Breast cancer risk in relation to TP53 codon 72 and CDH1 gene polymorphisms in the Bangladeshi women

Shabnaz, Samia; Ahmed, Maizbha Uddin; Islam, Md. Jahirul; Islam, Md. Reazul; Al-Mamun, Mir Md. Abdullah; Islam, Mohammad Safiqul; Hasnat, Abul

doi:10.1007/s13277-015-4612-7

Cited by 28 publications

(18 citation statements)

References 69 publications

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“…To maintain the stability of the meta-analysis after the non-inclusion of deviant studies of HWE and sensitivity analysis, we evaluated the influence of each study on pooled OR. After the exclusion of studies [39][40][41][42], no study has shown a significant influence of the pooled OR effect in each of the different genetic models ( Table 2).…”

Section: Resultsmentioning

confidence: 99%

TP53 p.Arg72Pro polymorphism and Breast Cancer Risk: A meta-analysis of case-control studies

Diakité¹,

Kassogue²,

Dolo³

et al. 2020

Preprint

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Background :The effect of the p.Arg72Pro variant of the P53 gene on the risk of developmentof breast cancer remains variable in populations. However, the use of strategiessuchas pooling age-matched controls with disease cases may provide a solid meta-analysis. Our goal was to perform a meta-analysis in order to assessthe association of p.Arg72Provariant of P53 gene with breast cancer risk. Methods : Databases such as PubMed, Genetics Medical Literature, Harvard University Library, Web of Science and Genesis Library were used to search articles. Age-matched case-control studies on breast cancer that have evaluated the genotype frequencies of the p.Arg72Pro of P53 gene were selected. The fixed and random effects (Mantel-Haenszel) were calculated using pooled odds ratio of 95% CI to determine the risk of disease. Inconsistency was calculated to determine heterogeneity among the studies. The publication bias was estimated using the funnel plot. Results : Twenty-one publications with cases age-matched controls including7841disease cases and 8876controls were evaluated in this meta-analysis. Overall, our results suggested that p.Arg72ProP53 was associated with a risk for breast cancer for the dominant model (OR= 1.09, 95% CI = 1.02-1.16; P= 0.01) and the additive model (OR= 1.09, 95% CI = 1.01-1.17; P= 0.03), but not in the recessive model (OR = 1.07, 95% CI = 0.97-1.16; P= 0.19). According to the ethnic group, allele Pro has been associated with breast cancer risk in Europeans for the dominant and additive models. Conclusions : This meta-analysis found a significant association between p.Arg72Pro in the P53 gene and the risk of breast cancer. Individuals carrying at least one Pro allele of the P53 gene are more likely to have breast cancer with dominant and additive models than individualsharboringthe Arg allele.

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Section: Resultsmentioning

confidence: 99%

TP53 p.Arg72Pro polymorphism and Breast Cancer Risk: A meta-analysis of case-control studies

Diakité¹,

Kassogue²,

Dolo³

et al. 2020

Preprint

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“…In our study, none of the studied SNPs showed any significant correlations with patients’ epidemiological or tumor or histological features. Shabnaz et al also did not find any correlation between − 160C/A polymorphisms with clinicopathological characteristics of BC patients [18]. However, Tipirisetti et al noted a positive correlation between the − 160A allele occurrences in patients with advanced stage [19].…”

Section: Discussionmentioning

confidence: 99%

E-cadherin genetic variants predict survival outcome in breast cancer patients

et al. 2016

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BackgroundE-cadherin is a major component of adherens junctions that regulates cell shape and maintains tissue integrity. A complete loss or any decrease in cell surface expression of E-cadherin will interfere with the cell-to-cell junctions’ strength and leads to cell detachment and escape from the primary tumor site. In this prospective study, three functional single nucleotide polymorphisms (−347G/GA, rs5030625; −160C/A, rs16260; +54C/T, rs1801026), were found to modulate E-cadherin expression.Methods577 DNA samples from breast cancer (BC) cases were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR–RFLP).ResultsWe detected no significant correlations between each polymorphism and the clinical parameters of the patients whereas the GACC haplotype was significantly associated with low SBR grading. Overall survival analysis showed that both −347G/G and +54C/C wild (wt) genotypes had a significantly worse effect compared to the other genotypes (non-wt). Moreover, carrying simultaneously both the −347 and +54 wt genotypes confers a significantly higher risk of death. However, with metastatic recurrence, the death-rate was null in patients carrying the non-wt genotypes, and attained 37% in those carrying the wt genotype. A multivariate analysis showed that these two polymorphisms are independent prognostic factors for overall survival in BC patients.ConclusionsOur results support the fact that E-cadherin genetic variants control disease severity and progression and could be a marker of disease outcome. These findings could be useful in selecting patients that should be monitored differently.

