The Contribution of PDCD6 Polymorphisms to Oral Cancer Risk

Shih, Liang‐Chun; He, Jie-Long; Chang, Wen‐Yu; Hsu, Chiao‐Po; Hsia, Te‐Chun; Wang, Yun-Chi; Yang, Jia-Sing; Mong, Mei-Chin; Tsai, Chia-Wen; Bau, Da‐Tian

doi:10.21873/cgp.20332

Cited by 4 publications

(5 citation statements)

References 34 publications

(41 reference statements)

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“…In this study, we also found that alcoholism seems to be one of the risk factors for oral cancer in the investigated population (Table I). However, in our previous findings, a less positive combined influence of alcohol in association with specific genotypes was found (11,12). More frequently, no combined effect was found (6-8, 10, 65-69).…”

Section: Discussionmentioning

confidence: 51%

“…Almost 90% of oral cancers are linked to cigarrete smoking, alcoholism, and poor diet (52,53). In Taiwan, betel quid chewing has been reported to be the most dangerous contributor to oral cancer many times (11)(12)(13)(54)(55)(56)(57). As a meta-analysis has suggested that smokers are five times more likely to develop oral cancer than non-smokers (58), our team has further found that smoking habits can synergistically enhance the influence of specific risk genotypes (9, 11-13, 56, 58-62).…”

Section: Discussionmentioning

confidence: 99%

“…All the protocols have been carefully checked and conducted following the principles of the Helsinki Declaration. More details on the sampling of the cases and controls are available in our previous studies (12,44). The demographic characteristics of all participants are listed in Table I.…”

Section: Methodsmentioning

confidence: 99%

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Association ofEZH2Genotypes With Oral Cancer Risk

Shih

Tsai

Lin

et al. 2022

In Vivo

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Background/Aim: The over-expression of enhancer of zeste homolog 2 (EZH2) protein is found in oral cancer tissues. However, the genetic role of the enhancer of EZH2 in the etiology of oral cancer is unknown. The aim of this study was to evaluate the association of EZH2 genotypes with oral cancer risk among Taiwanese. Materials and Methods: Three polymorphic variants of EZH2, rs887569 (C to T), rs41277434 (A to C), and rs3757441 (T to C), were analyzed regarding their association with oral cancer risk among 958 oral cancer patients and the same number of healthy controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). In addition, the interaction of EZH2 rs887569, rs41277434, and rs3757441 genotypes with personal behaviors such as smoking, alcohol drinking, and betel quid chewing were also examined.Results: The EZH2 genotypes rs887569, rs41277434, and rs3757441, were not significantly associated with oral cancer risk (p for trend=0. 1735, 0.5658, and 0.4606, respectively). The analysis of allelic frequency distribution also supported the findings that the variant alleles at EZH2 rs887569, rs41277434, and rs3757441 may not serve as determinants of oral cancer risk (all p>0.05). There was no interaction between EZH2 rs887569, rs41277434, or rs3757441 genotypes with personal smoking, alcohol drinking or betel quid chewing behaviors. Conclusion: EZH2 genotypes cannot predict oral cancer risk in Taiwan.Worldwide, oral cancer is ranked sixth among common cancers and has the incidence in Taiwan (1, 2). It has been reported that cancer of the oral cavity and oropharynx represented more than 475,000 newly diagnosed cases all of the world in 2020 (3, 4). In addition to environmental factors, such as tobacco smoking, alcohol drinking, betel quid chewing, and virus infection (5), genetic factors have been suggested to affect an individual's risk for oral cancer (6-13). Although the development of modern facilities is rapid and health care of cancer has been greatly improved in recent years, more than 450,000 patients worldwide are diagnosed with oral cancer annually, and oral cancer maintains a fiveyear survival rate of under 50% (14, 15). The fact that the newly diagnosed cases of oral cancer have been increasing for at least three decades has urged genomic scientists to find more practical and feasible markers for early detection of oral cancer to help decrease its incidence (16).Human enhancer of zeste homolog 2 (EZH2) gene is located on the long arm of chromosome 7 at 7q35, contains 2669

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Section: Discussionmentioning

confidence: 51%

Section: Discussionmentioning

confidence: 99%

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Association ofEZH2Genotypes With Oral Cancer Risk

