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Human papillomavirus and p53 mutations in head and neck squamous cell carcinoma among Japanese population.

Maruyama H, Yasui T, Ishikawa-Fujiwara T, Morii E, Yamamoto Y, Yoshii T, Takenaka Y, Nakahara S, Todo T, Hongyo T, Inohara H - Cancer Sci. (2014)

Bottom Line: Oropharyngeal carcinoma was more frequently HPV-positive than non-oropharyngeal carcinoma (34.4% vs 3.6%, P < 0.001), and HPV16 accounted for 91.1% of HPV-positive tumors.In oropharyngeal carcinoma, which showed an increasing trend of HPV prevalence over time (P < 0.001), HPV infection was inversely correlated with tobacco smoking, alcohol drinking, p53 mutations, and a disruptive mutation (P = 0.003, <0.001, <0.001, and <0.001, respectively).A disruptive mutation was never found in virus-related HNSCC, whereas it was independently associated with primary site, such as the oropharynx and hypopharynx (P = 0.01 and 0.03, respectively), in virus-unrelated HNSCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Otorhinolaryngology - Head and Neck Surgery, Osaka University Faculty of Medicine, Suita, Japan.

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Related in: MedlinePlus

Pattern of p53 mutations in human papillomavirus-unrelated head and neck tumors from never- and ever-smokers. One hundred sixty-five mutations are represented in 112 patients. Never-smokers showed a higher prevalence of G:C to A:T transitions at CpG sites than ever-smokers (*P = 0.04). Ever-smokers showed a higher prevalence of G:C to T:A transversions than never-smokers (**P = 0.04). Others represent insertion and deletion.
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fig02: Pattern of p53 mutations in human papillomavirus-unrelated head and neck tumors from never- and ever-smokers. One hundred sixty-five mutations are represented in 112 patients. Never-smokers showed a higher prevalence of G:C to A:T transitions at CpG sites than ever-smokers (*P = 0.04). Ever-smokers showed a higher prevalence of G:C to T:A transversions than never-smokers (**P = 0.04). Others represent insertion and deletion.

Mentions: The prevalence of any p53 mutation was not associated with tobacco smoking in virus-unrelated HNSCCs, as shown in Table 6, whereas tobacco carcinogen is known to link with a specific type of mutagenesis.(25) We addressed the pattern of p53 mutations in virus-unrelated HNSCCs, in relation to tobacco exposure. One hundred and twelve of 232 (48.3%) tumors harbored a total of 165 p53 mutations (22 tumors with two distinct mutations, 6 with three, 2 with four, 2 with five, and 1 with six), including 118 missense mutations, 12 nonsense mutations, 8 frame-shifts, and 27 silent mutations (detail of the mutations in Table S1), although six tumors harbored only silent mutations. The codon distribution of p53 mutations differed depending on tobacco exposure. In ever-smokers, 19 of 143 (13.2%) mutations were detected at codons described as “hotspots” for transversions (codon 157, one mutation; codon 158, six mutations; codon 245, six mutations; codon 248, five mutations; codon 273, one mutation),(26) whereas, in never-smokers, mutations at hotspots were found only at codon 245, accounting for 2 of 22 (9.1%) mutations. Figure 2 shows the types of mutations according to smoking status. Transversions accounted for 39.2% of mutations in ever-smokers, whereas the vast majority (81.8%) of mutations in never-smokers were transitions. Two types of mutations showed consistent difference in relation to smoking. G:C to T:A transversions were more prevalent in ever-smokers than in never-smokers (22.4% vs 4.5%, P = 0.04), whereas G:C to A:T transitions at CpG sites were less prevalent in ever-smokers than in never-smokers (10.5% vs 27.3%, P = 0.04).


Human papillomavirus and p53 mutations in head and neck squamous cell carcinoma among Japanese population.

Maruyama H, Yasui T, Ishikawa-Fujiwara T, Morii E, Yamamoto Y, Yoshii T, Takenaka Y, Nakahara S, Todo T, Hongyo T, Inohara H - Cancer Sci. (2014)

Pattern of p53 mutations in human papillomavirus-unrelated head and neck tumors from never- and ever-smokers. One hundred sixty-five mutations are represented in 112 patients. Never-smokers showed a higher prevalence of G:C to A:T transitions at CpG sites than ever-smokers (*P = 0.04). Ever-smokers showed a higher prevalence of G:C to T:A transversions than never-smokers (**P = 0.04). Others represent insertion and deletion.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4317800&req=5

fig02: Pattern of p53 mutations in human papillomavirus-unrelated head and neck tumors from never- and ever-smokers. One hundred sixty-five mutations are represented in 112 patients. Never-smokers showed a higher prevalence of G:C to A:T transitions at CpG sites than ever-smokers (*P = 0.04). Ever-smokers showed a higher prevalence of G:C to T:A transversions than never-smokers (**P = 0.04). Others represent insertion and deletion.
Mentions: The prevalence of any p53 mutation was not associated with tobacco smoking in virus-unrelated HNSCCs, as shown in Table 6, whereas tobacco carcinogen is known to link with a specific type of mutagenesis.(25) We addressed the pattern of p53 mutations in virus-unrelated HNSCCs, in relation to tobacco exposure. One hundred and twelve of 232 (48.3%) tumors harbored a total of 165 p53 mutations (22 tumors with two distinct mutations, 6 with three, 2 with four, 2 with five, and 1 with six), including 118 missense mutations, 12 nonsense mutations, 8 frame-shifts, and 27 silent mutations (detail of the mutations in Table S1), although six tumors harbored only silent mutations. The codon distribution of p53 mutations differed depending on tobacco exposure. In ever-smokers, 19 of 143 (13.2%) mutations were detected at codons described as “hotspots” for transversions (codon 157, one mutation; codon 158, six mutations; codon 245, six mutations; codon 248, five mutations; codon 273, one mutation),(26) whereas, in never-smokers, mutations at hotspots were found only at codon 245, accounting for 2 of 22 (9.1%) mutations. Figure 2 shows the types of mutations according to smoking status. Transversions accounted for 39.2% of mutations in ever-smokers, whereas the vast majority (81.8%) of mutations in never-smokers were transitions. Two types of mutations showed consistent difference in relation to smoking. G:C to T:A transversions were more prevalent in ever-smokers than in never-smokers (22.4% vs 4.5%, P = 0.04), whereas G:C to A:T transitions at CpG sites were less prevalent in ever-smokers than in never-smokers (10.5% vs 27.3%, P = 0.04).

Bottom Line: Oropharyngeal carcinoma was more frequently HPV-positive than non-oropharyngeal carcinoma (34.4% vs 3.6%, P < 0.001), and HPV16 accounted for 91.1% of HPV-positive tumors.In oropharyngeal carcinoma, which showed an increasing trend of HPV prevalence over time (P < 0.001), HPV infection was inversely correlated with tobacco smoking, alcohol drinking, p53 mutations, and a disruptive mutation (P = 0.003, <0.001, <0.001, and <0.001, respectively).A disruptive mutation was never found in virus-related HNSCC, whereas it was independently associated with primary site, such as the oropharynx and hypopharynx (P = 0.01 and 0.03, respectively), in virus-unrelated HNSCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Otorhinolaryngology - Head and Neck Surgery, Osaka University Faculty of Medicine, Suita, Japan.

Show MeSH
Related in: MedlinePlus