Mutational activation of K-ras in nonneoplastic exocrine pancreatic lesions in relation to cigarette smoking status

Cancer

Volumn 85, Issue 2, 1999, Pages 326-332

  Berger, David H ^a   Chang, Hong ^a   Wood, Moira ^a   Huang, Lingyi ^a   Heath, C W ^b   Lehman, Theresa ^c   Ruggeri, Bruce A ^a,d  

^a DREXEL UNIVERSITY COLLEGE OF MEDICINE   (United States)

^b AMERICAN CANCER SOCIETY   (United States)

^c Bioserve Biotechnology Inc   (United States)

^d CEPHALON INC   (United States)

Author keywords

Cigarette smoking; K ras; Ligase chain reaction; Pancreatic adenocarcinoma; Restriction frag merit length polymorphism

Indexed keywords

AMINO ACID SUBSTITUTION; ARTICLE; CANCER RISK; CIGARETTE SMOKING; CODON; GENE ACTIVATION; GENE MUTATION; HISTOPATHOLOGY; HUMAN; HUMAN TISSUE; ONCOGENE K RAS; PANCREAS ADENOCARCINOMA; PANCREAS DISEASE; POLYMERASE CHAIN REACTION; PRIORITY JOURNAL; REPRODUCIBILITY; RESTRICTION FRAGMENT LENGTH POLYMORPHISM; TISSUE PREPARATION;

ADULT; AGE FACTORS; AGED; AGED, 80 AND OVER; CARCINOMA, DUCTAL, BREAST; GENES, RAS; GENETIC MARKERS; HUMANS; MALE; MIDDLE AGED; PANCREATIC DISEASES; PANCREATIC NEOPLASMS; POINT MUTATION; POLYMERASE CHAIN REACTION; POLYMORPHISM, RESTRICTION FRAGMENT LENGTH; SMOKING;

EID: 0032943628     PISSN: 0008543X     EISSN: None     Source Type: Journal    
DOI: 10.1002/(SICI)1097-0142(19990115)85:2<326::AID-CNCR9>3.0.CO;2-O     Document Type: Article

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