“p53 mutation spectrum and its role in prognosis of oral cancer patients: A study from Gujarat, West India”

Rg, Singh; Patel, Kinjal D.; Patel, Prabhudas S.

doi:10.1016/j.mrfmmm.2015.12.001

Cited by 24 publications

(29 citation statements)

References 28 publications

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“…p53 mutations occur at exons 5-9 in nearly half of patients with OSCC, and G to A or G to T mutations are the predominant mutations that were observed and associated with CS and BQ chewing. Similar p53 mutations in oral cavity tumors have been found (14)(15)(16)(17). These findings suggest an important contributive role of tobacco carcinogens in p53 mutations in a series of Taiwanese patients with OSCC.…”

Section: Introductionsupporting

confidence: 77%

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking– and Betel Quid Chewing–Related Human Oral Cancer

Tsou¹,

Hu²,

Liu³

et al. 2019

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Cigarette smoking (CS) and betel quid (BQ) chewing are two known risk factors and have synergistic potential for the development of oral squamous cell carcinoma (OSCC) in Taiwan. The p53 mutation characteristics in OSCC (G to A or G to T mutations) are similar to that of acrolein-induced DNA damage. Acrolein is a major cigarette-related carcinogen that preferentially causes p53 mutations and inhibits DNA repair function in lung cancer. We hypothesize that acrolein is associated with OSCC carcinogenesis.Methods: A total of 97 patients with OSCC and 230 healthy subjects with CS and/or BQ chewing histories were recruited. Slot blot analysis of Acr-dG adducts, an indicator of acrolein-induced DNA damage in buccal DNA, and LC/MS-MS analysis of 3-HPMA levels, urinary Acr metabolites, were performed.Results: Our results showed that the level of Acr-dG adducts in buccal cells was 1.4-fold higher in patients with OSCC than in healthy subjects with CS and/or BQ chewing histories (P < 0.001). In addition, in healthy subjects, CS and BQ chewing were associated with significantly higher levels of 3-HPMA, indicating that CS and BQ chewing promotes acrolein absorption. However, 3-HPMA levels in patients with OSCC were significantly lower than those in healthy subjects, indicating impaired acrolein metabolism.Conclusions: In this study, we provide a novel mechanism by which increased acrolein uptake and impaired metabolism may contribute to the synergistic potential of CS and BQinduced OSCC.Impact: Elevated acrolein-induced DNA damage (Acr-dG adducts) detected in buccal swabs may serve as an early indicator to identify patients at risk of developing OSCC. a The P < 0.05 versus smoking (CS) by Student t test.

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Section: Introductionsupporting

confidence: 77%

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking– and Betel Quid Chewing–Related Human Oral Cancer

Tsou¹,

Hu²,

Liu³

et al. 2019

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Recently, we observed different type of base pair changes and the multiple mutations in p53 gene in oral cancer patients which suggest DNA insults by several different carcinogens which are present in smokeless tobacco. Our results on p53 mutation spectrum strongly support the notion that ethnic/geographic and differences in tobacco consuming habits are the major cause of variations in the p53 mutations [32]. Thus, the p53 mutational pattern has been recommended to be a clinically appropriate "molecular sensor" for genotoxic exposure to carcinogens present in the environment and endogenous mutagens [33].…”

Section: Fig 3 Mutant P53 Contributes To Tumorigenesissupporting

confidence: 81%

“…Further, detection of p53 mutation in apparently normal adjacent mucosa along with mutation with tumor tissues should be done for prognostication. p53 mutations also affect the survival rate as cases with truncating and transcriptionally non-active p53 mutations had poor disease free as well as overall survival [32]. However, the results of a recent meta-analysis by Tandon et al [74] highlights that the existing data regarding the prognostic importance of p53 are indecisive and there is a great heterogeneity observed in various studies.…”

Section: P53 Alterations and Clinicopathological Characteristicsmentioning

confidence: 99%

CLINICAL IMPLICATIONS OF p53 ALTERATIONS IN ORAL CANCER PROGRESSION: A REVIEW FROM INDIA

Patel¹,

Vajaria²,

Rg³

et al. 2018

Exp. Onc.

