Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this study was to study the expression of estrogen receptor-beta (ER-beta) in prostatic adenocarcinoma and correlate it with Gleason grade and clinical outcome. Immunohistochemical evaluation was performed on prostate needle biopsies from 53 patients (T1-T3pN0M0). ER-beta and ER-alpha transcripts were also studied by semiquantitative reverse transcriptase polymerase chain reaction in PC-3 and LNCaP prostate carcinoma cell lines. ERbeta was expressed in 93% of adenocarcinomas and was positively associated with primary Gleason grade (P = 0.028 for percentage of positive cells and P = 0.046 using a semiquantitative scale) and Gleason score (P = 0.010 for percentage of positive cells and P = 0.014 using a semiquantitative scale). ER-beta expression in the benign epithelium of prostates with adenocarcinoma was detected in 92% of cases and in the stroma in 47% of cases. A trend for longer time to treatment failure was noted for cases with low ER-beta expression after curatively intended radiotherapy (P = 0.082). PC-3, an aggressive prostate cancer cell line with invasive properties in nude mice, expressed higher levels of ER-beta than LNCaP, a nonmetastasizing cell line, whereas no difference for ER-alpha transcripts could be observed. Our findings suggest that ER-beta, as detected by PPG5/10 antibody, may have a role in the process of dedifferentiation of prostate adenocarcinomas, with higher levels present in less differentiated tumors.
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PMID:Prostate carcinoma expression of estrogen receptor-beta as detected by PPG5/10 antibody has positive association with primary Gleason grade and Gleason score. 1215 65

Telomerase activation, a cardinal requirement for immortalization, is a crucial step in the development of malignancy and requires the induction of the catalytic component, human telomerase reverse transcriptase (hTERT), encoded by the hTERT gene. By reverse transcription-PCR, using primers within the reverse transcriptase domain of hTERT, we investigated telomerase messenger in 8 adenomatous and 9 dysplastic polyps, and in 32 paired cancer-normal mucosa specimens, one liver and one spleen metastasis from patients resected for sporadic colorectal cancer. Telomerase messenger was absent or very low in normal mucosa and in adenomatous polyps. Dysplastic polyps and adenocarcinoma samples showed hTERT mRNA, with higher levels in cancer tissues compared to dysplastic lesions. A high telomerase messenger level was shown to be associated with late-staged cancers and with metastasis; thus, detection of telomerase messenger may be useful in the early diagnosis of colon cancer, and telomerase may be a new target for therapeutic intervention.
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PMID:Evaluation of telomerase mRNA (hTERT) in colon cancer. 1216 91

The features and functions of prostatic neuroendocrine (NE) cells remain ill-defined. Neuroendocrine differentiation (NED) in adenocarcinoma of the human prostate (CaP) is associated with more aggressive disease, but the underlying mediators are poorly understood. We examined these issues in transgenic mice that utilize regulatory elements from the cryptdin-2 gene (Defcr2) to express simian virus 40 large T antigen (TAg) in prostatic NE cells. CR2-TAg mice develop prostatic intraepithelial neoplasia at 8 weeks of age, 1 week after the onset of TAg expression. An invasive phase follows 2-4 weeks later, with lymph node, liver, lung, brain, and bone metastases appearing within 16 weeks. DNA microarray studies revealed 122 mRNAs that were increased >/=2-fold in duplicate assays of 16-week-old CR2-TAg versus normal prostates. Thirty two transcripts encode proteins associated with neurons and endocrine cells (e.g. basic helix loop helix, SRY-related high mobility group box and sine-oculis homeobox transcription factors, Hu RNA-binding proteins, neuronatin, Racgap1, collapsin response mediator protein-1, synaptotagmin-1, proprotein convertase, and secretogranins). Follow-up studies of candidate mediators and biomarkers of differentiation/growth in the microarray data set involved real time quantitative reverse transcriptase-PCR assays of laser capture microdissected NE cells from CR2-TAg prostates plus liver metastases, and immunohistochemical comparisons of transgenic mouse prostates and 35 human CaP samples. Our findings include (a) expression of the bHLH mouse achaete-scute homolog (mASH1) in normal and CR2-TAg NE cells and foci of NED in human CaP, (b) glutamic acid decarboxylase and its product (gamma-aminobutyric acid) in neoplastic NE cells juxtaposed next to cohorts of normal gamma-aminobutyric acid receptor expressing secretory cells (a potential route for paracrine interactions between these two epithelial lineages), and (c) aromatic l-amino-acid decarboxylase, but not its dopamine/serotonin products, in CR2-TAg NE cells and NED. These results underscore the value of CR2-TAg mice for characterizing normal NE cell biology and tumorigenesis.
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PMID:Molecular characterization of a metastatic neuroendocrine cell cancer arising in the prostates of transgenic mice. 1222 43

