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)

This study aimed to investigate the expression of cellular Fas-associated death domain-like interleukin-1beta-converting enzyme (FLICE)/caspase-8 inhibitory protein (c-FLIP) in endometrial carcinoma and its possible implications. c-FLIP protein was detected in 42 endometrial carcinoma tissues and in 22 normal proliferative endometrial tissues by immunohistochemistry. In addition, c-FLIP messenger ribonucleic acid (mRNA) was evaluated in 20 endometrial carcinomas and in 18 normal proliferative endometria by semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) using SYBR Green I(TM). The relationship between c-FLIP protein level and tumor cell proliferation and that between c-FLIP protein level and clinicopathologic parameters of patients with endometrial carcinoma was analyzed. c-FLIP protein expression was significantly higher in neoplastic tissues than in normal tissues (P < 0.01), and similar result was obtained from RT-PCR analysis of c-FLIP mRNA (P < 0.01). Furthermore, c-FLIP protein was significantly associated with proliferating cell nuclear antigen-labeling index (P < 0.01), clinical stage (P < 0.05), the presence of invasion to > 1/2 myometrium (P < 0.05), and lymph node metastasis (P < 0.01). Multivariate analysis of variance also confirmed the association of c-FLIP with clinical stage (P < 0.05) and with lymph node metastasis (P < 0.05), while its association with myometrial invasion was marginal (P = 0.059). It is concluded that c-FLIP might contribute to the carcinogenesis and aggressiveness of endometrial carcinoma and might be a useful prognostic factor in the tumor.
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PMID:Expression of cellular FLICE/caspase-8 inhibitory protein is associated with malignant potential in endometrial carcinoma. 1601 21

Human mammaglobin (hMAM) has recently been recognized as a breast associated glycoprotein. Although the biological role of hMAM is unknown, it has been previously reported that hMAM gene expression is a marker of low biological and clinical aggressiveness of breast cancer (BC). In this study, 148 cases of BC tissues were investigated for hMAM mRNA expression by reverse transcriptase-polymerase chain reaction (RT-PCR). In order to evaluate its prognostic value, hMAM was correlated with age of patients, type and size of tumor, nodal stage, histologic grade, c-erbB-2 over expression, Ki67 labelling index, estrogen receptor (ER) status and progesterone receptor (PGR) status. Fisher's exact test was used to examine the association between different parameters and hMAM. hMAM was expressed in 138/148 (93%) of BC tissues examined. Among the 10 hMAM negative cases, 8 were invasive ductal carcinomas (microscopically higher G3 grade) and 2 infiltrating lobular carcinomas. We found a significant association (p = 0.020) between absence of hMAM mRNA and G3 histologic grade but not with any other prognostic parameters studied. The present study indicates that lack of hMAM expression is restricted to the BC with G3 grading. Further studies are needed to clarify the biological basis and the clinical significance of our results.
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PMID:Relationship between human mammaglobin mRNA expression in breast cancer tissue and clinico-pathologic features of the tumors. 1676 20

Organ-specific homing of malignant cells involves interactions mediated through cell adhesion molecules and their receptors on the cell surface. Identification of peptides that mimic these receptor-ligand interactions is critical for analyzing the functional role of these proteins and is therapeutically significant to target or block organ-specific homing of tumor cells. Following three cycles of in vivo biopanning using a phage display peptide library injected into mice, we identified 11 unique peptides that were specific for homing to lung, liver, bone marrow, or brain. We developed a bioinformatics strategy to identify putative cell adhesion molecules (CAM) involved in tumor cell migration, invasion, and metastasis based on identified organ-specific peptides. Structural information, including surface exposure and the binding preference of any of these residues in the identified proteins, was examined. These studies resulted in identification of Semaphorin 5A (mouse, Sema5A; human, SEMA5A) and its receptor Plexin B3. The gene expression profile of these proteins in tumors and tumor cell lines was assessed using virtual microarray and serial analysis of gene expression (SAGE) databases and was further confirmed using reverse transcriptase polymerase chain reaction (RT-PCR). Our data demonstrate an association between the expression of SEMA5A and Plexin B3 and the aggressiveness of pancreatic and prostate cancer cells. In summary, using a combined experimental and bioinformatics approach, we have identified functional tumor-specific CAMs, which may be critical for organ-specific metastasis.
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PMID:Identification of functional cell adhesion molecules with a potential role in metastasis by a combination of in vivo phage display and in silico analysis. 1741 95

