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Preferential Formation of Benzo[a]pyrene Adducts at Lung Cancer Mutational Hotspots in P53
A direct etiological link between a defined chemical carcinogen and human cancer is provided and targeted adduct formation rather than phenotypic selection appears to shape the P53 mutational spectrum in lung cancer.
Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers
- G. Pfeifer, M. Denissenko, M. Olivier, N. Tretyakova, S. Hecht, P. Hainaut
- Biology, MedicineOncogene
- 21 October 2002
The available data suggest that p53 mutations in lung cancers can be attributed to direct DNA damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations.
Expression of base excision repair enzymes in rat and mouse liver is induced by peroxisome proliferators and is dependent upon carcinogenic potency.
It is suggested that DNA base excision repair may be an important factor in peroxisome proliferator-induced carcinogenesis and that induction of DNA repair might provide further evidence supporting a role of oxidative DNA damage by perox isome proliferators.
Cytosine methylation determines hot spots of DNA damage in the human P53 gene.
- M. Denissenko, J. X. Chen, M. Tang, G. Pfeifer
- Biology, ChemistryProceedings of the National Academy of Sciences…
- 15 April 1997
Results show that methylated CpG dinucleotides, in addition to being an endogenous promutagenic factor, may represent a preferential target for exogenous chemical carcinogens.
Targeting of lung cancer mutational hotspots by polycyclic aromatic hydrocarbons.
- L. E. Smith, M. Denissenko, G. Pfeifer
- Biology, ChemistryJournal of the National Cancer Institute
- 17 May 2000
The data suggest that PAHs contribute to the mutational spectrum in human lung cancer.
Role of ICAM1 in invasion of human breast cancer cells.
The results corroborate the previous genetic finding that variations in the ICAM region are associated with the occurrence of metastases and establish a causal role of ICAM1 in invasion of metastatic human breast carcinoma cell lines.
Suppression of RAD21 gene expression decreases cell growth and enhances cytotoxicity of etoposide and bleomycin in human breast cancer cells
- Josephine M. Atienza, R. Roth, M. Denissenko
- Biology, MedicineMolecular Cancer Therapeutics
- 1 March 2005
It is concluded that RAD21 is a novel target for developing cancer therapeutics that can potentially enhance the antitumor activity of chemotherapeutic agents acting via induction of DNA damage.
Sunlight induces pyrimidine dimers preferentially at 5-methylcytosine bases.
The results suggest that CPDs containing 5-methylcytosine may play an important role in formation of sunlight-induced skin tumors and that methylation of CpG sequences, besides being involved in spontaneous mutagenesis processes, can also create preferential targets for environmental mutagens and carcinogens.
Expression of Base Excision DNA Repair Genes Is a Sensitive Biomarker for in Vivo Detection of Chemical-induced Chronic Oxidative Stress
It is concluded that expression of base excision DNA repair genes is a sensitive in vivo biomarker for chemically induced oxidative stress to DNA that can be successfully used for the identification of the molecular source of radicals responsible for DNA damage in vivo.
Slow repair of bulky DNA adducts along the nontranscribed strand of the human p53 gene may explain the strand bias of transversion mutations in cancers
Mapping the BPDE adduct distribution in the transcribed strand of the p53 gene and quantifying the rates of repair for individual damaged bases in exons 5, 7, and 8 suggest that both preferential adduct formation and slow repair lead to hotspots for mutations at codons 157, 248 and 273.