Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0282612 (PIN)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fas (Apo-1/CD95) is a cell-surface receptor involved in cell death signaling through binding of Fas ligand. Mutations of the Fas gene might be involved in proliferative diseases of the prostate by prolongation of programmed cell death of prostatic epithelial cells. Using the laser capture microdissection method, Fas gene mutations were examined on genomic DNA extracted from lesions with high-grade prostatic intraepithelial neoplasia (HGPIN), a possible precursor of prostatic cancer (PCA), and from PCA. A total of 193 lesions, 111 with HGPIN, 55 with PCA, and 27 benign glands, were microdissected from 27 patients with PCA. Polymerase chain reaction-amplified products were directly sequenced. Loss of heterozygosity (LOH) was examined at four sites of known polymorphisms. Fas gene mutations were detected in HGPIN: 4 of 27 (14.8%) cases or 4 of 111 (3.6%) lesions. All were point mutations: three missense and one nonsense in the death domain. Benign proliferative glands adjoining HGPIN and/or PCA, and PCA never showed mutations. LOH was found in 31.3% of PCA and 25% of HGPIN lesions, but was never found in benign glands. Exclusive occurrence of Fas mutations in HGPIN might underlie the development of these lesions. Occasional findings of LOH in HGPIN and PCA suggested that genetic instability might occur during the early phase of prostatic carcinogenesis.
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PMID:Fas gene mutations in prostatic intraepithelial neoplasia and concurrent carcinoma: analysis of laser capture microdissected specimens. 1131 Aug 21

Human monocytes/macrophages (M/M) are the major targets for human immunodeficiency virus type 1 (HIV-1) infection. To characterize the global effects of acute HIV-1 infection on gene expression in M/M, the expression levels of 550 host cell RNA transcripts in U937 human promonocytes at 2-3 days after HIV-1 infection were assessed using cDNA microarray analysis and were compared to those in the infected HUT78, a CD4+ T cell line. Confirmed by semiquantitative RT-PCR, our results showed that 12 genes were up-regulated and 26 genes were down-regulated in the infected U937 cells at 2-3 days post-infection, whereas 8 genes were up-regulated and 20 genes were down-regulated in the infected HUT78 cells at 2-3 days post-infection. These genes encode a host of proteins with divergent functions in a variety of cellular processes including apoptosis (FAS, Fas ligand, PIN, HSP90beta, bcl-2, bcl-x), cell signal transduction (Ras, RGS1, IRF-1, STAT3), receptor-mediated signaling transduction (CD71, CD69, CD3delta), cell cycle and growth (c-myc, cytokines, kinase), transcriptional regulation (EWS, CREB-2), and chemotaxis (beta-chemokines, RANTES), supporting the general effects of HIV-1 infection on cells of different origin. Although most identified genes were regulated similarly in both infected cell lines, differences in gene regulation, such as c-myc, CD71, CD69, and beta-chemokines, between the two infected cell lines were also identified in this study. These differences may further our understanding of the pathogenicity of HIV and enable the discovery of novel therapeutic approach for AIDS.
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PMID:HIV-1 infection initiates changes in the expression of a wide array of genes in U937 promonocytes and HUT78 T cells. 1588 42