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“…Sarrió et al [36] 2003 Spain 45/20 N.S. Cattaneo et al [42] 2006 Central Italy (Lazio) 99/246 N.S. Yu et al [39] 2006 Taiwan 468/470 Minor allele carriers (rs16260 A) were 30% more likely to be breast cancer cases than women with only the major allele (C).…”

Section: Discussionmentioning

confidence: 99%

“…Cattaneo et al [42] investigated a sample of the Italian population and found no association between the -160 C/A SNP and breast cancer risk (OR = 1.35, 95 % CI = 0.84-2.17). Lei et al [37] found the same result among the Swedish as well as Czech populations.…”

Section: The Role Of E-cadherin Polymorphisms In Breast Cancer Riskmentioning

confidence: 99%

“…These mutations lead to truncated proteins of E-cadherin, abnormal alterations of the E-cadherin's calcium binding sites, or increases in its proteolytic this study, we found significant association between the CDH1 -160 C/A polymorphism and breast cancer in recent studies. -160C/A SNP within the CDH1 promoter region is a functional polymorphism that may affect transcription efficiency in vitro [42]. There is no doubt that E-cadherin inactivation plays an important role in the development of breast cancers.…”

Section: The Role Of E-cadherin Polymorphisms In Breast Cancer Riskmentioning

confidence: 99%

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The role of E-cadherin - 160C/A polymorphism in breast cancer

Luo

Huang

Tao³

et al. 2016

Open Life Sciences

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Open Life Sci. 2016; 11: 110-115 invasion and metastases. These characteristics are results of genetic deregulation. Accumulation of genetic mutations results in increasingly aggressive phenotypes [5]. E-cadherin in Breast Cancer Structure and Functions of E-CadherinThe CDH1 gene is located on human chromosome 16q22.1 and encodes for the E-cadherin protein [6]. The E-cadherin glycoprotein is composed of three major structural domains: a single transmembrane domain, connected with a cytoplasmic domain, and an extracellular domain comprising five tandemly repeated domains called EC1-EC5, which are exclusive to cadherins [7]. The extracellular domain of E-cadherin is essential for cell to cell adhesion, as well as for the correct folding and homo/hetero dimerisation of the proteins. The cytoplasmic domain of E-cadherin interacts with the catenins (α-, β-, γ-and p120 catenin) anchored to the actin cytoskeleton, establishing cadherin-catenin complexes [8]. Conformation of E-cadherin is only stable upon Ca 2+ binding to its highly conserved, negatively charged extracellular motifs [9]. Its stabilization at the cell membrane and accurate function occur by association to cytoplasmic p120-catenin [10]. E-cadherin forms adherens junction with its binding partner β-catenin and actin filaments. This complex is critical to inhibit individual epithelial cell motility and to provide homeostatic tissue architecture [11,12] (Figure 1). Signaling Pathways Regulated by E-CadherinIn addition to its role in cell to cell adhesion, E-cadherin is involved in a number of signaling pathways in carcinogenesis [13]. For the Wnt/β-catenin pathway, free β-catenins may accumulate in the cytoplasm attributed Abstract: Breast cancer is the most prevalent cancer in women worldwide. Numerous studies have suggested that the E-cadherin adhesion system is dysregulated in cancer cells. These impaired functions of E-cadherin contribute to releasing cancer cells from the primary lesion to cell dedifferentiation. Some studies have shown that polymorphism may affect E-cadherin expression, and then play a role in susceptibility to breast cancer. However, the results remained controversial. In this short review, we summarize the functions of E-cadherin and the signaling pathways it regulates, and assess the association between CDH1 polymorphisms and breast cancer susceptibility. This study suggests that genetic variation in CDH1 and -160C/A polymorphism may have an association with breast cancer risk. The assessment of CDH1 polymorphisms may be used for the identification of patients suitable for anti-CDH1 therapy.

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Breast cancer risk in relation to TP53 codon 72 and CDH1 gene polymorphisms in the Bangladeshi women

Cited by 28 publications

References 69 publications

TP53 p.Arg72Pro polymorphism and Breast Cancer Risk: A meta-analysis of case-control studies

TP53 p.Arg72Pro polymorphism and Breast Cancer Risk: A meta-analysis of case-control studies

E-cadherin genetic variants predict survival outcome in breast cancer patients

The role of E-cadherin - 160C/A polymorphism in breast cancer

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