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 expression levels of the Wilms' tumor gene WT1 were examined in 56 cases of head and neck squamous cell carcinoma (HNSCC) using quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR). They included 4 cases of floor of mouth, 9 of gingiva, 25 of tongue, 10 of oropharynx, 3 of hypopharynx, and 5 larynx squamous cell carcinoma (SCC). All (100%) of 4 cases of floor of mouth, 5 (56%) of 9 gingiva, 17 (68%) of 25 tongue, 8 (80%) of 10 oropharynx, all (100%) of 3 hypopharynx, and all (100%) of 5 larynx SCC overexpressed the WT1 gene in the range of 3.07 x 10(-4)-8.60 x 10(-1) levels (the WT1 expression level in K562 leukemic cells was defined as 1.0). Thus, 42 (75%) out of 56 cases of HNSCC overexpressed the WT1 gene. The high expression level of the WT1 gene significantly correlated with poor histological tumor differentiation and high tumor stage of HNSCC. Immunohistochemical analysis confirmed the expression of WT1 protein in 6 cases (one floor of mouth, 2 tongue, 2 oropharynx, and one larynx SCC) with overexpression of the WT1 gene. The direct sequencing analysis of the WT1 genomic DNA showed no mutations in any of 10 exons of the WT1 gene in 5 different HNSCC. These findings suggest an important role of the wild-type WT1 gene in the tumorigenesis of HNSCC.
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PMID:Overexpression of the Wilms' tumor gene WT1 in head and neck squamous cell carcinoma. 1282 78

The expression levels of the Wilms' tumor gene WT1 were examined in 34 primary thyroid cancers (24 papillary, 5 follicular, 1 anaplastic, and 4 medullary carcinomas), 17 thyroid follicular adenomas, and 6 normal-appearing thyroid tissues using quantitative real-time reverse transcriptase-polymerase chain reaction (RT-PCR). In 33 of 34 thyroid cancers, the WT1 mRNA was expressed at levels ranging from 5.0 x 10 (-5) to 8.3 x 10 (-2) levels (WT1 expression level in K562 leukemic cells was defined as 1.0). The WT1 mRNA expression levels were significantly higher than those in either thyroid follicular adenomas (P < 0.001) or normal-appearing thyroid tissues (P < 0.01). Immunohistochemical analysis confirmed the expression of WT1 protein in 20 of 21 thyroid cancers with WT1 mRNA expression. WT1 protein was also detected in 6 of 7 follicular adenomas with WT1 mRNA expression. However, the intensity of staining of WT1 protein in adenoma cells was weaker than that in cancer cells and its expression was restricted to approximately 30-80% of adenoma cells in the tumors examined. The direct sequencing analysis of the WT1 genomic DNA showed no mutations in any of the 10 exons of the WT1 gene in all of the 9 different thyroid cancers. These findings indicate an important role of the wild-type WT1 gene in the tumorigenesis of primary thyroid cancer.
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PMID:Overexpression of the Wilms' tumor gene WT1 in primary thyroid cancer. 1284 69

In the last few years molecular genetic studies of childhood cancer have acquired great importance. Advances in these techniques have increased knowledge of the various genes involved in tumoral development. Genetic alterations can occur in three large groups of genes: oncogenes, tumor suppressor genes, and DNA repair genes. Cytogenetic analyses (karyotyping) are complemented by various molecular techniques, such as fluorescence in situ hybridization (FISH), reverse transcriptase-polymerase chain reaction (RT-PCR) and spectral karyotyping (SKY). These are the most reliable techniques and improve the sensitivity of karyotyping. The present article reviews the most representative and best characterized genes involved in the molecular etiology of childhood cancer, both hematologic malignancies (leukemia and lymphoma) and solid tumors (brain tumors, neuroblastoma, Wilms' tumor, hepatoblastoma, rhabdomyosarcoma, Ewing's sarcoma and retinoblastoma). Molecular techniques have enabled more precise diagnosis as well as identification of new prognostic factors and the development of more effective treatments. These techniques can also be useful in identifying minimal residual disease during and after treatment for leukemias, neuroblastomas and sarcomas, with the aim of predicting recurrence.
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PMID:[The role of molecular genetics in childhood cancer]. 1451 4

