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)

We examined the expression of alpha 1, alpha 2, alpha 3, alpha 4, alpha 5 and beta 1 integrin on 36 transitional cell cancers (TCCs) in the bladder by immunohistochemistry. Only alpha 2, alpha 3 and beta 1 were detected on normal transitional cell epithelium, but four TCCs (12.5%) revealed positive staining for alpha 1, seven (19.4%) for alpha 4 and seven (20%) for alpha 5. These altered expressions of integrin alpha chain were more frequent in histologically higher stage or grade of TCC, and a correlation was found between increased alpha 5 expression and histological stage. alpha 5 was positive in 6 (35.3%) of 17 invasive TCCs whereas only 1 (5.9%) of 17 superficial TCCs. Flow cytometric analysis on bladder cancer cell lines showed that T24 and HT1376, which are undifferentiated TCC cell lines, highly expressed alpha 5 and beta 1. Also, SCaBER, which is derived from urinary bladder squamous cell cancer and which is recognised as the most malignant phenotype after metaplasia of transitional epithelium, had alpha 5 and beta 1. However, RT4, which is derived from transitional cell papilloma, showed no expression of alpha 5. Furthermore, reverse transcriptase-polymerase chain reaction (RT-PCR) showed the presence of mRNA of alpha 5 on T24, SCaBER and HT1376, but not on RT4. Taken together, it seems that the presence of alpha 5 integrin might be a more malignant phenotype in transitional cell carcinoma.
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PMID:Correlation between integrin alpha 5 expression and the malignant phenotype of transitional cell carcinoma. 856 38

The CD44 cell adhesion molecule is a surface glycoprotein mainly expressed in lymphoid tissues. Recently, abnormal variants of CD44 including alternatively-spliced large molecular variants, have been reported in many neoplastic tissues. We studied the variation in the size of CD44 molecules in 25 transitional cell carcinomas and 11 normal transitional epithelial tissues, using the reverse transcriptase-polymerase chain reaction (RT-PCR) followed by electrophoresis and Southern blot hybridization. Whereas 23 of 25 (92.0%) tumor tissues expressed CD44 splice variants with large molecular size, only 1 of 11 (9.1%) normal tissues expressed the abnormal variants. Urine sediments from 5 of 7 (71.4%) patients also was positive for the CD44 splice variants. CD44 splice variants are increased markedly in human transitional cell carcinoma. In conclusion, detection of CD44 splice variants using the RT-PCR, which is a convenient molecular biological technique, may be useful in combination with other diagnostic methods such as cytology, flow cytometry, and tumor antigens.
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PMID:Expression of CD44 splice variants in human transitional cell carcinoma. 874 26

Alterations in the p53 gene are a predominant component in the development of transitional cell carcinoma (TCC), but the particular pathways distal to p53 alterations which contribute to urothelial transformation are not defined. Here, the p21WAF1/CIP1 gene, a p53 inducible and p53 independent gene product, was studied in TCC. p21WAF1/CIP1 expression was measured by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) from five cell lines and 28 tumor specimens (14 superficial, 14 muscle invasive). This was expressed as a ratio of the gene product to L7, a ribosomal housekeeping gene. In addition, exons 4 through 8 of the p53 gene as well as exon 2 of the p21WAF1/CIP1 gene were assayed for mutations by polymerase chain reaction/single stranded conformation polymorphism analysis (PCR/SSCP). Candidate mutations were verified by sequencing. p21WAF1/CIP1/L7 expression was significantly decreased in invasive lesions compared to superficial lesions (P<0.002). p53 mutations were detected by PCR/SSCP in seven tumors [25%] (one superficial, six invasive) and p21WAF1/CIP1/L7 expression was significantly decreased in all tumors that had p53 mutations (P<0.007). PCR/SSCP analysis of exon 2 in p21WAF1/CIP1 detected band shifts in four/28 tumor specimens (two superficial, two invasive), which sequencing and comparison to autologous normal matched DNA revealed as novel mutations.
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PMID:Novel p21WAF1/CIP1 mutations in superficial and invasive transitional cell carcinomas. 893 28

