Association of Caspase-8 Genotypes With the Risk for Nasopharyngeal Carcinoma in Taiwan

Shih, Liang‐Chun; Tsai, Chia-Wen; Chang, Wen-Shin; Shen, Te Chun; Wang, Yun-Chi; Yang, Jia-Sing; Lin, Meng-Liang; Wang, Zhihong; Bau, Da‐Tian

doi:10.21873/anticanres.14562

Cited by 9 publications

(9 citation statements)

References 34 publications

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“…Moreover, Wang et al [8] also reached the same conclusion for esophageal cancer. While different conclusions were obtained, Lin et al [11] reported that there was no correlation between CAV1 (rs7804372) polymorphism and gastric cancer susceptibility. Hsu et al [12] evaluated the relationships between six single nucleotide polymorphism of the CAV1 gene and hepatocellular cancer risk in a Taiwanese population.…”

Section: Discussionmentioning

confidence: 98%

“…[6] The carcinogenic role of CAV1 has been identified in several tumors, suggesting CAV1 as a novel therapeutic target for tumors. Several studies have explored the relationship between CAV1 polymorphisms and susceptibility to breast cancer, [7] esophageal carcinoma, [8] colorectal cancer, [9] gastric cancer, [10,11] hepatocellular, [12] and other cancers. [13,14] However, the results of the CAV1 rs7804372 (T29107A) polymorphism and susceptibility to digestive cancer remain controversial.…”

Section: Introductionmentioning

confidence: 99%

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CAV1 rs7804372 (T29107A) polymorphism might be a potential risk for digestive cancers

Chen¹,

Zhang²,

Bai

et al. 2021

Medicine

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Background: Caveolin-1 (CAV1) is an essential structural component of caveolae, regulates cellular processes through complex cellular signaling pathways, and influences tumorigenicity. However, the role of the CAV1 (rs7804372) polymorphism in digestive cancers remains inconclusive. The meta-analysis was performed to evaluate the effect of CAV1 polymorphism on digestive cancer susceptibility and to provide a basis for precise treatment. Methods: The databases of PubMed, EMBASE, Google Scholar and CNKI were used to retrieve the published studies on CAV1 (rs7804372) polymorphism and susceptibility to digestive cancers up to June 2020. Two researchers conducted study screening, data extraction, and methodological quality evaluation separately according to inclusion and exclusion criteria. Review Manager 5.3 software was used to conduct the meta-analysis. Results: Six case-control studies were enrolled, including 2477 patients with digestive cancers and 2477 healthy controls. The pooled results showed that the CAV1 rs7804372 (T29107A) polymorphism increased the risk of digestive cancer occurrence in the allele ( T vs. A : odds ratio (OR) 1.33, 95% confidence interval (CI): 1.15–1.53, P < .01), homozygous ( TT vs. AA : OR 1.72, 95% CI: 1.31–2.26, P < .01), heterozygous ( TA vs. AA : OR 1.47, 95% CI: 1.21–1.78, P < .01), dominant ( TT vs. TA + AA : OR 1.32, 95% CI: 1.18–1.48, P < .01), and recessive comparing models ( TT + TA vs. AA : OR 1.61, 95% CI: 1.26–2.07, P < .01). Conclusion: Our results indicate that the CAV1 (rs7804372) polymorphism may modify the occurrence of digestive cancers, and the presence of T allele or TT genotype of the CAV1 (rs7804372) may increase the risk of digestive cancers.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

CAV1 rs7804372 (T29107A) polymorphism might be a potential risk for digestive cancers

Chen¹,

Zhang²,

Bai

et al. 2021

Medicine

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“…Typically, CDKs and cyclins are precisely regulated to guarantee accurate cellcycle progression. For instance, a subtle dysregulation in the G 1 to S phase transition due to cell cycle-related genes or proteins may be associated with various types of cancer (18)(19)(20)(21)(22)(23). In particular, cyclin D1 (CCND1) genotypes were found to be significantly associated with non-solid tumor childhood ALL risk (5).…”

Section: Discussionmentioning

confidence: 99%

Contribution of Cyclin-dependent Kinase Inhibitor 1B Genotypes to Childhood Leukemia Risk

