Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

By G. Pfeifer, M. Denissenko, Magali Olivier, N. Tretyakova, S. Hecht, Pierre Hainaut. Oncogene, 2002

1,114 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/48c74fab2588eb1d0635434c0746b6ad33b7f2c4

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Citations in the corpus

Potential Predictive Value of TP53 and KRAS Mutation Status for Response to PD-1 Blockade Immunotherapy in Lung Adenocarcinoma (2016, background): “449 It is well known that smoking-related lung cancers were characterized by greater 450 mutation burden, higher rate of transversion and more frequent KRAS mutation than that 451 occurred in never smokers(21, 32, 46, 47).”
Genomic features of response to combination immunotherapy in patients with advanced non-small cell lung cancer (2018, background): “, 2017), and is perhaps expected given the function of TP53 (Levine and Oren, 2009) and its known association with smoking (Pfeifer et al., 2002).”
The Catalogue of Somatic Mutations in Cancer (COSMIC) (2008, background): “If p.G12 is mutated, GAP cannot deactivate KRAS signaling, leading to a huge overac-tivation of downstream elements promoting growth (Scheffzek et al., 1997 of KRAS mutations to be missense changes at p.G12 (Fig.”
American Society of Clinical Oncology treatment of unresectable non-small-cell lung cancer guideline: update 2003. (2004, background): “Our understanding of the molecular mechanisms by which tobacco smoke causes lung cancer continues to grow [281-285].”
A small cell lung cancer genome reports complex tobacco exposure signatures (2009, neutral): “Erin D Pleasance(1), Philip J Stephens(1), Sarah O'Meara(1),(2), David J McBride(1), Alison Meynert(3), David Jones(1), Meng-Lay Lin(1), David Beare(1), King Wai Lau(1), Chris Greenman(1), Ignacio Varela(1), Serena Nik-Zainal(1), Helen R Davies(1), Gonzalo R Ordoñez(1), Laura J Mudie(1), Calli Latim”
iArc monogrAphs on the evAluAtion oF cArcinogenic risks to humAns (2012, background): “Loss of heterozygosity and point mutations in the p53 tumour-suppressor gene have also been linked with tobacco smoke carcinogens in cancer of the lung and of the larynx (Pfeifer et al., 2002; NIOSH, 2009).”
Deciphering Signatures of Mutational Processes Operative in Human Cancer (2013, positive): “…in tumors of the lung and skin have shown that the classes of mutations found match those induced experimentally by tobacco carcinogens and ultraviolet light respectively, the major known exogenous carcinogenic inﬂuences in these cancer types (Hainaut and Pfeifer, 2001; Pfeifer et al., 2002, 2005).”
Signatures of mutational processes in human cancer (2013, neutral): “There are signatures characterized predominantly by C>T (1A/B, 6, 7, 11, 15, 19), C>A (4, 8, 18), T>C (5, 12, 16, 21) and T>G mutations (9, 17), with others showing distinctive combinations of mutation classes (2, 13, 14).”
Mutational Processes Molding the Genomes of 21 Breast Cancers (2012, background): “For example, G>T/C>A transversions predominate in smokingassociated lung cancer, a pattern compatible with DNA damage induced by tobacco carcinogens such as benzo[a]pyrene diolepoxide (Pfeifer et al., 2002).”
TP53 Variations in Human Cancers: New Lessons from the IARC TP53 Database and Genomics Data (2016, background): “These hotspots have been linked to tobacco smoking and aromatic amines but their exact origin and functional role in bladder cancer remain unknown [Pfeifer et al., 2002].”
TP53 mutations in human cancers: origins, consequences, and clinical use. (2010, background): “…T transversions at specific G:C base pairs oriented with the (premutated) guanine on the nontranscribed strand (codons 157, 158, 245, 248, and 273)(Pfeifer et al. 2002; Pfeifer et al. 2003), and exposure to dietary aflatoxinB1 and G to T transversions at the third base of codon 249 (AGG to AGT)…”