Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0684249 (lung carcinoma)
 23,830 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the expression of the genes encoding the A and B chains of platelet-derived growth factor (PDGF) in a number of human leukemia cell lines. Steady-state expression of the A-chain RNA was seen only in the promonocytic leukemia cell line U937 and in the T-cell leukemia cell line MOLT-4. It has previously been reported that both PDGF A and PDGF B genes are induced during megakaryoblastic differentiation of the K562 erythroleukemia cells and transiently during monocytic differentiation of the promyelocytic leukemia cell line HL-60 and U937 cells. In this study we show that PDGF A RNA expression was induced in HL-60 and Jurkat T-cell leukemia cells and increased in U937 and MOLT-4 cells after a 1- to 2-h stimulation with an 8 pM concentration of transforming growth factor beta (TGF-beta). PDGF A RNA remained at a constant, elevated level for at least 24 h in U937 cells, but returned to undetectable levels within 12 h in HL-60 cells. No PDGF A expression was induced by TGF-beta in K562 cells or in lung carcinoma cells (A549). Interestingly, essentially no PDGF B-chain (c-sis proto-oncogene) RNA was expressed simultaneously with PDGF A. In the presence of TGF-beta and protein synthesis inhibitors, PDGF A RNA was superinduced at least 20-fold in the U937 and HL-60 cells. PDGF A expression was accompanied by secretion of immunoprecipitable PDGF to the culture medium of HL-60 and U937 cells. The phorbol ester tumor promoter tetradecanoyl phorbol acetate also increased PDGF A expression with similar kinetics, but with a mechanism distinct from that of TGF-beta. These results suggest a role for TGF-beta in the differential regulation of expression of the PDGF genes.
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PMID:Regulation of platelet-derived growth factor gene expression by transforming growth factor beta and phorbol ester in human leukemia cell lines. 347 82

Platelet-derived growth factor (PDGF) is synthesized and secreted by mesenchymal cells. We used immunohistochemistry and in situ hybridization to determine whether immunoreactivity for PDGF and PDGF receptor (PDGF-R) might be a prognostic indicator in lung carcinoma. We compared these results with those of immunohistochemistry for anti-proliferating cell nuclear antigen (anti-PCNA). Indirect immunohistochemistry and in situ hybridization were performed for PDGF B-chain, PDGF-R beta and PCNA antibodies, and PDGF B mRNA on frozen, paraffin-embedded sections of 92 surgically resected lung carcinomas (39 squamous cell carcinomas, 47 adenocarcinomas, 2 large-cell carcinomas, 2 adenosquamous carcinomas, and 2 double carcinomas). Clinicopathologic data (sex, age, stage, survival period, histologic type, and degree of cell differentiation) were evaluated using a statistical analysis system. PDGF reactivity was positive in tumor cell cytoplasm in some cases of squamous cell carcinoma (64%) and adenocarcinoma (55%) and in all cases of large-cell carcinoma, adenosquamous carcinoma, and double carcinoma. PDGF-R reactivity was detected only in tumor stroma. Positive PDGF staining was associated with a poor prognosis in patients with lung carcinoma, independent of age, sex, stage, and degree of cell differentiation (risk ratio = 2.53, p = 0.03). PDGF B mRNA was detected in 100% of PDGF-positive squamous cell carcinomas and in 85% of adenocarcinomas. There was no correlation between PDGF expression and PCNA index in lung carcinomas. Together, these results suggest that immunohistochemistry for PDGF B-chain may predict the outcome for lung carcinoma patients.
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PMID:Expression in lung carcinomas of platelet-derived growth factor and its receptors. 938 86