Differential display in combination with arbitrarily primed polymerase chain reaction (PCR) fingerprinting has become one of the most powerful techniques to identify and isolate mRNAs that are differentially expressed in pairs of biological samples. However, in many cases the cDNA band corresponding to the differentially amplified product contains several cDNA species that comigrate with the cDNA of interest due to the poor resolution of the fingerprinting gels, thus hampering further analysis and identification of the desirable cDNA. To improve the electrophoretic resolution of differentially amplified cDNAs, we have utilized Resolver Gold agarose gel electrophoresis (Ingenius) as an additional step to overcome downstream problems encountered during RNA fingerprinting experiments. To illustrate the power of the modified differential display procedure we present a detailed analysis of the cDNA products differentially displayed in tumor biopsies obtained from a noninvasive (grade II, Ta) and an invasive (grade III, T2-T4) human bladder transitional cell carcinoma (TCC). Several genes that were differentially expressed in this tumor pair were identified. These included: tropomyosin 4, the protein disulfide isomerase precursor (PDI), MRP14, signal transducer CD24, keratins 8 and 13, cytochrome oxidase subunit IV (COXIV), putative transcription factor HOX-1.3, as well as two novel genes of yet unknown function. All of the identified cDNAs were shown to be truly differentially expressed by Northern blotting, reverse transcriptase-PCR (RT-PCR), and two-dimensional polyacrylamide gel electrophoresis (2-D PAGE) analysis of the corresponding lesions.
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PMID:Identification of true differentially expressed mRNAs in a pair of human bladder transitional cell carcinomas using an improved differential display procedure. 1019 29

We investigated the expression of platelet-derived endothelial cell growth factor/thymidine phosphorylase (PD-ECGF/TP) in primary bladder cancer, its association with clinicopathologic findings, and their prognostic value. mRNA was extracted from 20 bladder cancer specimens and 6 normal bladder mucosal tissues. Relative amounts of PD-ECGF/TP mRNA were evaluated by reverse transcriptase-polymerase chain reaction (RT-PCR) and compared with the level of glyceraldehyde-3-phosphate dehydrogenase mRNA (used as an internal standard). PD-ECGF/TP expression was examined by immunohistochemistry in 85 patients who underwent cystectomy for bladder cancer. Serum PD-ECGF/TP levels were measured in 23 patients using a sandwich-type enzyme-linked immunosorbent assay. By RT-PCR analysis, expression of PD-ECGF/TP was found to be 7-fold higher in invasive tumors than in superficial tumors (P<0.01) and 9-fold higher than in normal bladder (P<0.01). Out of 85 transitional cell carcinoma tissue samples, 69 (81%) were evaluated as PD-ECGF/TP-positive by immunohistochemical staining. PD-ECGF/TP expression correlated significantly with tumor grade (P = 0.001), depth of invasion (P = 0.012), and lymphatic invasion (P = 0.01). No correlation was found between expression of PD-ECGF/TP and the number of tumors, tumor configuration, lymph node involvement, venous invasion, c-erbB-2 expression, or overall survival. We could not detect a significant serum level of PD-ECGF/TP in any patient. The results suggest that PD-ECGF/TP might give valuable information for bladder cancer management, though it may not be a good new tumor marker for bladder cancer.
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PMID:Expression of platelet-derived endothelial cell growth factor/thymidine phosphorylase in human bladder cancer. 1066 52

Cytogenetic and loss of heterozygosity (LOH) studies demonstrated chromosome 3p deletions in transitional cell carcinoma (TCC). We recently cloned the tumor suppressor gene FHIT (fragile histidine triad) at 3p14.2, one of the most frequently deleted chromosomal regions in TCC of the bladder, and showed that it is the target of environmental carcinogens. Abnormalities at the FHIT locus have been found in tumors of the lung, breast, cervix, head and neck, stomach, pancreas, and clear cell carcinoma of the kidney. We examined six TCC derived cell lines (SW780, T24, Hs228T, CRL7930, CRL7833, and HTB9) and 30 primary TCC of the bladder for the integrity of the FHIT transcript, using reverse transcriptase-polymerase chain reaction (RT-PCR) to investigate a potential role of the FHIT gene in TCC of the bladder. In addition, we tested expression of the Fhit protein in the six TCC-derived cell lines by Western blot analysis and in 85 specimens of primary TCCs by immunohistochemistry. Three of the six cell lines (50%) did not show the wild-type FHIT transcript, and Fhit protein was not detected in four of the six cell lines (67%) tested. Fhit expression also was correlated with pathological and clinical status. A significant correlation was observed between reduced Fhit expression and advanced stage of the tumors. Overall, 26 of 30 (87%) primary TCCs showed abnormal transcripts. Fhit protein was absent or greatly reduced in 61% of the TCCs analyzed by immunohistochemistry. These results suggested that loss of Fhit expression may be as important in the development of bladder cancer as it is for other neoplasms caused by environmental carcinogens.
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PMID:Loss of FHIT expression in transitional cell carcinoma of the urinary bladder. 1066 70