We previously showed that Wilms tumor gene (WT1) expression level, measured by quantitative reverse transcriptase polymerase chain reaction (RT-PCR), was useful as an indicator of minimal residual disease (MRD) in leukemia and myelodysplastic syndrome. However, in conventional quantitative RT-PCR (CQ-PCR), RT-PCR must be performed for various numbers of cycles depending on WT1 expression level. In the present study, we developed a new real-time quantitative RT-PCR (RQ-PCR) method for quantitating WT1 transcripts. Results of intraassay and interassay variability tests demonstrated that the real-time WT1 assay had high reproducibility. WT1 expression levels measured by the RQ- and the CQ-PCR methods were strongly correlated (r = 0.998). Furthermore, a strong correlation was observed among WT1 transcript values normalized with 3 different control genes (beta-actin, ABL, and glyceraldehyde-3-phosphate dehydrogenase) and between relative WT1 transcript values with WT1 expression in K562 cells as the reference and absolute WT1 transcript copy numbers per microgram RNA. When WT1 expression and minor bcr-abl expression were concurrently monitored in 2 patients with bcr-abl-positive acute lymphoblastic leukemia, both MRDs changed mostly in parallel, indicating the reliability and validity of our RQ-PCR method. In conclusion, this RQ-PCR method is convenient and reliable for monitoring MRD and enables routine clinical use of a WT1 assay.
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PMID:Monitoring minimal residual disease in leukemia using real-time quantitative polymerase chain reaction for Wilms tumor gene (WT1). 1468 94

Wilms' tumor gene WT1 mRNA is a new marker of leukemic blast cells for AML, ALL, and CML. The minimal residual disease(MRD) of leukemia can be detected at frequencies as low as 1 in 10(3) to 10(4) normal bone marrow cells and 1 in 10(5) normal peripheral blood mononuclear cells by means of the quantitation of WT1 mRNA (WT1 assay) using reverse transcriptase-polymerase chain reaction. Thus, the WT1 assay makes it possible to rapidly assess the effectiveness of treatment and to evaluate the degree of eradication of leukemic cells in individual leukemia patients. Furthermore, the WT1 assay can continuously assess the disease progression of myelodysplastic syndrome(MDS) and predict the evolution of MDS to overt AML within 6 months. Moreover, WT1 protein is highly immunogenic, thus, WT1 peptide-based cancer immunotherapy is effective.
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PMID:[Development of a new inspection diagnostic method: genetic screening of cancer]. 1520 29

The WT1 gene is highly expressed in various types of leukemia, particularly in acute type leukemia. The extent of minimal residual disease (MRD) of leukemia can be evaluated by measuring the WT1 gene expression level using a quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) method. The WT1 transcript assay can be applied to almost all patients with leukemia regardless of the presence or absence of chimeric DNA markers. Furthermore, because of the fact that WT1 expression levels increase significantly at relapse compared with those at the time of diagnosis, and because of the decrease in background levels of WT1 expression in bone marrow following allogeneic SCT, the WT1 transcript assay possesses a high degree of sensitivity following allogeneic SCT. Frequent monitoring of the WT1 gene expression level predicts the risk of relapse following allogeneic SCT, and furthermore, the kinetics of WT1 transcripts predict the efficacy of immunomodulation therapy such as donor leukocyte infusion.
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PMID:WT1 gene transcript assay for relapse in acute leukemia after transplantation. 1522 32

Telomerase activity is essential for maintaining the termini of linear chromosomes. Telomerase consists of both a RNA and a specialized reverse transcriptase. Our objective for this study was to determine the molecular and cytogenetic features of the chicken telomerase reverse transcriptase (chTERT) gene and protein. The TERT mRNA from gastrula stage embryos was found to be 4497 bp in length, translating into a protein of 1346 amino acids (aa). The chTERT protein shares 45% aa identity with human TERT (hTERT). A distinctive feature of chTERT, as compared to human and other vertebrate TERTs, is the larger size of the protein due mainly to a considerably longer N-terminal flexible linker region (144 aa longer than in human). Chicken TERT was mapped to chromosome 2q21 near an interstitial telomere site. Several transcription factor binding motifs in the 5' flanking/promoter region of chTERT were similar to those found associated with hTERT (E-box, Ik1, MAZ, Sp1 sites), whereas several c-Myb sites were found associated with chTERT only and c-Ets-2 and WT1 were associated with hTERT only. Results presented here should promote structure-function studies of chTERT, as well as contribute to the comparative analysis of TERT regulation and function in vertebrates utilizing the telomere clock mechanism to different degrees.
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PMID:The chicken telomerase reverse transcriptase (chTERT): molecular and cytogenetic characterization with a comparative analysis. 1536 46

