• Asian Pacific Journal of Cancer Prevention
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• v.14 no.2
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• pp.723-726
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• 2013

Background: Breast cancer is worldwide the most common cancer in women and is a major public health problem. Genes with high or low penetrance are now clearly implicated in the onset of breast cancer, mostly the BRCA genes. All women in families at high risk of breast cancer do not develop tumours, even when they carry the familial mutation, suggesting the existence of genetic and environmental protective factors. Several studies have shown that consanguinity is linked to a decreased or an increased risk of breast cancer, but to the best of our knowledge, there is no study concerning the association between consanguinity and the occurrence of tumours in women with high risk of breast cancer. The objective of this study was to examine whether parental consanguinity in families with genetic predisposition to breast cancer affect the risk of siblings for having this cancer. Materials and Methods: Over a six-year period, 72 different patients with a histological diagnosis of breast or ovarian cancer from 42 families were recruited for genetic counselling to the Department of Medical Genetics, Rabat. Consanguinity rate was determined in cases and compared to the consanguinity rate in the Moroccan general population. Results: Consanguinity rates were 9.72% in patients and 15.3% in controls, but the difference was statistically not significant (p>0.001) and the mean coefficient of consanguinity was lower in breast cancer patients (0.0034) than in controls (0.0065). Conclusions: Despite the relatively small sample size of the current study, our results suggest that parental consanguinity in Moroccan women might not be associated with an altered risk of breast cancer. Large scale studies should be carried out to confirm our results and to develop public health programs.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.22
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• pp.9739-9745
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• 2014

Purpose: We aimed to evaluate the effects of hormone receptor, HER2, and epidermal growth factor receptor (EGFR) expression on epithelial ovarian cancer (EOC) prognosis and investigate whether or not phenotypic subtypes might exist. Materials and Methods: The medical records of 82 patients who were diagnosed with EOC between 2003 and 2012 and treated by platinum-based chemotherapy were retrospectively evaluated. Expression of EGFR, oestrogen (ER), progesterone (PR), and cerbB2 (HER2) receptors were assessed immunohistochemically on paraffin-embedded tissues of these patients. Three phenotypic subtypes were defined according to ER, PR, and HER2 expression and associations of these with EGFR expression, clinicopathologic features, platinum sensitivity, and survival were investigated. Results: When we classified EOC patients into three subtypes, 63.4% had hormone receptor positive (HR(+)) (considering breast cancer subtypes, luminal A), 18.3% had triple negative, and 18.3% had HER2(+) disease. EGFR positivity was observed in 37 patients (45.1%) and was significantly more frequent with advanced disease (p=0.013). However, no significant association with other clinicopathologic features and platinum sensitivity was observed. HER2(+) patients had significantly poorer outcomes than HER2(-) counterparts (triple negative and HR positive patients) (p=0.019). Multivariate analysis demonstrated that the strongest risk factor for death was residual disease after primary surgery. Conclusions: Triple negative EOC may not be an aggressive phenotype as in breast cancer. The HER2 positive EOC has more aggressive behaviour compared to triple negative and HR(+) phenotypes. EGFR expression is more frequent in advanced tumours, but is not related with poorer outcome. Additional ovarian cancer molecular subtyping using gene expression analysis may provide more reliable data.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.4
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• pp.1501-1506
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• 2015

Gemcitabine is an anti-cancer drug with clinically uses in the treatment of various neoplasms, including breast, ovarian, non-small cell lung, pancreaticand cervical cancers, T-cell malignancies, germ cell tumours, and hepatocellular carcinomas. However, it has also been reported to have many adverse effects. Naturally occurring anti-mutagenic effects, especially those of plant origin, have recently become a subject of intensive research. The present study was therefore designed to investigate the anti-mutagenic effects of Salvia merjamie (Family: Lamiaceae) plant extracts against the mutagenic effects of gemcitabine. The anti-mutagenic properties of Salvia merjamie were tested in Inbred SWR/J male and female mice bone marrow cells. The mice were treated in four groups; a control group treated with 30 mg/kg body weight gemcitabine and three treatment groups, each with 30 mg/kg body weight gemcitabine together with, respectively, 50, 100 and 150 mg/kg body weight Salvia merjamie extract. Chromosomal aberration and mitotic index assays were performed with the results demonstrating that Salvia merjamie extract protects bone marrow cells in mice against gemcitabine induced mutagenicity. This information can be used for the development of a potential therapeutic anti-mutagenic agents.