This study evaluated the presence of Human Papillomavirus (HPV) DNA in the cervix and peripheral blood of women with cervical intraepithelial neoplasia (CIN I, II, and III) and healthy individuals. Overall, 139 paired peripheral blood and cervix samples of healthy women and women with CIN I, II, and III (n = 68) were tested for HPV DNA by using standard procedures. Polymerase chain reaction (PCR) sequencing determined HPV types. Quantification of HPV16 E6 and E2 genes was performed to determine viral load and physical state. HPV DNA was detected in the cervix (21.1% in healthy individuals; 48.8–55.5% in CIN patients), blood (46.4% in healthy individuals; 44.1–77.7% in CIN patients) and paired peripheral blood and cervix samples (24% in healthy individuals; 32.5–44.4% in CIN patients). The most frequent types found in the cervix were HPV16, 18, 31, 33, 58, and 70, while HPV16, 18, 33, 58, and 66 were the most frequent types found in the blood. HPV DNA in the cervix was associated with previous sexually transmitted infections (STIs) (p = 0.023; OR: 2.978; CI:1.34–7.821), HPV DNA in the blood (p = 0.000; OR: 8.283; CI:3.700–18.540), and cervical lesions (CIN I/II or III) (p = 0.007). Binomial logistic regression showed that HPV DNA in the blood (p = 0.000; OR: 9.324; CI:3.612–24.072) and cervical lesions (p = 0.011; OR: 3.622; CI:1.338–9.806) were associated with HPV DNA in the cervix. However, we did not find an association between HPV DNA in the blood and cervical lesions (p = 0.385). Our results showed that only HPV DNA found in the cervix was associated with cervical lesions.

This study evaluated the presence of HPV DNA in the cervix and peripheral blood of women with cervical intraepithelial neoplasia (CIN I, II, and III) and healthy individuals. Overall, 139 paired peripheral blood and cervix samples of healthy women and women with CIN I, II, and III (n= 68) were tested for HPV DNA by using standard procedures. PCR-sequencing determined HPV types. Quantification of HPV16 E6 and E2 genes was performed to determine viral load and physical state. HPV DNA was detected in the cervix (21.1% in healthy individuals; 48.8-55.5% in CIN patients), blood (46.4% in healthy individuals; 44.1-77.7% in CIN patients), and paired peripheral blood and cervix samples (24% in healthy individuals; 32.5-44.4% in CIN patients). The most frequent types found in the cervix were HPV16, 18, 31, 33, 58, and 70, while HPV16, 18, 33, 58, and 66 were the most frequent types found in the blood. HPV DNA in the cervix was associated with previous sexually transmitted infections (STIs) (P=0.023; OR: 2.978; CI:1.34-7.821), HPV DNA in the blood (P=0.000; OR: 8.283; CI:3.700-18.540), and cervical lesions (CIN I/II or III) (P=0.007). Binomial logistic regression showed that HPV DNA in the blood (P=0.000; OR: 9.324; CI:3.612-24.072) and cervical lesions (P=0.011; OR: 3.622; CI:1.338-9.806) were associated with HPV DNA in the cervix. However, we did not find an association between HPV DNA in the blood and cervical lesions (P=0.385). Our results showed that only HPV DNA found in the cervix was associated with cervical lesions.

This study evaluated the presence of Human Papillomavirus (HPV) and Bovine Leukemia Virus (BLV) DNA in breast cancer (BC) samples from women in Northeastern Brazil. We analyzed 186 formalin-fixed, paraffin-embedded tissue block samples using PCR and qPCR to detect HPV and BLV DNA. BLV DNA was not detected in any BC patients. However, HPV DNA was found in 46.2\% of the BC samples: 44.6\% were positive for HPV16, 3.5\% for HPV31, and 2\% were coinfected with HPV16 and HPV31. Additionally, we found an association between HPV-positive BC and Ki-67 expression (P=0.03, OR=1.85; CI=1.02-3.34), as well as between HPV31-positive BC and mitotic index (P=0.047). Although BLV was not detected in BC patients from Northeastern Brazil, the association between HPV and cell proliferation markers warrants further investigation, as HPV may contribute to the aggressiveness of BC in these patients.

Introduction: Matrix metalloproteinases (MMP) have been identified as biomarkers for several diseases, including cancer. MMP-26 is constitutively expressed in some cancer cells of epithelial origin. Despite this, there is a lack of studies regarding the expression of MMP-26 on prostatic carcinoma. Aim: Here, we investigate the expression of the MMP-26 peptide in benign and malign prostatic tissues. Patients and Methods: For this, 150 specimens, including atrophy (N = 25), prostatic intraepithelial neoplasia (PIN) (N = 25), benign prostatic hyperplasia (BPH) (N = 50), and prostatic adenocarcinoma (PA) (N = 50), were immunohistochemically (IHC) examined for the expression of MMP-26. Results: MMP-26 expression was positive in 70 (46.7%) out of the 150 samples, being more prevalent in the PA group (46/50 cases,92%), followed by PIN (22/25 cases, 88%). The BPH group showed only 2/50 (4%) positive cases, and the atrophy group showed no reactivity. ROC curve analysis showed that MMP-26 immunoexpression had a higher area under the curve between PA vs atrophy+PIN+BPH (AUC=0.94; 95% CI 0.9-0.98), PA+PIN vs atrophy+BPH (AUC=0.97; 95% CI 0.94-0.99) and PA vs atrophy+BPH (AUC=0.97; 95% CI 0.95-1.00) groups. In addition, the expression and intensity of the MMP-26 reaction showed a significant association with total PSA values ( P =0.001). Conclusions: Our results showed that MMP-26 immunoexpression was useful to differentiate a group of benign and malignant samples in prostate tumors. This characteristic could assist in the predictive assessment and, consequently, in the development of new strategies for the diagnosis, prognosis, and treatment of prostate cancer.

In this study, we evaluated the presence of early and late Human Papillomavirus (HPV) proteins in retinoblastoma Brazilian patients. For this, 8 formalin-fixed paraffin-embedded retinoblastoma tissue blocks were used. HPV DNA presence was determined by in situ hybridization (ISH). Immunohistochemistry were performed to verify HPV16/18 E6, E1^E4, and L1 proteins. HPV was detected in all retinoblastoma tumors and viral DNA was labeled in tumor cells, retinal layers and optical nerve structures. In addition, E1^E4, E6 and L1 proteins were detected in all samples in the same areas where HPV DNA was detected. Our data showed the presence and expression of early and late HPV proteins in retinoblastoma tumors from Brazilian children. However, further studies should be performed to clarify the role of HPV infection in retinoblastoma tumor.