The aim of this study was to analyze the expression and clinical role of DJ-1, a negative regulator of PTEN (phosphatase and tensin homolog deleted on chromosome 10), in ovarian carcinoma, and investigate the putative association between DJ-1 levels and expression of its transcriptional regulators specificity protein 1 (Sp1) and specificity protein 3 (Sp3). Effusions (n = 72) and solid tumors (n = 57, 42 primary and 15 metastases) were analyzed for DJ-1 messenger RNA (mRNA) expression using reverse transcriptase-polymerase chain reaction. Most specimens (48 effusions, 50 solid tumors) were additionally analyzed for Sp1 and Sp3 mRNA expression. PTEN protein expression was analyzed in 201 effusions and 92 solid tumors using immunohistochemistry. DJ-1 mRNA was expressed in more than 80% of specimens, with no preferential anatomical site. DJ-1 expression was positively associated with Sp1 expression in effusions (P = .03) and with Sp1 (P = .02) and Sp3 (P = .002) expression in solid tumors. In effusions, DJ-1 expression was higher in postchemotherapy compared with prechemotherapy specimens (P = .012). Higher DJ-1 levels (P = .027) and more advanced FIGO stage (IV versus III; P = .003) correlated with shorter progression-free survival in univariate analysis for patients with postchemotherapy effusions. PTEN expression was low in effusions and solid tumors (23% and 13%, respectively), and its expression showed no association with DJ-1 levels or survival. Our data show that DJ-1 is frequently expressed in advanced-stage ovarian carcinoma at all anatomical sites and is coexpressed with its transcriptional regulators Sp1 and Sp3. In contrast, PTEN expression is infrequent in this disease. These findings may provide one of the molecular mechanisms that mediate cancer cell survival and aggressiveness in this tumor.
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PMID:Expression and clinical role of DJ-1, a negative regulator of PTEN, in ovarian carcinoma. 1794 81

To characterize cancer-related gene expression changes in oral squamous cell carcinomas (OSCCs), we compared the gene expression profiles in OSCC-derived cell lines with human normal oral keratinocytes (HNOKs). Microarray analysis identified 166 genes that were up-regulated in OSCC-derived cell lines. Gene ontology analysis showed that cancer-related function had the highest significance. Among the genes mapped to the cancer-related network with the highest significance, the receptor for hyaluronan-mediated motility (RHAMM) was evaluated further for mRNA and protein expression in the OSCC cell lines, primary OSCCs. Overexpression of RHAMM protein was observed in all cell lines compared to HNOKs. Immunohistochemical analysis showed highly expressed RHAMM in primary OSCCs, whereas most corresponding normal tissues had no or significant down-regulation of protein immunoreactivity. Real-time quantitative reverse transcriptase-polymerase chain reaction data agreed with the protein expression. Moreover, the RHAMM expression status was correlated with the TNM stage (P<0.001). The results suggested that RHAMM expression may be correlated with tumor aggressiveness and offer clues to the development of new treatments for human OSCCs.
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PMID:Hyaluronan-mediated motility: a target in oral squamous cell carcinoma. 1842 26

