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)

By reverse transcriptase-polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemistry, MGSA-alpha, -beta, -gamma, and CXCR2 mRNA expression and proteins are detected in 7 out of 10 human melanoma lesions. The biological consequence of constitutive expression of the MGSA/GRO chemokine in immortalized melanocytes was tested in SCID and nude mouse models. Continuous expression of MGSA/GRO-alpha, -beta, or -gamma in immortalized melan-a mouse melanocytes results in nearly 100% tumor formation for each of the clones tested, whereas clones expressing only the neomycin resistance vector form tumors <10% of the time. Moreover, antibodies to the MGSA/GRO proteins slow or inhibit the formation of tumors in the SCID mouse model and block the angiogenic response to conditioned medium from the tumor-producing clones. Transcription of the MGSA/GRO chemokines is regulated by an enhancesome-like complex comprised of the nuclear factor-kappaB (NF-kappaB), HMG(I)Y, IUR, and Sp1 elements. In Hs294T melanoma cells the half life of the IKB protein is shortened in comparison to normal retinal epithelial cells, facilitating the endogenous nuclear localization of NF-kappaB. We propose that this endogenous nuclear NF-kappaB, working in concert with the 115-kDa IUR-binding factor, promotes constitutive expression of MGSA/GRO genes.
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PMID:Mechanism and biological significance of constitutive expression of MGSA/GRO chemokines in malignant melanoma tumor progression. 936 13

The human melanoma cell line SKmel-23 has been used to investigate the sub-lethal damage that can occur as a result of exposing melanin containing cells to light (532 nm) from a frequency doubled Q-switched (Nd:YAG) laser. A dose response curve was obtained, which indicates that at energy levels of 0.6 J/cm2 and below no effect on either the viability or growth rate of the cell line was observed. Above this, cells rapidly died and at an energy level of 2.0 J/cm2, only approximately 15% of cells survived. This contrasts with the effects on the G361 melanoma line, which contains far less melanosomes, as an LD50 for this cell line was approximately 5.5 J/cm2. Exposing SKmel-23 cells to 0.4 J/cm2 of 532 nm light results in a diminution of the number of melanosomes within cells as well as a marked decrease in melanin content, as determined by spectrophotometric assay and electron microscopy. Using the reverse transcriptase polymerase chain reaction technique, the reduction in melanin content of the cells was accompanied by a selective decrease in mRNA coding for tyrosinase, the first enzyme in the biosynthetic pathway for melanin. No decrease in the mRNA coding for the GAPDH protein was observed. Our finding has implications for understanding the control processes that regulate the melanin content of cells and suggests that the model described can be used to further investigate changes that may occur in cells as a result of their exposure to sub-lethal levels of laser light.
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PMID:Sub-lethal effects of exposing the human melanoma cell line SKmel-23 to 532 nm laser light. 937 46

Monoclonal antibody 57B specifically detects MAGE-3 gene protein expression. MAGE-derived peptides are recognized by CD8+ T cells and applied in immunotherapy. We examined formalin-fixed, paraffin-embedded tissue of 61 melanoma (primary, n = 40; metastatic, n = 21) and 46 control cases (junctional, dermal, compound, Spitz, Reed, and balloon-cell nevi) by immunohistochemistry using the alkaline phosphatase anti-alkaline phosphatase method after antigen retrieval. Immunoreactivity was rated positive at 20 positive cells per tumor or more. Staining pattern was homogeneous, scattered, or focal. All control samples and internal controls were immunonegative. Staining with monoclonal antibody 57B showed a specificity of 100% with a sensitivity of 44%. Immunopositivity (overall, 44% of melanomas) increased along with tumor, node, and metastasis stage; pT1 showed 13%, pT2 22%, pT3a 29%, pT3b 45%, pT4 100%, pTxN1 60%, and pTxNxM1a 63% of samples positive. The staining pattern was homogeneous on pT1 to pT3a tumors, homogeneous or focal in pT3b and pT4a, and homogeneous, focal, or scattered in pTxN1 and pTxNxM1a. The frequency of immunopositivity relates well to data on mRNA expression using reverse transcriptase polymerase chain reaction in a subgroup analyzed by both methods. Monoclonal antibody 57B can be used to allow profiling of melanomas using routine archival tissue, when considering immunotherapeutic approaches involving MAGE-3-derived epitopes.
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PMID:MAGE-3 immunoreactivity in formalin-fixed, paraffin-embedded primary and metastatic melanoma: frequency and distribution. 940 5

