSOR GENE; VIRUS CARCINOGENESIS;

DNA METHYLATION; EPIGENESIS, GENETIC; HELICOBACTER INFECTIONS; HELICOBACTER PYLORI; HUMANS; INFLAMMATION; RISK; SIGNAL TRANSDUCTION; STOMACH NEOPLASMS; TRANSLATIONAL MEDICAL RESEARCH;

EID: 84857068434     PISSN: 10780432     EISSN: 15573265     Source Type: Journal    
DOI: 10.1158/1078-0432.CCR-11-2011     Document Type: Review

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