Cytokeratin 20 (CK20) is an epithelial protein expressed almost exclusively in the gastrointestinal (GI) tract and is widely used as immunohistochemical marker for routine diagnosis. In contrast, CK20 gene expression is not an established marker for the classification of tumours and the detection of disseminated cancer cells in colorectal cancer. Recently, real-time reverse transcriptase polymerase chain reaction (RT-PCR) has provided the means for reproducible and quantitative investigation of molecular markers. This report directly compares CK20 mRNA and protein expression in serial sections of archival, formalin-fixed, paraffin-embedded (FFPE) colorectal adenocarcinomas. CK20 expression was detected by immunohistochemistry (IHC) in 60/63 (95.2%) cases, by conventional RT-PCR in 58/60 (96.7%) and by quantitative RT-PCR using the LightCycler (LightCycler is a trademark of a Member of the Roche Group) System in 29/32 (90.6%) microdissected cases, one case yielding variable results. Despite the high detection rate of all three techniques, marked heterogeneity of CK20 expression was seen between different cases and also within individual cases. CK20 expression profiles were not related to particular histopathological features of the tumours. A good correlation (r = 0.8964) was found between CK20 mRNA and protein expression by comparing quantitative RT-PCR with IHC in 32 cases. This was also true for selected heterogeneous tumour cells within individual cases. Both RT-PCR and IHC are therefore valuable tools for CK20 detection in colorectal adenocarcinoma, with real-time RT-PCR providing supplementary quantitative information. This suggests a promising supportive role for quantitative RT-PCR in molecular pathology.
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PMID:Quantification of CK20 gene and protein expression in colorectal cancer by RT-PCR and immunohistochemistry reveals inter- and intratumour heterogeneity. 1223 79

Ultrastructural studies have shown that Clara cell-type is a more common type of adenocarcinoma than alveolar type II cell-type, and that both types may provide better prognosis than other types, indicating an importance of differentiation toward peripheral airway cells. Pulmonary surfactant protein (SP)-A is a specific marker for both alveolar type II cells and Clara cells in peripheral lung tissues, while SP-C and Clara cell 10 kD protein (CC10) may be particularly and highly specific to alveolar type II cells and Clara cells, respectively. The aims of this study were to assess the differentiation of adenocarcinoma cells in pleural effusions by evaluating the expression of these cell markers and to evaluate their values as diagnostic tools for judging the cause of pleural effusion. We examined pleural effusions from 52 patients; 20 with primary lung adenocarcinomas, 6 with small cell lung carcinomas, 11 with metastatic malignant tumors and 15 with non-neoplastic diseases. The cell pellets from effusions were subjected to immunocytochemical staining for SP-A, proSP-C, a precursor of SP-C, and CC10. By this immunocytochemical study for SP-A and proSP-C, 10 (50%) and 6 (30%) of 20 adenocarcinomas, respectively, showed a positive immunoreactivity in their effusion cells, while none of them expressed CC10. Alveolar type II cells therefore may be the main progenitor cells of some adenocarcinomas. In pleural effusions from patients with primary lung adenocarcinomas, reverse transcriptase-polymerase chain reaction (RT-PCR) for SP-A mRNA showed a sensitivity of 83%, while, in all remaining patients, these assays were negative. In conclusion, we demonstrated that lung adenocarcinomas, which are partially differentiated toward alveolar type II cells, are not as rare as previously thought, and that both the RT-PCR and immunocytochemical analyses for SP-A and pro-SP-C could be worthy indicators of differential diagnosis.
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PMID:Assessment of differentiation in adenocarcinoma cells from pleural effusion by peripheral airway cell markers and their diagnostic values. 1244 49