Tenascin-C is a modular glycoprotein composed of domains of amino acid repeats. All forms of tenascin-C have eight constant fibronectin type III repeats, but additional fibronectin type III repeats can be spliced into a variable domain found between the fifth and sixth constant repeats. Four extra repeats, named A, B, C and D, have been examined previously. Here, we have used in situ hybridization to determine the tissue origins of the novel AD1 and AD2 repeats. In the embryonic-day-10 chicken embryo, transcripts encoding the AD2 repeat are limited to the tips of lung bronchioles and the base of feather buds. In contrast the AD1 hybridization signal was widespread. Quantitative in situ hybridization reveals AD1-containing transcripts represent up to 85% of the total tenascin-C mRNA in some tissues (developing bone), and are undetectable in others (e.g. radial glia). Avian and human tumor cell lines were examined for the expression of the AD1 repeat using the reverse transcriptase polymerase chain reaction (RT-PCR). Transcripts encoding six different tenascin-C splice variants incorporating the AD1 repeat were found in the fibrosarcoma cell line, QT6. Many human tumor cells, including malignant melanoma and ductal breast carcinoma, were positive for AD1 tenascin-C expression. In addition, we found evidence of AD1 tenascin-C expression in samples of excised human tumors. Our results show that a novel variant may be a major part of the tenascin-C of the embryonic extracellular matrix, and may also be found in the stroma surrounding some human tumors.
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PMID:The expression of tenascin-C with the AD1 variable repeat in embryonic tissues, cell lines and tumors in various vertebrate species. 940 2

The long-term action of azidothymidine, reverse transcriptase inhibitor, on cultivated U-937 (human promyelocyte leukemia) and MeWo (human melanoma) cells led to the concentration-dependent decrease in the length of telomeric chromosomal repeats. Telomere shortening was accompanied by temporary retardation of cell proliferation. Combined with the data obtained previously, these results suggest that azidothymidine inhibits telomerase functioning in cultivated cells.
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PMID:[Azidothymidine, blocking telomerase functioning, shortens telomeric repeats in transformed human cells]. 944 12

We report a case of malignant melanoma associated with human papillomavirus (HPV) in a 37-year-old woman. The patient has had numerous brown papular and nodular tumors, 5 to 30 mm in diameter, on her left leg for > 15 years, some of them coalescing rapidly in the last 12 months to a multilobulated black nodule diagnosed as malignant melanoma by histology and immunohistochemistry. HPV type 16 DNA was detected in the melanoma specimen by reverse transcriptase polymerase chain reaction (rt-PCR) and in situ hybridization (ISH) of the tumor tissues. This is the first report of melanoma associated with HPV 16.
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PMID:Association of human papillomavirus type 16 with malignant melanoma. 950 74

The tenascin-R (TN-R) gene encodes a multidomain extracellular matrix protein belonging to the tenascin family, previously detected only in the central nervous system. In this report, we describe the structure of the 5' region of the human TN-R gene and characterize the activity of its promoter. We cloned two previously unreported nontranslated exons (exons 1 and 2, 539 and 101 bp in length, respectively) separated by a large (> or = 40-kb) intron. The intron between exons 2 and 3 (containing the ATG codon) is 122 kb in length. Tenascin-R transcripts in fetal, adult, and neoplastic human brain contain both exons 1 and 2, as demonstrated by S1 nuclease analysis and reverse transcriptase-polymerase chain reaction. The human TN-R promoter displays relatively unusual features in terms of sequence in that it lacks any TATA box, CAAT box, GC-rich regions, or initiator element. The promoter displays its activity only in cultured cells of neural and glial origin, not in transformed epithelial cells and melanoma cells. All the elements required for the full and cell-specific activity of the promoter are contained in the 57-bp sequence closest to the transcription startpoint.
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PMID:Structure of 5' region of human tenascin-R gene and characterization of its promoter. 953 7

