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 purpose of this article is to review the available means to investigate whether an elevated serum prostate-specific antigen (PSA) after radical prostatectomy may be explained by the presence of residual benign tissue. To answer this question, one may consider the following features: the kinetics of recurrent/ persistent PSA, the incidence of rising PSA in the presence of capsular incisions exposing benign glands only, the level of urinary PSA and the ratio of free/total PSA in the urine, the results of anastomotic biopsy samples, and the detection of circulating prostate cells by PSA reverse transcriptase-polymerase chain reaction (RT-PCR) after surgery. Capsular incisions exposing benign tissue are not associated with a significant risk of biochemical failure. In case of an organ-confined cancer with negative surgical margins but a rising postoperative PSA, the systematic reevaluation of the initial pathological slides constantly shows capsular effraction or focal positive margins that have been overlooked at the first evaluation. Even when anastomotic biopsies document only benign tissue, the study of PSA doubling time is usually characteristic of the coexistence of residual tumoral cells. However, in a few cases, the persistent negative results of the detection of circulating prostate cells by PSA, RT-PCR in patients with organ-confined cancer and negative margins but elevated postoperative PSA might be explained by the presence of residual benign prostatic hyperplasia tissue. Most of the data in the literature are in favor of the responsibility of persistent/recurrent cancer in the recurring PSA rather than that of benign prostatic hyperplasia/normal residual tissue. Therefore, a persistent/recurrent detectable level of PSA is the serum after radical prostatectomy characterizes biochemical failure.
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PMID:The significance of recurrent PSA after radical prostatectomy: benign versus malignant sources. 1046 14

The elevation of circulating hepatocyte growth factor (HGF) concentrations is associated with tumor progression and prognosis in cancer patients. We aimed to clarify whether peripheral blood mononuclear cells (PBMC) of cancer patients can produce circulating HGF. In sera and PBMC supematants of 39 cancer patients and 55 control subjects, we measured HGF concentrations by enzyme-linked immunosorbent assay and analyzed HGF expression in PBMC by reverse transcriptase-polymerase chain reaction and Western blotting. Compared with primary cancer patients and control subjects, recurrent cancer patients showed higher serum HGF concentrations (p < 0.05, p < 0.01 respectively), higher HGF concentrations in PBMC supernatants (p < 0.01 for both) and more frequent HGF mRNA expression in PBMC. Additionally, HGF mRNA was induced in PBMC of a control subject cultured with the sera of recurrent cancer patients. These results indicate that PBMC of recurrent cancer patients can produce HGF and that their sera may contain substances that induce HGF mRNA expression.
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PMID:Hepatocyte growth factor production by peripheral blood mononuclear cells of recurrent cancer patients. 1150 46

A key hallmark of cancer, unlimited replication, requires cancer cells to evade both replicative senescence and potentially lethal chromosomal instability induced by telomere dysfunction. The majority of cancers overcome these critical barriers by upregulating telomerase, a telomere-specific reverse transcriptase. However, a subset of cancers maintains telomere lengths by the telomerase-independent Alternative Lengthening of Telomeres (ALT) pathway. The presence of ALT is strongly associated with recurrent cancer-specific somatic inactivating mutations in the ATRX-DAXX chromatin-remodeling complex. Here, we generate an ALT-positive adenocarcinoma cell line following functional inactivation of ATRX and telomerase in a telomerase-positive adenocarcinoma cell line. Inactivating mutations in ATRX were introduced using CRISPR-cas9 nickase into two prostate cancer cell lines, LAPC-4 (derived from a lymph node metastasis) and CWR22Rv1 (sourced from a xenograft established from a primary prostate cancer). In LAPC-4, but not CWR22Rv1, abolishing ATRX was sufficient to induce multiple ALT-associated hallmarks, including the presence of ALT-associated promyelocytic leukemia bodies (APB), extrachromosomal telomere C-circles, and dramatic telomere length heterogeneity. However, telomerase activity was still present in these ATRX^KO cells. Telomerase activity was subsequently crippled in these LAPC-4 ATRX^KO cells by introducing mutations in the TERC locus, the essential RNA component of telomerase. These LAPC-4 ATRX^KO TERC^mut cells continued to proliferate long-term and retained ALT-associated hallmarks, thereby demonstrating their reliance on the ALT mechanism for telomere maintenance. IMPLICATIONS: These prostate cancer cell line models provide a unique system to explore the distinct molecular alterations that occur upon induction of ALT, and may be useful tools to screen for ALT-specific therapies.
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PMID:Functional Loss of ATRX and TERC Activates Alternative Lengthening of Telomeres (ALT) in LAPC4 Prostate Cancer Cells. 3161 8

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