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p53 plays a central role in prevention of normal cell from the development of the malignant phenotype. Somatic alterations (mutations, loss of heterozygosity, deletions) in p53 are a hallmark of most human cancers and cause defects in normal p53 function. However, in the tumors harboring wild-type p53, there are alterations in the regulation of the p53. Thus, understanding why p53 is unable to perform its role as a tumor suppressor in these wild-type tumors is very crucial. Germ-line polymorphisms in p53 are also anticipated to cause measurable disturbance in p53 function. Over-expression as well as polymorphic variants of MDM2 might have effects on cancer development. In addition, degradation of p53 by E6 protein of high risk human papillomavirus is also suggested as one of the mechanisms which attenuate p53 responses in oral carcinogenesis. p53 has also been demonstrated to mediate cellular responses upon various DNA damaging cancer therapies, importantly, apoptosis. These responses have been implicated in an individual’s ability to respond to these cancer therapies. Thus, exploring mechanisms by which normal function of p53 is affected in the comprehensive way in oral cancer might aid in the identification of tumor characteristics, prognosis and thus in the development of a new approach to treat the oral cancer.

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“…Mutant p53 proteins usually causes the accumulation of p53 protein at a very high levels, and the mutant p53 protein itself can inhibit normal p53 protein levels [ 11 ]. In recent years, several reports have shown that p53 expression can serve as a promising biomarker for predicting various tumors [ 14 – 19 ]. Many studies have also reported the prognostic value of p53 expression in RCC, but the results were still conflicting [ 20 – 41 ].…”

Section: Discussionmentioning

confidence: 99%

“…Mutant p53 cannot be effectively bound to DNA , and the p21 protein cannot act as the “stop signal” for cell division, which results in tumors formation [ 12 , 13 ]. It is reported that p53 expression predicts prognosis in various multiple cancer types including breast cancer [ 14 ], gastric cancer [ 15 ], multiple myeloma [ 16 ], colorectal cancer [ 17 ], cervical cancer [ 18 ], and oral cancer [ 19 ]. Many studies have investigated the prognostic role of p53 expression in RCC, but the results are conflicting [ 20 – 41 ].…”

Section: Introductionmentioning

confidence: 99%

Prognostic and clinicopathological value of p53 expression in renal cell carcinoma: a meta-analysis

et al. 2017

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BackgroundThe prognostic value of p53 expression in renal cell carcinoma (RCC) had been investigated in previous studies; however, the results remain inconsistent. This study was performed to investigate the prognostic and clinicopathological significance of p53 protein expression in RCC.Materials and MethodsLiterature was identified from PubMed, Embase, Web of Science, and Cochrane database, which investigated the relationships between p53 expression and outcomes. Hazard ratios (HRs) for survival outcomes and odds ratios (ORs) for clinical parameters associated with p53 were extracted from eligible studies. Heterogeneity was assessed using the I2 value. The fixed-effects model was used if there was no evidence of heterogeneity; otherwise, the random-effects model was used. Publication bias was evaluated using Begg's funnel plots and Egger's regression test.ResultsA total of 2,013 patients from 22 studies were included in the meta-analysis. The results showed that p53 positive expression is associated with poor overall survival (OS) (HR = 2.17, 95% confidence [CI]: 1.51–3.13) and cancer-specific survival (CSS) (HR = 1.59, 95% CI: 1.19–2.12) in RCC. In addition, p53 positive expression was closely correlated with TNM stage (III/IV vs. I/II: OR = 2.51, 95% CI: 1.05–6.00), Fuhrman grade (III/IV vs. I/II: OR = 1.80, 95% CI: 1.24–2.63), and distant metastasis (M1 vs. M0: OR = 1.70, 95% CI: 1.16–2.49), but not related to lymph node involvement (N1 vs. N0: OR = 1.32, 95% CI: 0.80–2.18), primary tumor stage (pT3/pT4 vs. pT1/pT2: OR = 1.16, 95% CI: 0.88–1.53), and sex (n = 2, male vs. female, OR = 1.09, 95% CI: 0.70–1.68).ConclusionsThis study suggests that p53 positive expression is correlated with poor prognosis and advanced clinicopathological features in patients with RCC, which indicates that p53 is a potentially effective therapeutic target.

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“p53 mutation spectrum and its role in prognosis of oral cancer patients: A study from Gujarat, West India”

Cited by 24 publications

References 28 publications

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking– and Betel Quid Chewing–Related Human Oral Cancer

Acrolein Is Involved in the Synergistic Potential of Cigarette Smoking– and Betel Quid Chewing–Related Human Oral Cancer

CLINICAL IMPLICATIONS OF p53 ALTERATIONS IN ORAL CANCER PROGRESSION: A REVIEW FROM INDIA

Prognostic and clinicopathological value of p53 expression in renal cell carcinoma: a meta-analysis

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