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BackgroundHuman papillomavirus (HPV) is the most common sexually transmitted virus in women worldwide. The persistence of the virus may cause warts that are considered benign lesions and low or high grade intraepithelial lesions (LSIL/HSIL). Immunological system plays an important role in the resolution of infections. In this context, we highlight the chemokines, which are important regulators in the development of viral infections and inflammation. Among which CXCL12 stands out, due to its pro-inflammatory features, acting as chemoattractant recruiting immune cells. Several polymorphisms were identified in CXCL12 gene including rs1801157 in the 3′-untranslated region, which is characterized by a substitution of a guanine for an adenine.MethodsIn this study, 195 women were classified as HPV non-infected and 169 as HPV-infected. HPV-DNA was detected by polymerase chain reaction (PCR) and the polymorphism was assessed in blood cells through restriction fragment length polymorphism analysis.ResultsHPV infection was more incident in women who had more than 4 sexual partners during lifetime (p = 0.007), among those who presented lower number of pregnancies (p = 0.017). HPV was more prevalent among allele A carriers confirmed by logistic regression analysis adjusted for several confounding factors [ORADJ = 4.985; CI95% (2.85–8.72), p < 0.001]. An association between allele A carriers and HSIL development (p = 0.003) was also observed.ConclusionsIn the present study, we demonstrated that CXCL12 rs1801157 is independently associated with HPV infection and exerts influence in HSIL development, suggesting it as a promising susceptibility biomarker for HPV infection and lesions development.

About 20% of breast cancer patients overexpress the Human Epidermal growth factor Receptor-2 (HER2), also known as ErbB2. HER2overexpression is associated with enhanced tumor malignancy and its overexpression is related to specific target therapy against breast tumors and other cancers. HER2-mediated pathways in tumor cells act on behalf of the tumor conferring aggressive characteristics. Several reports demonstrated the occurrence of toxicity during the anti-HER2 therapy and this fact has been associated with the generation of reactive species and oxidative stress. However, the link between HER2 and oxidative stress signaling is still poorly understood. The aim of this review is to point out the interplay between oxidative stress and HER2 signaling in breast cancer. An overview regarding HER2 biology and oxidative stress pathways is provided with a special focus in studies that implicate on HER2-generation of reactive species and oxidative stress during trastuzumab-based treatments.

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