TP73 alterations in cervical carcinoma

Craveiro, Rogéria; Costa, Sandra; Pinto, Daniela; Salgado, L.; Carvalho, L.; Castro, Carolina Moreno; Bravo, Isabel; Lopes, Carlos; Silva, Isabel; Medeiros, Rui

doi:10.1016/j.cancergencyto.2003.08.020

Cited by 28 publications

(9 citation statements)

References 30 publications

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“…According to previous reports, in our population we may consider that more that 95% of the cases of invasive cervical cancer are in association to HPV-16 and-18 (Smith et al, 2007, Medeiros et al, 2005) , Smith J, 2007. Previously reported studies indicate that several genetic J U S T A C C E P T E D polymorphisms may determine cervical cancer onset and progression (Silva et al, 2013, Craveiro et al, 2012, Araujo et al, 2012, Catarino et al, 2008, Santos et al, 2006, Santos et al, 2005, Coelho et al, 2005, Craveiro et al, 2004. Future studies may include HPV genotyping to evaluate its role in disease progression and clinical outcome under the influence of the genetic background.…”

Section: Several Reports Showed An Association Between Parp1 Val762almentioning

confidence: 60%

Base excision repair pathway:PARP1genotypes as modulators of therapy response in cervical cancer patients

et al. 2016

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Section: Several Reports Showed An Association Between Parp1 Val762almentioning

confidence: 60%

Base excision repair pathway:PARP1genotypes as modulators of therapy response in cervical cancer patients

et al. 2016

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“…Increasing evidences suggest that genetic polymorphisms may have an important contribution on cancer susceptibility and tumour behaviour, particularly in hormone related cancers [28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

DNA repair polymorphisms might contribute differentially on familial and sporadic breast cancer susceptibility: a study on a Portuguese population

Costa

Pinto

Pereira

et al. 2006

Breast Cancer Res Treat

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The purpose of this study was to evaluate the role of polymorphisms in DNA repair genes as genetic indicators of susceptibility to familial and sporadic breast cancer. We analysed DNA samples from 285 breast cancer patients and 442 control subjects, for XRCC1 Arg399Gln, XPD Lys751Gln, RAD51 G135C and XRCC3 Thr241Met polymorphisms using PCR-RFLP. We observed that women carriers of XRCC1 399Gln genotypes and without family history of breast cancer have a protective effect concerning this disease (OR = 0.54 95% CI 0.35-0.84; p = 0.006). Furthermore, we found that carriers of XRCC3 241Met genotypes without FH have an increased susceptibility of breast cancer (OR = 2.21 95% CI 1.42-3.44; p < 0.001). Additionally, we verified an increased risk of breast cancer in women with FH and carrying RAD51 135C genotypes (OR = 2.17 95% CI 1.19-3.98; p = 0.012). Our results suggest XRCC1 Arg399Gln and XRCC3 Thr241Met DNA repair polymorphisms as important biomarkers to sporadic breast cancer susceptibility, as well as, RAD51 G135C polymorphism as a real risk modifier in familial breast cancer cases.

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“…There are fewer epidemiological studies to examine the association between p73 , MDM2 and MDM4 polymorphisms and HPV16-associated cancer risk. A Portuguese study reported a significant association between the p73 4/14 GC/AT polymorphism and cervical cancer 35 and a Japanese study reported a borderline significant association between this p73 polymorphism and risk for cervical cancer 36 . In our previous case-control study among non-Hispanic whites, we found that these polymorphisms have been shown to be individually associated with risk for subsites of squamous cell carcinomas of the head and neck, especially in never-smokers 20–22 , while there are no studies that simultaneously investigate the combined effects of these polymorphisms on risk of HPV16-associated oral cancer.…”

Section: Discussionmentioning

confidence: 99%

Combined p53‐related genetic variants together with HPV infection increase oral cancer risk

Wang

Sturgis

Zhang

et al. 2011

Intl Journal of Cancer

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To explore the role of polymorphisms of p53-related genes in etiology of oral cancer, we investigated joint effects of seven putatively functional polymorphisms of p53 (codon 72 Arg/Pro), p73 (4/14 GC/AT), MDM2 (A2164G and T2580G), and MDM4 (rs11801299 G>A, rs10900598 G>T, and rs1380576 C>G) on risk of HPV16-associated oral cancer in a case-control study with 325 cases and 335 cancer-free controls. We found that HPV16 seropositivity alone was associated with an increased risk of oral cancer [adjusted odds ratio (OR), 3.1; 95% confidence interval (CI), 2.1–4.6]. After combining genotypes of seven polymorphisms and using the low-risk group (0–3 combined risk genotypes) and HPV16 seronegativity as the reference group, the medium-risk (4 combined risk genotypes) and high-risk groups (5–7 combined risk genotypes) and HPV16 seronegativity were associated with only an OR of 1.6 (95% CI, 1.1–2.5) and 1.2 (95% CI, 0.7–1.9) for oral cancer risk, respectively, while the low-risk, medium-risk, and high-risk groups and HPV16 seropositivity were significantly associated with a higher OR of 2.1 (95% CI, 1.2–3.6), 4.0 (95% CI, 1.8–9.1), and 19.1 (95% CI, 5.7–64.2), respectively. Notably, such effect modification by these combined risk genotypes was particularly pronounced in young subjects (aged < 50 years), never smokers, and patients with oropharyngeal cancer. Taken together, these findings suggest that the combined risk genotypes of p53-related genes may modify risk of HPV16-associated oral cancer, especially in young patients, never-smokers, and patients with oropharyngeal cancer. Larger studies are needed to validate our findings.

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TP73 alterations in cervical carcinoma

Cited by 28 publications

References 30 publications

Base excision repair pathway:PARP1genotypes as modulators of therapy response in cervical cancer patients

Base excision repair pathway:PARP1genotypes as modulators of therapy response in cervical cancer patients

DNA repair polymorphisms might contribute differentially on familial and sporadic breast cancer susceptibility: a study on a Portuguese population

Combined p53‐related genetic variants together with HPV infection increase oral cancer risk

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