Although it is well established that some protein tyrosine kinases have a prognostic value in breast cancer, the involvement of protein tyrosine phosphatases (PTPs) is poorly substantiated for breast tumors. Three of these enzymes (PTP-gamma, LAR, and PTPL1) are already known to be regulated by estrogens or their antagonists in human breast cancer cells. We used a real-time reverse transcriptase polymerase chain reaction method to test the expression levels of PTP-gamma, LAR and its neuronal isoform, and PTPL1 in a training set of RNA from 59 breast tumors. We sought correlations between levels of these molecular markers, current tumor markers, and survival. We then quantified the expression level of the selected phosphatase in 232 additional samples, resulting in a testing set of 291 breast tumor RNAs from patients with a median follow-up of 6.4 years. The Spearman nonparametric test revealed correlations between PTPL1 expression and differentiation markers. Cox univariate analysis of the overall survival studies demonstrated that PTPL1 is a prognostic factor [risk ratio (RR)=0.45], together with the progesterone receptor (PR) (RR=0.52) and node involvement (RR=1.58). In multivariate analyses, PTPL1 and PR retained their prognostic value (RRs of 0.48 and 0.55, respectively). This study demonstrates for the first time that PTPL1 expression level is an independent prognostic indicator of favorable outcome for patients with breast cancer. In conjunction with our mechanistic studies, this finding identifies PTPL1 as an important regulatory element of human breast tumor aggressiveness and sensitivity to treatments such as antiestrogens and antiaromatase.
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PMID:Expression of the putative tumor suppressor gene PTPN13/PTPL1 is an independent prognostic marker for overall survival in breast cancer. 1900 8

ING5 can interact with p53, thereby inhibiting cell growth and inducing apoptosis. To clarify the roles of ING5 in gastric tumorigenesis and progression, its expression was examined by immunohistochemistry on a tissue microarray containing gastric nonneoplastic mucosa (n = 119), dysplasia (n = 50), and carcinomas (n = 429), with its comparison with clinicopathologic parameters of the carcinomas. ING5 expression was analyzed in gastric carcinoma tissues and cell lines (MKN28, MKN45, AGS, GT-3 TKB, and KATO-III) by Western blot and reverse transcriptase-polymerase chain reaction. ING5 protein was found to distribute to the nuclei of gastric carcinoma cells with similar messenger RNA levels. An increased expression of ING5 messenger RNA was observed in gastric carcinoma in comparison with paired mucosa (P < .05). Lower expression of nuclear ING5 was detected in gastric dysplasia and carcinoma than that in nonneoplastic mucosa (P < .05). Gastric nonneoplastic mucosa and metastatic carcinoma showed more expression of cytoplasmic ING5 than did gastric carcinoma and dysplasia (P < .05). Nuclear ING5 expression was negatively correlated with tumor size, depth of invasion, lymph node metastasis, and clinicopathologic staging (P < .05), whereas cytoplasmic ING5 was positively associated with depth of invasion, venous invasion, lymph node metastasis, and clinicopathologic staging (P < .05). Nuclear ING5 was more expressed in older than younger carcinoma patients (P < .05). There was a higher expression of nuclear ING5 in intestinal-type than diffuse-type carcinoma (P < .05), whereas it was the converse for cytoplasmic ING5 (P < .05). Survival analysis indicated that nuclear ING5 was closely linked to favorable prognosis of carcinoma patients (P < .05), albeit not independent. It was suggested that aberrant ING5 expression may contribute to pathogenesis, growth, and invasion of gastric carcinomas and could be considered as a promising marker to gauge aggressiveness and prognosis of gastric carcinoma.
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PMID:The altered expression of ING5 protein is involved in gastric carcinogenesis and subsequent progression. 2106 63