Angiogenesis plays a critical role in metastasis and tumor growth. Human tumors, including colorectal adenocarcinoma, secrete angiogenic factors, inducing proliferation and chemotaxis of microvascular endothelial cells, eventually leading to tumor neovascularization. The chemokine interleukin 8 (IL-8; CXCL8) exerts potent angiogenic properties on endothelial cells through interaction with its cognate receptors CXCR1 and CXCR2. As CXCR1 and CXCR2 expression is differentially regulated in tissue-specific endothelial cells and effects of IL-8 on intestinal endothelial cells are not defined, we characterized the potential IL-8-induced angiogenic mechanisms in primary cultures of human intestinal microvascular endothelial cells (HIMEC) and IL-8 receptor expression in human intestinal microvessels. CXCR1 and CXCR2 expression on HIMEC were defined using reverse transcriptase-PCR, immunohistochemistry, flow cytometry, and Western blot analysis. IL-8-induced downstream signaling events were assessed using immunoblot analysis and immunofluorescence. The angiogenic effects of IL-8 on HIMEC were determined using proliferation and chemotaxis assays. HIMEC responded to IL-8 with rapid stress fiber assembly, chemotaxis, enhanced proliferation, and phosphorylation of extracellular signal-regulated protein kinase 1/2 (ERK 1/2). HIMEC express CXCR2, but not CXCR1. Neutralizing antibodies to CXCR2 diminished IL-8-induced chemotaxis and stress fiber assembly. Specific inhibitors of ERK 1/2 and phosphoinositide 3-kinase abrogated endothelial tube formation and IL-8-induced chemotaxis in HIMEC. IL-8 elicits angiogenic responses in microvascular endothelial cells isolated from human intestine by engaging CXCR2. We confirmed tissue expression of CXCR2 in human intestinal microvessels. Supported by the notion that malignant colonic epithelial cells overexpress IL-8, CXCR2 blockade may be a novel target for anti-angiogenic therapy in colorectal adenocarcinoma.
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PMID:Angiogenic effects of interleukin 8 (CXCL8) in human intestinal microvascular endothelial cells are mediated by CXCR2. 1249 58

It has been suggested that thyroid transcription factor-1 (TTF-1) is frequently expressed in human lung cancer, especially in adenocarcinoma and small cell lung cancer, and the TTF-1 expression is closely related with the expression of surfactant protein. We hypothesized that TTF-1 is expressed in human lung cancer cell lines and its expression might be related to the expression of surfactant protein. To test this, expressions of TTF-1 and surfactant protein A (SP-A) were immunohistochemically evaluated in 16 human lung cancer cell lines. In addition, expressions of mRNAs for TTF-1 and SP-A were analyzed by reverse transcriptase-polymerase chain reaction (RT-PCR) and sequencing. As a result, nuclear staining of TTF-1 was observed in two of six adenocarcinoma cell lines, none of seven small cell lung cancer cell lines, and none of three squamous lung cancer cell lines. Among the 16 cell lines, six cell lines (PC3, LC2/Ad, A549, RERF-LC-OK, HI1017, and PC9) expressed significant amounts of mRNA for TTF-1. In contrast, cytoplasmic staining of TTF-1 was observed in five of six adenocarcinoma cell lines, in six of seven small cell lung cancer cell lines, and in all three squamous cell lung cancer cell lines. One of the two adenocarcinoma cell lines those showed positive nuclear staining and cytoplasmic SP-A staining released a significant amount of SP-A in culture supernatant. Our present study demonstrates that the frequency of TTF-1 expression in the nucleus was very low in human lung cancer cell lines; however, their cytoplasmic positivities should be further investigated.
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PMID:Expression of thyroid transcription factor-1 in 16 human lung cancer cell lines. 1249 91

