Huang Sc

Cytokine regulation networks in the cancer microenvironment.

During carcinoma formation, cancer cells release various cytokines and growth factors into their surroundings and recruit and reprogram many other types of cells in order to establish a tumor microenvironment. Consequently, the tumor tissues almost always contain a large number of endothelial cells, fibroblasts, and infiltrating inflammatory cells that in turn produce a variety of cytokines. The cytokines produced by these cells have been posited as key factors in modulating immune response either against or in favor of tumorigenesis in the microenvironment. The interactions that take place between immune and cancer cells are complex, involving multiple cascades of cytokines, chemokines, and/or growth factors. In this review, we address the essential pro- and anti-tumorigenic roles of cytokines in the tumor microenvironment. As the interaction of cytokines, growth factors, and cancer cells forms a comprehensive network at the tumor site that is then responsible for the overall progression or rejection of the tumor, the current review links the microenvironment-derived cytokines and growth factors to a number of different kinds of human carcinogenesis models. Multifunctional cytokines, extracellular matrix mediators, and regulatory cytokines in the cancer environment are all shown to be key factors in the different cancer immune-editing systems. The characterization of cytokine networks in various types of cancer cells may yield important information for understanding the immune-related mechanisms of cancer development, and this knowledge may have subsequent application in cancer immunotherapy.

Extracellular matrix proteases - cytokine regulation role in cancer and pregnancy.

The extracellular matrix proteases act in diverse physiological and pathological processes involving tumor growth, angiogenesis, and pregnancy through the cleavage of extracellular matrix (ECM) and non-matrix proteinaceous substrates. Matrix metalloproteinases (MMPs) constitute a main family among the ECM proteases. Endogenous tissue inhibitors of metalloproteinases (TIMPs), as one kind of MMPs inhibitors (MMPIs), reduce the excessive proteolytic ECM degradation by MMPs. The balance between MMPs and TIMPs plays a major role in cancer tumorigenesis, angiogenesis, as well as embryo implantation and trophoblastic invasion during pregnancy. A variety of literature concerns the correlated changes in MMPs and MMPIs during the formation of cancer and pregnancy-related complications. Importantly, MMPs and TIMPs may act as regulators of signaling pathways through the cleavage of non-matrix substrates, including cytokines, chemokines, and growth factors. In this review, we concentrate on mutual interactions between ECM proteases and cytokines during cancer development and pregnancy. The current knowledge in the field of identified ECM proteases will be contributive to the innovative therapeutic intervention in both cancer and pregnancy-related processes.

Comparison of detection of human papillomavirus 16 DNA in cervical carcinoma tissues by Southern blot hybridisation and nested polymerase chain reaction

An association between human papillomavirus (HPV) and cervical neoplasia has been widely reported and HPV DNA is commonly detected in cervical carcinoma tissues. However, estimates of the prevalence of HPV infection differs among various detection methods. Seventy cases of cervical carcinoma were screened for HPV 16 infection by Southern blot hybridisation (SBH) and nested polymerase chain reaction (PCR). According to SBH, the prevalences of HPV 16 DNA in stage I (n = 40) and stage II (n = 30) cervical carcinomas were 52.5 and 63.3%, respectively, and the overall prevalence was 57.1% (40 of 70). By nested PCR, the prevalences of HPV 16 infection in stage I and II cervical carcinomas were 87.5 and 93.3%, respectively, and the overall prevalence was 90.3%. The prevalence of HPV DNA detected by nested PCR was significantly greater than that detected by SBH. The combined concordance of positive and negative results between SBH and nested PCR was 61.4%. The discrepancy resulted mainly from 25 cases (35.7%) that were positive by PCR but negative by SBH. A small copy number of HPV DNA in the these 25 cases was documented by a semi-quantitative PCR method. The nested PCR was more sensitive than SBH and detected cases with low amounts of HPV DNA. The detection of HPV infection varied between these two prevailing detection methods and this should be kept in mind in assessing various epidemiological data concerning HPV infection.