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Background and aims The causative role of high risk human papillomavirus (HR-HPV) in breast cancer development is controversial, though a number of reports have identified HR-HPV DNA in breast cancer specimens. Nevertheless, most studies to date have focused primarily on viral DNA rather than the viral transcription. The aim of this study was to investigate the presence of HR-HPV in breast cancer tissues at HPV DNA level and HPV oncogenes mRNA level by in situ hybridization (ISH). Methods One hundred and forty six (146) cases of breast invasive ductal carcinoma(IDC) and 83 cases of benign breast lesions were included in the study. Type specific oligonucleotide probes were used for the DNA detection of HPV 16,18 and 58 by ISH. HR-HPV oncogenes mRNA was assayed by novel RNAscope HR-HPV HR7 assay ISH. p16 protein expression was evaluated by immunohistochemistry (IHC). Results HR-HPV 16,18 and 58 DNA were detected in 52 out of 146 (35.6%) IDC and in 3 out of 83 (3.6%) benign breast lesions by ISH. The HR-HPV mRNAs was detected only in a few specimens with strong HPV DNA positivity(4/25) in a few scattered cancer cells with very weak punctate nuclear and/or cytoplasmic staining. p16 over-expression did not correlate with the HPV DNA positive breast cancer samples(17/52 HPVDNA+ vs 28/94 HPV DNA-, p = 0.731). Conclusions HR-HPVs certainly exist in breast cancer tissue with less active transcription, which implies that the causal role of HPV in breast cancer development need further study.

Objective To investigate the effect of c-Jun N-terminal kinase 1 (JNK1) or JNK2 overexpression on the proliferation and apoptosis of SCL-1 human cutaneous squamous cell carcinoma cell lines. Methods JNK1 and JNK2 were separately combined with pHBAD-EF1-MCS-3FLAG-CMV-GFP vector to construct the recombinant adenovirus expression vectors of JNK1 and JNK2. The recombinant vectors were used to infect SCL-1 cells. After the optimization of the infection conditions, the fold changes of over-expression were identified by real-time quantitative PCR (qRT-PCR) and Western blot analysis. CCK-8 assay was performed to determine the proliferative activity of SCL-1 cells. Cell colony forming ability was evaluated by cell colony formation assay. Wound healing assay was used to detect the scratch healing rate of SCL-1 cells. Cell apoptosis was determined by flow cytometry. The qRT-PCR was used to detect the mRNA levels of JNK1, JNK2 and c-Jun. The protein level of phosphorylated c-Jun was tested by Western blot analysis. Results The optimal infection condition of JNK1- and JNK2-overexpressing adenoviral vectors was multiplicity of infection (MOI) of 100. The expression levels of JNK1 and JNK2 in SCL-1 cells significantly increased 48 hours after the infection. Compared with the control group, the over-expression of JNK1 had no significant effect on the proliferation and anti-apoptosis ability of SCL-1 cells. The proliferation and anti-apoptosis ability of Ad-JNK2 was significantly enhanced compared with Ad-JNK1, and the phosphorylated c-Jun protein level was up-regulated. Conclusion JNK2 has the function of enhancing the proliferation and anti-apoptotic ability of SCL-1 human cutaneous squamous cell carcinoma cells.

Objective: Treatments for condylomata acuminata (CA) include pharmacotherapy and surgical therapies, but each treatment has its limitations. The aim of this study was to investigate the virus clearance rate, wart cure rate and safety of 5 methods on CA. Methods: 361 patients diagnosed with CA were divided into groups A (2.0-4.0 cm) according to the maximum diameter of their lesion. Five treatments were compared in each group, and the clinical outcomes were evaluated during follow-ups. Results: A 5-aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) is preferred if the maximum lesion diameter is 2.0- 4.0 cm, an ALA-PDT retreatment (after cryotherapy or CO2 laser treatment) should be the first choice. Conclusions: The treatments for CA should be chosen according to the maximum diameter of each patient's lesion.

Combination of a photosensitizer, 5-aminolevulinic acid (ALA), with photodynamic therapy (PDT) has been widely used to treat skin squamous cell carcinoma (SCC). However, a portion of SCC patients do not respond well to PDT. The molecular reason for this resistance is not clear. We hypothesize that mitogen-activated phosphorylation kinase (MAPK) plays a key role in mediating SCC resistance to PDT. To determine whether inhibition of MAPK signaling enhances the anti-tumor effect of ALA-PDT in SCC. The human squamous carcinoma cell line, SCL-1, was either untreated or treated with various combinations of ALA, PDT light source and inhibitors of MAPK signaling components. ALA-PDT treatment significantly decreased cell viability, increased the percentage of annexin-V positive cells and resulted in formation of apoptotic bodies. ALA-PDT treated cells showed increased levels of p-MEK, p-ERK1/2, p-p38, p-Elk-1, p-JNK and p-c-Jun. Addition of inhibitors for ERK1/2 (PD98059), p38 (SB203580) and JNK (SP60125) reversed the changes and led to a more dramatic decrease in SCL-1 cell viability than seen with ALA-PDT alone. Inhibition of the MAPK pathway enhances the cytotoxic effect of ALA-PDT on SCL-1.