Pancreatic cancer is one of the most lethal types of cancer in the world. The incidence of pancreatic cancer increases each year with no significant decrease in mortality. Pancreatic cancer is a complex disease, and this complexity is partly attributed to late diagnosis, an aggressive phenotype, environmental factors and lack of effective treatment options. Surgical resection followed by adjuvant chemotherapy is the treatment of choice for early stage cancer, whereas gemcitabine is the standard first line therapy for patients with advanced stage disease. Treatment regimens comprising folinic acid, 5-fluorouracil, irinotecan, oxaliplatin and nab-paclitaxel have demonstrated modest effects in improving median survival rates. A number of other chemotherapeutics are currently undergoing clinical trials as components of combination therapies with gemcitabine. An increasing number of novel molecular targets and cellular pathways are being identified, which highlights the complexity of this disease. The development of chemoresistance to gemcitabine is multifactorial and there exists an interplay between pancreatic cancer cells, the tumor microenvironment and cancer stem cells. These components appear to be governed by a complex network of non-coding RNAs such as micro RNAs and long non-coding RNAs. In the present study, studies describing previous research on the understanding of the factors associated with the development of chemoresistance to gemcitabine in pancreatic cancer are reviewed. A comprehensive understanding of the multiple pathways of chemoresistance is key to develop next generation therapeutics to pancreatic cancer.

Background: India has a large population of HIV-positive individuals, including men who have sex with men (MSM), and the incidence of human papillomavirus (HPV)-related cancers is high. In developed countries, HIV-positive MSM exhibit the highest prevalence of anal HPV infection and incidence of anal cancer. Little is known about anal HPV infection in HIV-positive Indian MSM. Methods: We evaluated 300 HIV-positive MSM from 2 cities in India. Men were tested for anal HPV infection using L1-HPV DNA polymerase chain reaction with probes specific for 29 types and a mixture of 10 additional types. CD4⁺ level and plasma HIV viral load were measured. Participants completed an interviewer-administered questionnaire including a sexual history. Results: The prevalence of anal HPV was 95% (95% confidence interval: 91% to 97%). The 3 most common types were HPV 35 (20%), HPV 16 (13%), and HPV 6/11 (13%). History of taking antiretroviral medications decreased risk of anal HPV 16 infection [relative risk (RR): 0.6 (0.4–1.0)]. Having an increased number of vaginal sex partners lowered risk of any anal HPV infection. Ever having receptive sex increased risk of any anal HPV [RR: 1.2 (1.1–1.4)] and anal HPV 16 [RR: 6.5 (1.8–107)]. Conclusions: Almost all Indian HIV-positive MSM had anal HPV infection. The prevalence of HPV 16 was lower and the prevalence of other oncogenic HPV types was higher than in similar populations in North America and Europe. Vaccine-based prevention strategies for HPV infection in India should consider potential differences in HPV type distribution among HIV-infected MSM when designing interventions.

Virological monitoring of hepatitis B virus (HBV) DNA is critical to the management of HBV infection. With several HBV DNA quantification assays available, it is important to use the most efficient testing system for virological monitoring. In this study, we evaluated the performance characteristics and comparability of three HBV DNA quantification systems: Abbott HBV real-time PCR (Abbott PCR), artus HBV real-time PCR with QIAamp DNA blood kit purification (artus-DB), and artus HBV real-time PCR with the QIAamp DSP virus kit purification (artus-DSP). The lower limits of detection of these systems were established against the WHO international standards for HBV DNA and were found to be 1.43, 82, and 9 IU/ml, respectively. The intra-assay and interassay coefficients of variation of plasma samples (1 to 6 log ₁₀ IU/ml) ranged between 0.05 to 8.34% and 0.16 to 3.48% for the Abbott PCR, 1.53 to 26.85% and 0.50 to 12.89% for artus-DB, and 0.29 to 7.42% and 0.94 to 3.01% for artus-DSP, respectively. Ninety HBV clinical samples were used for comparison of assays, and paired quantitative results showed strong correlation by linear regression analysis (artus-DB with Abbott PCR, r = 0.95; Abbott PCR with artus-DSP, r = 0.97; and artus-DSP with artus-DB, r = 0.94). Bland-Altman analysis showed a good level of agreement for Abbott PCR and artus-DSP, with a mean difference of 0.10 log ₁₀ IU/ml and limits of agreement of −0.91 to 1.11 log ₁₀ IU/ml. No genotype-specific bias was seen in all three systems for HBV genotypes A, C, and D, which are predominant in this region. This finding illustrates that the Abbott real-time HBV and artus-DSP systems show more comparable performance than the artus-DB system, meeting the current guidelines for assays to be used in the management of hepatitis B.

The hypothesis to be tested was that the prevalence of human papillomavirus (HPV) and cervical intraepithelial neoplasia would be significantly higher in HIV seropositive women as compared with seronegative controls. Secondary aims were to determine the risk factors for HPV and cervical intraepithelial neoplasia and the HPV types in HIV-positive women. A cross-sectional study of women 18 to 49 years old was done. Seventy-five women who were HIV seropositive and 58 seronegative women, of whom 27 had HIV-positive partners, participated in the study. A Pap smear and a cervical swab for HPV were done. Women with Pap smear abnormality underwent colposcopy and large loop excision procedures if indicated. Ten (13.3%) HIV-positive women had high-grade squamous intraepithelial lesion as compared with 2 (3.4%) seronegative women (odds ratio [OR] 4.3; 95% CI = 0.9-41.7; p =.048). Among the HIV-positive women, 28 (37.3%) had high-risk HPV, whereas only 9 (15.5%) had high-risk HPV among seronegative women (OR 3.2; 95% CI = 1.3-8.3; p =.009). Among women who were positive for high-risk HPV, the HIV-positive women were significantly more likely to have more than 1 HPV type (OR 7.4; 95% CI = 1.4-43.7; p =.005). Women who had coitus at less than 18 years of age were more likely to have high-risk HPV infection (OR 2.9; 95% CI = 1.2-6.2; p =.013) even after controlling for HIV status. HIV-positive women have a higher risk for multiple HPV infections as compared with seronegative women. Behavioral factors dominate HIV in determining HPV infections and resultant cervical neoplasia.