Assessment of the Prognostic Value of Methylation Status and Expression Levels of FHIT, GSTP1 and p16 in Non-Small Cell Lung Cancer in Egyptian Patients

Haroun, Riham Abdel-Hamid; Zakhary, Nadia I.; Mohamed, Mohamed R.; Abdelrahman, Abdelrahman Mohamed; Kandil, Eman; Shalaby, Kamal A.

doi:10.7314/apjcp.2014.15.10.4281

Cited by 26 publications

(22 citation statements)

References 31 publications

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“…Studies have shown that high methylation in the FHIT promoter region was closely associated with loss of heterozygosity. The loss of FHIT expression in lung cancer was mainly due to high methylation in its promoter region (16). In the present study, there were statistically significant differences in the methylation status of p16, RASSF1A and FHIT promoters between cancer patients and controls.…”

Section: Diagnostic Value Of Tumor Markers In Lung Cancersupporting

confidence: 48%

Establishment of Two Data Mining Models of Lung Cancer Screening Based on Three Gene Promoter Methylations Combined with Telomere Damage

et al. 2017

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Section: Diagnostic Value Of Tumor Markers In Lung Cancersupporting

confidence: 48%

Establishment of Two Data Mining Models of Lung Cancer Screening Based on Three Gene Promoter Methylations Combined with Telomere Damage

et al. 2017

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“…GSTP1 is expressed at the highest level in the lung tissue among all GST isozymes, accounting for 83% of all GST isozymes (15). Therefore, GSTP1 plays an important role in the detoxification of inhaled carcinogens, such as activated polycyclic aromatic hydrocarbons (PAHs), benzo(a)pyrene and tobacco carcinogens (16). It has even been suggested to be the most important GST influencing lung cancer risk (17).…”

Section: Discussionmentioning

confidence: 99%

Correlation between metabolic enzyme GSTP1 polymorphisms and susceptibility to lung cancer

Wang

Ren

Zhang

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to determine the frequency distribution and characteristics of polymorphic alleles and genotypes in glutathione S-transferase π 1 (GSTP1) exon 5, and to explore the correlation between GSTP1 exon 5 polymorphisms and susceptibility to lung cancer using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Patients were diagnosed with lung cancer from May 2006 to October 2008 by postoperative pathological examination. A total of 150 patients, including 115 males and 35 females, aged 31-76 years (mean, 57.1 years) were enrolled. The control group consisted of 152 healthy volunteers who received physical examination at outpatient clinics. Genomic DNA was extracted from the peripheral venous blood of the 302 subjects, and the GSTP1 genotype was determined by PCR-RFLP and restricted enzyme digestion of PCR products. GSTP1 polymorphisms were analyzed in the 302 subjects. The C and G allele frequencies of GSTP1 in the control and lung cancer groups showed no significant difference (P=0.135); the frequencies of three different genotypes, A/A, A/G and G/G, of GSTP1 in the control and lung cancer groups exhibited no significant differences between the two groups (P=0.223). GSTP1 genotype frequencies in the study population fitted the Hardy-Weinberg equilibrium, demonstrating that the genotype results of this study conform to this genetic law. Overall, 50.7% of the subjects in the lung cancer group carried the non-A/A genotype of GSTP1, which was higher than the 43.4% of the control group. The risk of lung cancer in subjects with the non-A/A genotype was 1.43-fold higher than that in those with the A/A genotype, but no statistical significance was found (P=0.138). GSTP1 exon 5 polymorphisms were demonstrated to be associated with lung cancer susceptibility on the whole. However, stratified analysis suggested the correlation of GSTP1 exon 5 polymorphisms with lung squamous cell carcinoma risk, and that exon 5 polymorphisms might increase the risk of lung squamous cell carcinoma. Exon 5 GSTP1 polymorphisms were not found to be a strong influencing factor in lung cancer risk, but may play a certain role.

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“…Haroun et al observed that the methylation frequencies of the genes tested in non-small cell lung carcinoma specimens were 53.6% for FHIT . 28 Jeong et al evaluated the methylation of FHIT in 60 BC samples; FHIT methylation was detected in 96.7% and the positive expression rate of FHIT in 87.3% of the patients. 27 Our data and previous studies indicate that FHIT promoter hypermethylation is a useful diagnostic biomarker of BC.…”

Section: Discussionmentioning

confidence: 99%

“…FHIT promoter hypermethylation is reversible, drug treatment through demethylation may be useful to delay tumorigenesis and progression, as well as improving prognosis. Inhibitors of DNA methylation such as 5-Aza-CdR and FdCyd were applied to human BC cells and induced apoptosis, 16 , 28 and FdCyd is now in clinical trials for the treatment of BC and other solid tumors. 29 – 31 More specifically, Stewart et al observed that there was a statistically significant increase in expression of FHIT as well as two other tumor suppressor genes, FUS1 and WWOX , in patients with tumor regression following decitabine, which is a demethylating agent.…”

Section: Discussionmentioning

confidence: 99%

The clinicopathological significance and drug target potential of FHIT in breast cancer, a meta-analysis and literature review

Wang

et al. 2015

DDDT

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FHIT is a bona fide tumor-suppressor gene and its loss contributes to tumorigenesis of epithelial cancers including breast cancer (BC). However, the association and clinicopathological significance between FHIT promoter hypermethylation and BC remains unclear. The purpose of this study is to conduct a meta-analysis and literature review to investigate the clinicopathological significance of FHIT methylation in BC. A detailed literature search was performed in PubMed, EMBASE, Web of Science, and Google Scholar databases. The data were extracted and assessed by two reviewers independently. Odds ratios with 95% corresponding confidence intervals were calculated. A total of seven relevant articles were available for meta-analysis, which included 985 patients. The frequency of FHIT hypermethylation was significantly increased in invasive ductal carcinoma compared to benign breast disease, the pooled odds ratio was 8.43, P<0.00001. The rate of FHIT hypermethylation was not significantly different between stage I/II and stage III/IV, odds ratio was 2.98, P=0.06. In addition, FHIT hypermethylation was not significantly associated with ER and PR status. FHIT hypermethylation was not significantly correlated with premenopausal and postmenopausal patients with invasive ductal carcinoma. In summary, our meta-analysis indicated that the frequency of FHIT hypermethylation was significantly increased in BC compared to benign breast disease. The rate of FHIT hypermethylation in advanced stages of BC was higher than in earlier stages; however, the difference was not statistically significant. Our data suggested that FHIT methylation could be a diagnostic biomarker of BC carcinogenesis. FHIT is a potential drug target for development of demethylation treatment for patients with BC.

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Assessment of the Prognostic Value of Methylation Status and Expression Levels of FHIT, GSTP1 and p16 in Non-Small Cell Lung Cancer in Egyptian Patients

Cited by 26 publications

References 31 publications

Establishment of Two Data Mining Models of Lung Cancer Screening Based on Three Gene Promoter Methylations Combined with Telomere Damage

Establishment of Two Data Mining Models of Lung Cancer Screening Based on Three Gene Promoter Methylations Combined with Telomere Damage

Correlation between metabolic enzyme GSTP1 polymorphisms and susceptibility to lung cancer

The clinicopathological significance and drug target potential of FHIT in breast cancer, a meta-analysis and literature review

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