Pei

Chang

Hsu

et al. 2022

In Vivo

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Background/Aim: Although genetic differences in cell-cycle control genes have been associated with cancer risk, to our knowledge, no report has specifically examined the role of gene variants in childhood acute lymphoblastic leukemia (ALL). Cyclin-dependent kinase inhibitor 1B (CDKN1B; also known as p27/KIP1) is a cell-cycle regulating gene. This study aimed at investigating the association between CDKN1B genotypes and childhood ALL risk. Materials and Methods: In 266 childhood ALL cases and 266 healthy controls, the CDKN1B rs34330 and 2066827 polymorphisms were genotyped, and the association of CDKN1B genotypes with childhood ALL risk were analyzed. Results: The genotypes of CDKN1B rs34330 and 2066827 were similarly distributed between the control and case groups (p for trend=0.8718 and 0.4030, respectively). The allelic frequency also exhibited no statistical difference (p=1.0000 and 0.6666, respectively). There was no significant interaction between CDKN1B genotypes and age or sex. Conclusion: CDKN1B genotypes were not found to be minor contributors to childhood ALL susceptibility in Taiwan.Acute lymphoblastic leukemia (ALL), the most common cause of cancer-related death among children, still presents a poor prognosis (1). The pathogenesis of childhood ALL remains largely unknown, and genetic variations and some risk factors, such as advanced parental age, have been reported to be the cause of childhood ALL (2-4). In recent years, a few novel polymorphic biomarkers have been reported to play a role in childhood ALL risk (5-8). Interestingly, there are still many more genomic factors waiting to be explored for the contribution of their genotypic and phenotypic patterns to the etiology of childhood ALL.The CDKN1B gene (also known as p27/KIP1), located on chromosome 12p13, encodes for cyclin-dependent kinase (CDK) inhibitor 1B, which plays a role in the suppressive regulation of the cell cycle (9-11), and may also play critical roles in leukemia (12). Under normal conditions, DNA can be affected by numerous DNA-damaging agents exogenous and endogenous, and such damaged cells undergo cell-cycle arrest to allow DNA adducts and errors to be removed. Therefore, dysregulation of cell-cycle arrest, or normal control, may result in the initiation of carcinogenesis (13,14). There are at least two well-known polymorphic sites of 1637

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“…Oral cancer XPC genotyping methodology. DNA from all participants was processed in typical polymerase chain reaction (PCR) processes as in our previous papers (25)(26)(27). The sequences of designed forward and reverse primers, corresponding restriction enzymes (New England BioLabs, Ipswich, MA, USA) and sizes of PCR products after enzyme digestion for oral cancer XPC genotyping identification are shown in Table II.…”

Section: Methodsmentioning

confidence: 99%

Interaction of DNA Repair Gene XPC With Smoking and Betel Quid Chewing Behaviors of Oral Cancer

Chang

Shih

et al. 2021

Cancer Genomics Proteomics

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Background/Aim: Xeroderma pigmentosum complementation group C (XPC) is reported to play important roles in DNA integrity and genomic instability, however, the contribution of XPC to oral carcinogenesis is largely uncertain. Therefore, we aimed at examining the contribution of XPC genotypes to oral cancer. Materials and Methods: The genotypes of XPC rs2228001 and rs2228000 were examined among 958 oral cancer patients and 958 control subjects by polymerase chain reaction-restriction fragment length polymorphism methodology and corresponding DNA repair capacity was checked. Results: First, the percentages of XPC rs2228001 AC and CC were higher among oral cancer patients than controls. Second, no significant association was observed regarding XPC rs2228000. Third, there was a synergistic influence of smoking and betel quid chewing behaviors and XPC rs2228001 genotype on oral cancer risk. Last, functional experiments showed DNA repair capacity was lower for AC/CC carriers than AA carriers. Conclusion: XPC rs2228001 C allele, which was associated with decreased DNA repair capacity, may interact with smoking and betel quid chewing behaviors on oral cancer risk.Oral cancer is the tenth most common cancer worldwide, and Taiwan has one of the highest incidences (1). Based on the most updated annual statistics from the government, oral cancer is of the fourth death-causing cancers among Taiwanese males (2). Uniquely, betel quid chewing, in addition to cigarrete smoking and alcohol drinking, has been identified as an effective environmental factor to oral cancer risk in Taiwan (3). The Taiwan government has embarked in population screen searching for the oral cancer candidates for early cure and medication to lower its incidence, however, the death rate and incidence of oral cancer were still high. Therefore, novel predictors for oral cancer risk are still needed.There are five major DNA repair systems, consisting of more than 130 genes, and teaming up to maintain the stability and integrity of the human genome. Among them, the nucleotide excision repair (NER) system is in charge of removing DNA crosslinks, bulky adducts, alkylating DNA adducts, oxidative DNA adducts and thymidine dimers (4-6). In NER machinery, four major steps (adduct recognition, lesion DNA incision, gapped DNA fulfilling and ligation) and several core players, including xeroderma pigmentosum complementation group C (XPC)-RAD23B, play critical roles as key enzymes (4, 5) Theoretically, subtle genetic 441 This article is freely accessible online.

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Association of Caspase-8 Genotypes With the Risk for Nasopharyngeal Carcinoma in Taiwan

Cited by 9 publications

References 34 publications

CAV1 rs7804372 (T29107A) polymorphism might be a potential risk for digestive cancers

CAV1 rs7804372 (T29107A) polymorphism might be a potential risk for digestive cancers

Contribution of Cyclin-dependent Kinase Inhibitor 1B Genotypes to Childhood Leukemia Risk

Interaction of DNA Repair Gene XPC With Smoking and Betel Quid Chewing Behaviors of Oral Cancer

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