We recently found a urinary molecular marker, Hepatoma-Up-Regulated Protein (HURP), for the detection of urinary bladder transitional cell carcinoma (TCC). In this study, the expression of HURP in 57 voided urine specimens was determined by semi-quantitative reverse transcriptase-polymerase chain reaction. HURP value was correlated with a variety of clinical parameters, including sex, age, tumor grade, stage, multiplicity, tumor shape and recurrence/metastasis during the follow-up period. The detection rate of HURP was 60.7% (17 out of 28) in voided urine of patients with TCC, 5.9% (1 out of 17) in non-TCC urological benign disease and 0% (0 out of 12) in healthy volunteers. HURP positivity (defined as above 0.1 cut-off value) was detected in 83.6% (92 out of 110) TCC specimens, 4.3% (1 out of 23) of non-TCC urinary cancer and 0% (0 out of 15) of benign urological disease. No relationship was found between the level of HURP and the above-mentioned clinical parameters other than recurrence of TCC patients. A higher level of tissue HURP was found in the patients having recurrence (Mann-Whitney U-test, p = 0.027).
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PMID:Prognostic significance of hepatoma-up-regulated protein expression in patients with urinary bladder transitional cell carcinoma. 1289 66

Prostate carcinoma and transitional cell carcinoma (TCC) occur in the prostate gland of older dogs and have morphologic similarities when evaluated by light microscopy. The dog is a commonly used animal model for studying human prostate carcinoma; therefore, it is important to accurately differentiate canine prostate carcinomas from TCCs. We investigated whether keratin 7 (K7) and arginine esterase (AE) would aid differentiation of canine prostate carcinoma from TCC. K7 expression was evaluated in normal and neoplastic canine prostate and bladder tissues using immunohistochemistry. The expression of AE messenger ribonucleic acid (mRNA) in normal and neoplastic canine prostate and bladder was detected using northern blots and reverse transcriptase-polymerase chain reaction (RT-PCR). In addition, AE enzyme activity was measured in normal and neoplastic canine prostate and bladder tissues. We found marked similarities in K7 expression in prostate carcinomas and TCCs. AE mRNA was present in high levels in normal prostatic tissue but was reduced in prostate carcinoma by northern blot assay. Nested RT-PCR detected AE mRNA both in TCCs (13 of 15) and in prostate carcinomas (13 of 13). Enzymatic activity of AE was high in normal prostate gland and in some prostate carcinomas, whereas normal bladder and TCCs produced lower levels of AE. In conclusion, K7 and AE cannot be used to differentiate TCC from prostate carcinoma in dogs.
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PMID:Canine prostate carcinomas express markers of urothelial and prostatic differentiation. 1501 26

Angiogenesis or the development of new blood vessels from the surrounding vasculature is essential for the growth and progression of solid tumors. Vascular endothelial growth factor (VEGF), a positive regulator of angiogenesis, plays a pivotal role in tumor angiogenesis and shows a high expression in almost all known tumors, including transitional cell carcinoma (TCC) of the bladder. A novel isoform, VEGF(165)b containing a novel exon 9, was recently identified in renal cell carcinoma and was shown to be down-regulated and inhibitory in nature. We aimed to analyze quantitatively expression of this isoform, VEGF(165)b, in TCC of the bladder and compare it to the benign part of the same organ. A real-time reverse transcriptase polymerase chain reaction protocol was set up to quantitate simultaneously the messenger ribonucleic acid levels of VEGF and VEGF(165)b from 34 clinical samples representing bladder cancer and matched benign tissue. Expression of VEGF(165)b showed a >or=3.0-fold change in 27 of 34 (79%) bladder tumors than the benign samples. Increased expression of VEGF(165)b was seen in superficial tumors as compared to invasive tumors, which was statistically significant (P < 0.001). Therefore, VEGF(165)b was up-regulated in TCC of the bladder.
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PMID:Differential expression of vascular endothelial growth factor165b in transitional cell carcinoma of the bladder. 1762 98

Inorganic arsenic increases urinary bladder transitional cell carcinoma in humans. In F344 rats, dimethylarsinic acid (DMA[V]) increases transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in transitional epithelium occur, it may contribute to carcinogenesis or cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the transitional epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase beta (Polbeta), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibility remains that DMA(V) may lower damage-induced increases in repair gene expression or cause post-translational modification of repair enzymes.
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PMID:Dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of DNA repair genes of bladder transitional epithelium in F344 rats. 1938 86


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