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Cited by 15Lung Cancer Treatments and MutationsLung Cancer Research StudiesLung Cancer Diagnosis and Treatment

p53 gene mutations and 17p allelic deletions in hepatocellular carcinoma from Japan

Nose, Haruhiko, Imazeki, Fumio, Ohto, Masao, Omata, Masao·1993·Cancer
DOI 10.1002/1097-0142(19930715)72:2
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Abstract

Point mutations in codon 12 of the K-ras protooncogene occur more frequently in lung adenocarcinomas from smokers (30%) than they do in lung adenocarcinomas from nonsmokers (7%), suggesting that smoking is an important factor in the induction of these mutations. The lack of well defined "early" premalignant or in situ glandular neoplasms of the lung, however, has not permitted direct evaluation of the chronology of ras activation in the development of lung adenocarcinomas. To circumvent the need to evaluate precursor lesions, we examined lung adenocarcinomas from former smokers for point mutations in K-ras. Mutations in codon 12 of K-ras were detected using polymerase chain reaction amplification and mutation-specific oligonucleotide probes. The types and frequencies of mutations found in adenocarcinomas obtained from 57 former smokers were compared to those found in 27 adenocarcinomas from patients who never smoked and to those found in 27 adenocarcinomas from patients who were current smokers. The overall prevalence of K-ras point mutations in lung adenocarcinomas obtained from former smokers (32%) was not different from that seen in adenocarcinomas from patients who were current smokers (30%, P = 0.83), and was greater than that seen in adenocarcinomas from patients who never smoked (7%, P = 0.015). This pattern was independent of the duration of abstinence from smoking. Furthermore, the predominant type of mutation found in tumors from former smokers was a guanine-to-thymine transversion, the specific type of mutation induced by benzo(a)pyrene, one of the chemical carcinogens found in tobacco smoke. These findings support previous findings that suggest that codon 12 of the K-ras oncogene may be a specific target of the mutagenic activity of tobacco smoke, and suggest that DNA alterations at this site can occur early and irreversibly during the development of adenocarcinomas of the lung

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Crossref · 10.1002/1097-0142(19930715)72:2<355::aid-cncr2820720208>3.0.co;2-w

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9 of 9 references verified0 citation errors · 0 not checkable

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  • This finding agrees with previous reports that complete loss of p53 function is associated with progression but not initiation of hepatitis B virus or aflatoxin B1-induced HCC in humans.

    “This finding agrees with previous reports that the complete loss of p53 function is associated with the progression but not initiation of hepatitis B virus or aflatoxin B1-induced HCC in humans (Hosono et al., 1993; Nose et al., 1993).”

    From Circadian Homeostasis of Liver Metabolism Suppresses Hepatocarcinogenesis (2016) · cites this paper as Nose et al., 1993

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Authors
Nose, H., Imazeki, F., Ohto, M., & Omata, M.
Venue
Cancer
Publisher
Wiley
Published
1993-07-15
Volume
72
Issue
2
Pages
355-360
DOI
10.1002/1097-0142(19930715)72:2
OpenAlex
W7131845346
Cited by
0
References
9
FWCI
0.00
Type
journal article
Language
en
Open access
closed
Licence
doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 8083 d)
Locations
Pure Amsterdam UMC (publishedVersion)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
  • Health Sciences › Medicine › Oncology › Lung Cancer Research Studies
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Diagnosis and Treatment
Keywords
K-ras oncogene, lung adenocarcinoma, smoking, codon 12 point mutation, tobacco smoke carcinogens, benzo[a]pyrene, carcinogenesis, former smokers, smoking abstinence

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