Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P42345 (mTOR)
 26,049 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ovarian cancers pose the greatest challenge for gynecological oncology. They are a heterogeneous, rapidly progressing and highly lethal group of malignancies and their etiology is still poorly understood. Among many hypotheses, explaining the pathogenesis of malignant tumors, chronic inflammation seems to play a significant role, which was proved in cervical, hepatic and esophageal cancers. The processes of inflammation and carcinogenesis are very much alike. Their similarity was experimentally confirmed by epidemiological, immunological, biochemical and genetic studies. Additionally this view is supported by indirect epidemiological and clinical evidence linking ovarian cancer with pelvic inflammatory disease, endometriosis or polycystic ovary syndrome. Chronic inflammation is a key factor in the pathogenesis of these illnesses. Moreover ovulation involving repeated damage and repair of the ovarian surface epithelium is in fact an inflammatory process. In this review, we focus on the role of inflammation in cancer initiation, promotion and progression with special emphasis on the ovarian cancer. We discuss the potential involvement of the fallopian tubes, endometriosis and microenvironment of tumors represented by cytokines, chemokines, growth factors and various enzymes that destroy the extracellular matrix. Considering that molecular biology is currently rapidly evolving, we focus on the function of the mammalian target of rapamycin (mTOR) kinase and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB) in the pathophysiology of inflammation and cancer.
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PMID:Inflammation and ovarian cancer--current views. 2370 Aug 63

Chlamydia trachomatis is the leading causative agent of bacterial sexually transmitted infections worldwide which can lead to female pelvic inflammatory disease and infertility. A greater understanding of host response during chlamydial infection is essential to design intervention technique to reduce the increasing incidence rate of genital chlamydial infection. In this study, we investigated proteome changes in epithelial cells during C. trachomatis infection by using an isobaric tags for relative and absolute quantitation (iTRAQ) labeling technique coupled with a liquid chromatography-tandem mass spectrometry (LC-MS(3) ) analysis. C. trachomatis (serovar D, MOI 1)-infected HeLa-229 human cervical carcinoma epithelial cells (at 2, 4 and 8 h) showed profound modifications of proteome profile which involved 606 host proteins. MGST1, SUGP2 and ATXN10 were among the top in the list of the differentially upregulated protein. Through pathway analysis, we suggested the involvement of eukaryotic initiation factor 2 (eIF2) and mammalian target of rapamycin (mTOR) in host cells upon C. trachomatis infection. Network analysis underscored the participation of DNA repair mechanism during C. trachomatis infection. In summary, intense modifications of proteome profile in C. trachomatis-infected HeLa-229 cells indicate complex host-pathogen interactions at early phase of chlamydial infection.
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PMID:Temporal proteomic profiling of Chlamydia trachomatis-infected HeLa-229 human cervical epithelial cells. 2713 21