A 7-year-old girl was hospitalized because of a tumorous mass in her left periorbital region. The tumor was removed by local excision. The soft-part tumor recurred in the parotid gland region 4 months later, and a second recurrence was noted on the left side of the neck 3 years and 3 months thereafter. The patient had not received chemotherapy or local irradiation. Histological and immunohistochemical examinations of the recurrent masses revealed morphological characteristics of small cell proliferation with desmoplastic stroma that were similar to those of the initial tumor. The cellular components showed immunoreactivity for desmin, cytokeratin, vimentin, and epithelial membrane antigen in part, but the cells were negative for myogenin, CD99, and neuron-specific enolase. These findings suggested a diagnosis of desmoplastic small cell tumor, despite its extra-abdominal location. The histological diagnosis was confirmed by reverse transcriptase polymerase chain reaction, which demonstrated an EWS-WT1 chimeric fusion gene. An in-frame fusion of EWS exon 9 and WT1 exon 8 was subsequently identified by cloning and sequencing. The chimeric fusion gene might be related to the tissue-specific phenotype of desmoplastic small cell tumors, although further investigation of this speculation is necessary.
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PMID:Desmoplastic small cell tumor of soft tissue: molecular variant of EWS-WT1 chimeric fusion. 1693 Mar 35

Ewing sarcoma/peripheral primitive neuroectodermal tumor (pPNET) is a rare primary tumor of the kidney with morphologic features similar to those of other primitive tumors. Previous studies have shown that these tumors frequently stain positively with immunostains against CD99 and FLI-1 and negatively with stains against WT-1, suggesting that these markers may be used for the distinction between Wilms tumor and pPNET. We present 30 cases of primary malignant neuroepithelial tumor with immunohistochemical profiles and reverse transcriptase polymerase chain reaction (RT-PCR) analysis and show that immunophenotypic overlap exists between Wilms tumor and pPNET. A subset of 30 neuroepithelial tumors from the National Wilms Tumor Study originally categorized as putative pPNETs of the kidney was stained with FLI-1, WT-1, and thyroid transcription factor-1. Bicolor fluorescence in situ hybridization studies were performed on 19 of the cases. Other data on these tumors were available from a previous study (Am J Surg Pathol 2001;25:133). Of 7 primary tumors that had the EWS/FLI-1 fusion transcript by RT-PCR, 6 exhibited strong immunopositivity for FLI-1. Nine that were negative by RT-PCR stained positively with the FLI-1 stain. Five fusion-negative cases stained with both FLI-1 and WT-1. Three fusion-negative cases were negative for FLI-1 but positive for WT-1. Five fusion-negative cases were negative for both FLI-1 and WT-1. Of the 30 cases, 29 were positive for CD99. Seven cases that were negative for the EWS-FLI-1 fusion by RT-PCR were positive by fluorescence in situ hybridization. All cases were negative for thyroid transcription factor-1. Reliance upon immunohistochemistry as the sole means of ancillary diagnosis in renal pPNET can lead to confusing results. We recommend molecular fusion studies for clarification of primitive renal tumors with unexpected immunophenotypic results.
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PMID:Immunohistochemistry of primary malignant neuroepithelial tumors of the kidney: a potential source of confusion? A study of 30 cases from the National Wilms Tumor Study Pathology Center. 1713 38

The Wilms' tumor suppressor gene (WT1) encodes a zinc finger transcription factor that is vital during development of several organs including metanephric kidneys. Despite the critical regulatory role of WT1, the pathways and mechanisms by which WT1 orchestrates development remain elusive. To identify WT1 target genes, we performed a genome-wide expression profiling analysis in cells expressing inducible WT1. We identified a number of direct WT1 target genes, including the epidermal growth factor (EGF)-family ligands epiregulin and HB-EGF, the chemokine CX3CL1, and the transcription factors SLUG and JUNB. The target genes were validated using quantitative reverse transcriptase-polymerase chain reaction, small interfering RNA knockdowns, chromatin immunoprecipitation, and luciferase reporter analyses. Immunohistochemistry of fetal kidneys confirmed that a number of the WT1 target genes had overlapping expression patterns with the highly restricted spatiotemporal expression of WT1. Finally, using an in vitro embryonic kidney culture assay, we found that the addition of recombinant epiregulin, amphiregulin, CX3CL1, and interleukin-11 significantly enhanced ureteric bud branching morphogenesis. Our genome-wide screen implicates WT1 in the transcriptional regulation of the EGF-family of growth factors as well as the CX3CL1 chemokine during nephrogenesis.
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PMID:Identification of novel Wilms' tumor suppressor gene target genes implicated in kidney development. 1743 Aug 90


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