CTLs recognize antigenic peptides bound to MHC class I Ags on the cell surface of tumor cells. Tumor-associated Ag (TAA) peptides are 8 to 10 amino acids long and can be derived from normal, mutated, or viral proteins. The majority of T cell-defined Ags have been identified in human melanoma cells. These were shown to be commonly expressed by different allogeneic melanomas that share the same MHC molecule. We have recently isolated Kb-restricted TAA peptides, which are mutations of the gap junction protein connexin 37, from the spontaneous C57BL/6 Lewis lung carcinoma (3LL). These peptides, named MUT 1 and MUT 2, serve as CTL epitopes and can induce CTL activity in vivo. Using CTL cross-reaction assays, peptide extraction, HPLC fractionation, and reverse transcriptase-PCR amplification, we show that clones of another spontaneous C57BL/6 lung carcinoma, CMT 64, share TAA peptides with the 3LL carcinoma. Vaccination with synthetic MUT 1 or MUT 2 induces CTLs that efficiently lyse CMT 64-derived clones, protects mice from CMT 64 metastasis, and affords therapy of established CMT 64 metastases. Hence, shared CTL epitopes exist between two spontaneous murine lung carcinomas.
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PMID:Identification of shared tumor-associated antigen peptides between two spontaneous lung carcinomas. 955 Apr 1

Hermansky-Pudlak Syndrome (HPS) is a rare, autosomal recessive disorder that is characterized by oculocutaneous albinism, a predisposition to mild bleeding caused by storage-pool deficient platelets, and a ceroid storage disorder. A gene responsible for HPS in Puerto Rico maps to chromosome 10q2 and isolation of the gene has been reported. We have now identified a variant HPS cDNA that contains the same 5' sequence as the published HPS gene and a unique 3' sequence. Analysis of genomic DNA suggests that the two cDNA are derived from alternative transcripts of a single gene; two polyadenylated transcripts were found in normal human melanocytes, human bone marrow cells, human melanoma cells, lymphoblastoid cell lines, and megakaryocytic leukemia cells by reverse transcriptase polymerase chain reaction and northern analysis. The splicing exhibited by this gene is identical to the splicing found to produce two alternative transcripts of the Chediak-Higashi Syndrome gene, another pigment disorder exhibiting platelet storage pool deficiency. These studies show that the HPS gene on chromosome 10 is complex and may have more than one biologically active transcript.
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PMID:Identification of a novel transcript produced by the gene responsible for the Hermansky-Pudlak syndrome in Puerto Rico. 957 45

The gene MTS1 encodes p16INK4, an inhibitor of cyclin-dependent kinase 4, and is frequently deleted, mutated, or silenced by promoter methylation in melanoma cells and in the germline of familial melanoma patients. Although MTS1 may thus be the candidate melanoma suppressor gene that maps to chromosome 9p21, it is not clear how dysfunction at that locus temporally relates to melanoma progression. To further test its role in sporadic melanoma, the expression of p16INK4-protein and -mRNA was characterized in melanomas and melanocytic nevi by immunocytochemistry and in situ reverse transcriptase-polymerase chain reaction. Histologic tissue sections were immunolabeled with anti-p16INK4 antibody for 108 melanocytic lesions, including common and atypical nevi, in situ melanomas, primary invasive melanomas, and metastatic tumors. A subset of the lesions was analyzed for expression of p16INK4-mRNA, employing forward and reverse intron-bridging primers for reverse transcriptase-polymerase chain reaction amplification of the transcript corresponding to exons 1 and 2 of MTS1. Strong immunolabeling was detected in the melanocytes of common nevi and of nevi with architectural disorder and cytologic atypia. By digital image analysis, in contrast, labeling intensity decreased significantly and progressively in the melanocytes of in situ, invasive, and metastatic melanomas. Results from the in situ reverse transcriptase-polymerase chain reaction analysis were confirmatory, showing a strong signal in the melanocytic nevi but progressive signal attenuation with increasing stage of melanoma. These data indicate correlation between gradual loss of expression of the MTS1 locus and progression of melanoma, further supporting an emerging role for the gene in the malignant transformation of melanocytes. The failure to demonstrate reduced expression in nevi suggests either that these lesions are not an early stage in melanoma development, in contrast to prevailing assumptions, or that loss of p16INK4 function is not an initiating event in melanocyte transformation.
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PMID:Expression of the tumor suppressor gene product p16INK4 in benign and malignant melanocytic lesions. 962 Mar 1


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