Shih

Tsai

Lin

et al. 2022

In Vivo

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“…MMP-7 genotyping methodology. Peripheral blood leucocytes from each subject in this study were extracted using the DNA applying QIAamp Blood Mini Kit (Blossom, Taipei, Taiwan) as per the previous publications (45)(46)(47)(48). The primer design, the corresponding restriction endonucleases and polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) conditions for MMP-7 genotyping are the same as in our previous publications (23,49).…”

Section: Methodsmentioning

confidence: 99%

The Contribution of Matrix Metalloproteinase-7 Promoter Genotypes to Hepatocellular Carcinoma Susceptibility

Yueh¹,

Tsao²,

Chien³

et al. 2022

Anticancer Res

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Background/Aim: Metalloproteinase-7 (MMP-7) has been previously found to be up-regulated in hepatocellular carcinoma (HCC) specimens and cells, favoring epithelialmesenchymal transition. However, the contribution of MMP-7 genotypes to HCC has not been revealed to date. The study aimed to evaluate the contribution of MMP-7 promoter A-181G (rs11568818) and C-153T (rs11568819) genotypes on the risk of HCC in Taiwan, where HCC incidence is extremely high compared to worldwide data. Materials and Methods: In this case-control study, MMP-7 genotypes and their association with cigarette smoking and alcohol drinking habits were determined in 298 HCC patients and 889 healthy subjects by a typical polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology. Results: Ever smokers

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“…All protocols were conducted following the principles documented in the Helsinki Declaration. The detail sampling of the cases and controls has been published in our previous studies (12,13). The demographics of participants are summarized in Table I.…”

Section: Methodsmentioning

confidence: 99%

The Contribution of Flap Endonuclease 1 Genotypes to Oral Cancer Risk

PAN

Chien

et al. 2022

Anticancer Res

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Background/Aim: Flap endonuclease 1 (FEN1) is a critical protein in DNA repair, genomic stability, and carcinogenesis. Functional polymorphisms in FEN1 promoter -69G>A (rs174538) and 3'UTR 4150G>T (rs4246215), have been associated with the susceptibility to several cancers, including lung, breast, esophageal, gastric, liver, colorectal, and gallbladder cancer, as well as glioma, endometriosis, and leukemia. However, the contribution of FEN1 variant genotypes to oral cancer has never been examined. Thus, we aimed to evaluate the contribution of FEN1 rs174538 and rs4246215 genotypes to oral cancer risk in Taiwan. Materials and Methods: The contribution of FEN1 genotypes to oral cancer risk was examined in 958 oral cancer patients and 958 age-and sex-matched healthy controls by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Results: The percentages of GG, AG, and AA genotypes at FEN1 rs174538 were 34.8%, 46.0%, and 19.2% among oral cancer patients and 37.8%, 45.2%, and 17.0% among healthy controls (p for trend=0.2788). The genotypic percentages of FEN1 rs4246215 were 35.9%, 45.9%, and 18.2% among oral cancer patients and 37.6%, 45.1%, and 17.3% among healthy controls (p for trend=0.7315). Overall, FEN1 rs174538 and rs4246215 were not differently distributed between the oral cancer patient and healthy control groups. The allele frequency analysis confirmed that FEN1 rs174538 and rs4246215 were non-differentially distributed among case and control groups (OR=1.11 and 1.05, 95%CI=0.98-1.27 and 0.93-1.20, p=0.1074 and 0.4491, respectively). Conclusion: FEN1 may contribute to oral cancer risk determination via protein expression and/or post-transcription modification, but may not be a practical genetic marker.Oral cancer is the fourth most prevalent and the fourth deathcausing cancer among males in Taiwan, where the incidence density of oral cancer is higher worldwide (1-3). In literature, several factors are revealed to contribute to the etiology of oral cancer in Taiwan, such as betel quid chewing, tobacco smoking, alcohol drinking, bad tooth brushing habits, and virus infection (4, 5). Interestingly, in recent years, specific inherited genotypes have been reported to contribute to personal oral cancer susceptibility (6-13). A better understanding of genomic, environmental and behavioral factors can contribute to precise and personalized oral cancer prediction and therapy.

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The Contribution of PDCD6 Polymorphisms to Oral Cancer Risk

Cited by 4 publications

References 34 publications

Association ofEZH2Genotypes With Oral Cancer Risk

Association ofEZH2Genotypes With Oral Cancer Risk

The Contribution of Matrix Metalloproteinase-7 Promoter Genotypes to Hepatocellular Carcinoma Susceptibility

The Contribution of Flap Endonuclease 1 Genotypes to Oral Cancer Risk

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