CYP3A5 is the major CYP3A form in the human lung, and it is inducible by dexamethasone in the human A549 lung adenocarcinoma cell line. In the present study, we characterized the nature and mechanism of this induction process. The induction of CYP3A5 mRNA was assessed by quantitative reverse transcriptase-polymerase chain reaction in A549 cells. About 4-fold induction was detected by nanomolar concentrations of dexamethasone and also by budenoside and beclomethasone dipropionate, glucocorticoids used for the inhalation treatment of bronchial asthma, whereas the CYP3A4 inducers mifepristone (RU486), rifampicin, clotrimazole, and nifedipine were without effect. The glucocorticoid induction was blocked by the glucocorticoid receptor (GR) antagonist RU486. In transient transfection assays to A549 cells, CYP3A5 5' regulatory region was activated by the dexamethasone treatment. In contrast, dexamethasone was unable to induce CYP3A5 transcription in GR-deficient COS-1 cells, but the induction could be achieved after GR cotransfection. The CYP3A5 expression was measured in alveolar macrophages from patients with respiratory diseases. The CYP3A5 expression level was decreased by smoking, but glucocorticoid therapy had no statistically significant effect. In conclusion, CYP3A5 is induced in the A549 cells by glucocorticoids through a GR-mediated pathway, whereas smoking may be able to depress CYP3A5 expression.
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PMID:Regulation of CYP3A5 by glucocorticoids and cigarette smoke in human lung-derived cells. 1253 30

Infection with Helicobacter pylori, a Gram-negative, microaerophilic, flagellated bacteria that adheres to human gastric mucosa, is strongly associated with gastric ulcers and adenocarcinoma. The mechanisms through which gastric epithelial cells recognize this organism are unclear. In this study we evaluated the interactions between the Toll-like receptors (TLRs) and H. pylori-mediated NF-kappa B activation and the induction of chemokine mRNA expression. By reverse transcriptase-PCR we determined that MKN45 gastric epithelial cells express low but detectable amounts of TLR2, -4, and -5 but no MD-2. To determine which, if any, TLRs may play a role in the response of epithelial cells to H. pylori, HEK293 cells were cotransfected with the NF-kappa B-Luc reporter, CD14 and MD2 expression plasmids, and expression plasmids for TLR2, TLR4, or TLR5. Infection of the cultures with H. pylori (strain 26695) induced NF-kappa B activity in cells transfected with TLR2 and TLR5, but not TLR4. Consistent with the HEK293 experiments, H. pylori-induced NF-kappa B activation was decreased in MKN45 gastric epithelial cells by transfection of dominant-negative versions of TLR2 and TLR5 but not TLR4. Highly purified lipopolysaccharide from H. pylori strain 26695 activated NF-kappa B in HEK293 via TLR2 but not TLR4. Partially purified flagellin from H. pylori was also capable of inducing NF-kappa B activation in HEK cells transfected with TLR5. Additionally, chemokine gene expression was induced by H. pylori in HEK293 cells following stable transfection with TLR2 or TLR5 expression plasmids. These studies demonstrate that gastric epithelial cells recognize and respond to H. pylori infection at least in part via TLR2 and TLR5. Furthermore, the unique lipopolysaccharide of H. pylori is a TLR2, not a TLR4 agonist.
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PMID:Toll-like receptor (TLR) 2 and TLR5, but not TLR4, are required for Helicobacter pylori-induced NF-kappa B activation and chemokine expression by epithelial cells. 1280 70

Oesophageal and gastric cancers are a significant cause of morbidity and mortality worldwide. Despite improvements in surgical techniques, radiation and chemotherapy, the prognosis of both cancers remains poor. Immunohistochemical and experimental studies indicate that the concept of micrometastasis is applicable to oesophageal and gastric cancer. New staging approaches, including immunohistochemistry and real-time reverse transcriptase-polymerase chain reaction (RT-PCR) of various markers, have been proposed for a more accurate staging of oesophageal and gastric cancer. Preliminary results suggest that real-time RT-PCR of markers for intestinal differentiation, such as guanylyl cyclase C (GC-C), might be useful for both the detection of premalignant conditions, such as intestinal metaplasia and the detection of micrometastasis from adenocarcinoma of the upper intestinal tract. Standard curative treatment options for oesophageal cancer include surgery or chemoradiotherapy. Chemotherapy is an option for the treatment of advanced and recurrent oesophageal cancer. Standard curative treatment for gastro-oesophageal junction and gastric cancer includes surgery and adjuvant chemoradiotherapy. Chemotherapy is an option for the treatment of advanced and recurrent gastric cancer.
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PMID:Pathological staging and therapy of oesophageal and gastric cancer. 1283 35


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