Inhibitor of growth 5, a tumor suppressor protein, can interact with p53, thereby inhibiting cell growth and inducing apoptosis. Inhibitor of growth 5 overexpression results in a reduction in colony-forming efficiency and cell population in S phase. To clarify the roles of inhibitor of growth 5 in tumorigenesis and progression of colorectal carcinomas, we examined inhibitor of growth 5 expression by immunohistochemistry on a tissue microarray containing colorectal carcinomas (n = 306), adenomas (n = 69), and nonneoplastic mucosa (n = 288) and compared this with clinicopathologic parameters of the carcinomas. In addition, inhibitor of growth 5 expression in colorectal carcinoma tissues and cell lines (DLD-1, HCT-15, SW480, and WiDr) was analyzed by Western blot and reverse transcriptase-polymerase chain reaction. It was found that the inhibitor of growth 5 protein was localized to the nuclei of colon carcinoma cells with no differences at mRNA levels. Among 18 frozen samples of colorectal carcinoma, significantly increased expression of inhibitor of growth 5 protein was observed in the carcinoma in comparison with adjacent mucosa in 14 cases (77.8%; P < .05), and 71.4% (10/14) of carcinoma cases exhibited up-regulated inhibitor of growth 5 mRNA expression. Decreased inhibitor of growth 5 expression was detected by immunohistochemistry in colorectal carcinoma, compared with non-neoplastic mucosa and adenoma (P < .05). Nuclear inhibitor of growth 5 expression was negatively correlated with tumor size, depth of invasion, degree of dedifferentiation, and Union Internationale Contre le Cancer staging (P < .05). In contrast, cytoplasmic inhibitor of growth 5 expression was positively correlated with depth of invasion, lymphatic invasion, and Union Internationale Contre le Cancer staging (P < .05). It was suggested that aberrant inhibitor of growth 5 expression may contribute to pathogenesis, growth, and invasion of colorectal carcinomas and could be considered as a promising marker to gauge aggressiveness of colorectal carcinomas.
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PMID:The nuclear to cytoplasmic shift of ING5 protein during colorectal carcinogenesis with their distinct links to pathologic behaviors of carcinomas. 2119 23

The expression of pyrimidine nucleoside phosphorylase (PyNPase) mRNA in tumor (T) and normal (N) biopsy specimens obtained from 41 cases of colorectal carcinoma was examined by the reverse transcriptase/polymerase chain reaction (RT-PCR). The higher T/N ratio of the expression of PyNPase mRNA correlated significantly with the presence of lymph vessel invasion (p=0.039), the positive lymph node metastasis (p=0.014) and the advanced stage of the disease (p=0.014). There was a significant con-elation between the results determined by enzyme activity and those determined by RT-PCR (p=0.005). The findings suggested that the determination of PyNPase mRNA by RT-PCR may give useful information on tumor aggressiveness of colorectal carcinoma and this method can be used instead of enzyme activity.
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PMID:Clinical significance of pyrimidine nucleoside phosphorylase in colorectal carcinoma. 2153 2

Alpha-1-antitrypsin (alpha 1AT) is present not only in the normal gastrointestine, but in malignant gastrointestinal tissue as well. We studied the expression of alpha 1AT mRNA in 30 cases of esophageal carcinoma using a Northern blot analysis. In addition, we also examined the expression of matrix metalloproteinase 7 (MMP7) mRNA in the latest 15 cases by reverse transcriptase-polymerase chain reaction (RT-PCR) method to clarify the relationship between the alpha 1AT and MMP7. In 25 of the 30, the expression of alpha 1AT mRNA in esophageal carcinomatous tissue (T) was lower than that in the corresponding normal tissue (N) of the esophagus. The T/N ratio of alpha 1AT mRNA expression showed a significant inverse correlation with the depth of tumor invasion, lymph node metastasis and stage of disease (p=0.042, p=0.0001 and p=0.002, respectively). The T/N ratio of alpha 1AT bad a converse correlation with that of MMP7 (p=0.034). The current study thus suggested that i) the lower expression of T/N expression may be a marker for the biological aggressiveness of esophageal carcinoma, and ii) the reduction of alpha 1AT may be partially correlated with the overexpression of MMP7 in tumor tissue.
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PMID:Significance of alpha-1-antitrypsin mRNA expression in esophageal carcinoma. 2154 94


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