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Evaluation of the cytotoxic potential of BT-cisplatin combination against the ovarian cancer cell lines OVCAR-3 and SKOV-3. (PDF 420 kb)

Background The role of excessive adiposity or its metabolic consequences in persistent HPV infection among general adult women remains unknown. Methods Using data from the National Health and Nutrition Examination Survey (NHANES) in 2003–2010, we compared adult women’s likelihood for any- or high-risk (HR) type HPV infection by degrees of excessive adiposity and metabolic health status. Results Any-type (41.1 % vs. 44.9 %, P = 0.045) or HR-type HPV prevalence (21.9 % vs. 25.4 %, P = 0.055) was comparable in women aged 20–59 years with or without central obesity. After adjusting for age, socioeconomic indicators, and lifetime sexual risks, centrally-obese women barely showed a different likelihood for any-type (aPR [adjusted prevalence ratio] = 0.91, P = 0.03) or HR-HPV infection (aPR = 0.92, P = 0.279). However, obesity (aPR = 0.76, P = 0.017) or centrally-obesity (aPR = 0.72, P = 0.003) was negatively correlated with HR-HPV infection in women reporting an early sex debut (

Evaluation of the cytotoxic potential of BT-cisplatin combination against the ovarian cancer cell lines OVCAR-3 and SKOV-3. (PDF 420 kb)

Background MicroRNAs (miRNAs) have emerged as master regulators of angiogenesis and other cancer-related events. Discovering new angiogenesis-regulating microRNAs (angiomiRs) will eventually help in developing new therapeutic strategies for tumor angiogenesis and cardiovascular diseases. Kaposi’s sarcoma (KS), which is induced by the etiological infectious agent KS-associated herpesvirus (KSHV), is a peculiar neoplasm that expresses both blood and lymphatic endothelial markers and possesses extensive neovasculature. Using KSHV and its proteins as baits will be an efficient way to discover new angiomiRs in endothelial cells. Kaposin B is one of the latent viral genes and is expressed in all KSHV tumor cells. Since Kaposin B is a nuclear protein with no DNA-binding domain, it may regulate gene expression by incorporating itself into a transcription complex. Results We demonstrated that c-Myc and Kaposin B form a transcription complex and bind to the miR-221/-222 promoter, thereby affecting their expression and anti-angiogenic ability. By small RNA sequencing (smRNA-Seq), we revealed that 72.1 % (173/240) of Kaposin B up-regulated and 46.5 % (113/243) of Kaposin B down-regulated known miRNAs were regulated by c-Myc. We also found that 77 novel miRNA were up-regulated and 28 novel miRNAs were down-regulated in cells expressing both c-Myc and Kaposin B compared with cells expressing Kaposin B only. The result was confirmed by RNA-IP-seq data. Conclusions Our study identifies known and novel c-Myc-regulated microRNAs and reveals that a c-Myc-oriented program is coordinated by Kaposin B in KSHV-infected cells. Electronic supplementary material The online version of this article (doi:10.1186/s12918-015-0242-3) contains supplementary material, which is available to authorized users.

Background Pediatric embryonal brain tumors (PEBTs), which encompass medulloblastoma (MB), primitive neuroectodermal tumor (PNET) and atypical teratoid/rhabdoid tumor (AT/RT), are the second most prevalent pediatric brain tumor type. AT/RT is highly malignant and is often misdiagnosed as MB or PNET. The distinction of AT/RT from PNET/MB is of clinical significance because the survival rate of patients with AT/RT is substantially lower. The diagnosis of AT/RT relies primarily on morphologic assessment and immunohistochemical (IHC) staining for a few known markers such as the lack of INI1 protein expression. However, in our clinical practice we have observed several AT/RT-like tumors, that fulfilled histopathological and all other biomarker criteria for a diagnosis of AT/RT, yet retained INI1 immunoreactivity. Recent studies have also reported preserved INI1 immunoreactivity among certain diagnosed AT/RTs. It is therefore necessary to re-evaluate INI1(+), AT/RT-like cases. Method Sanger sequencing, array CGH and mRNA microarray analyses were performed on PEBT samples to investigate their genomic landscapes. Results Patients with AT/RT and those with INI(+) AT/RT-like tumors showed a similar survival rate, and global array CGH analysis and INI1 gene sequencing showed no differential chromosomal aberration markers between INI1(−) AT/RT and INI(+) AT/RT-like cases. We did not misdiagnose MBs or PNETs as AT/RT-like tumors because transcriptome profiling revealed that not only did AT/RT and INI(+) AT/RT-like cases express distinct mRNA and microRNA profiles, their gene expression patterns were different from those of MBs and PNETs. The most similar transcriptome profile to that of AT/RTs was the profile of embryonic stem cells. However; the transcriptome profile of INI1(+) AT/RT-like tumors was more similar to that of somatic neural stem cells, while the profile of MBs was closer to that of fetal brain tissue. Novel biomarkers were identified that can be used to distinguish INI1(−) AT/RTs, INI1(+) AT/RT-like cases and MBs. Conclusion Our studies revealed a novel INI1(+) ATRT-like subtype among Taiwanese pediatric patients. New diagnostic biomarkers, as well as new therapeutic tactics, can be developed according to the transcriptome data that were unveiled in this work. Electronic supplementary material The online version of this article (doi:10.1186/s12920-015-0103-3) contains supplementary material, which is available to authorized users.