Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0376358 (prostate cancer)
 59,338 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The goal of this study was to determine if patients with stage D0-3 prostatic adenocarcinoma have detectable hematogenous micrometastasis. Polymerase chain reaction amplification of prostate-specific antigen mRNA, which is exclusively expressed by prostatic epithelial cells, was used to detect circulating prostatic cells. Peripheral venous blood was obtained from 17 control and 12 prostate cancer patients with stage D0-3 prostatic adenocarcinoma. Of the 12 cancer cases, four patients (stage D1-3) tested positive for prostate-specific antigen RNA, indicating the presence of circulating micrometastasis. The 17 negative controls all tested negative. Contrary to a long held hypothesis, these data point to the possibility that hematogenous metastasis may be a relatively early event in the natural history of human prostate cancer. These findings may have an important impact on our understanding and treatment of prostate cancer.
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PMID:Detection of hematogenous micrometastasis in patients with prostate cancer. 138 51

The RAS gene family includes three functional genes, H-RAS, K-RAS, and N-RAS, which have been most widely studied in human tumors. Point mutations most commonly occurring at codons 12, 13, or 61 of these genes allow the RAS protooncogene to be converted to a RAS oncogene. A variety of human tumors have been studied for RAS mutations to date, however, conflicting data has been reported regarding prostate cancer. Cell line studies and two American studies of clinical material have found a low incidence of RAS mutation in prostate cancer. The few mutations found were predominantly in the H-RAS gene. Conversely, a recent study of Japanese occult autopsy specimens found an approximate 25% incidence of K-RAS mutations. In this current study, DNA was extracted from 24 archival paraffin-embedded, formalin-fixed radical prostatectomy specimens. Twenty-one of the 24 cases had pathologic stage C disease, and paraffin blocks were selected having the most concentrated area of neoplasm. Twelve, seven, and five cases demonstrated moderate, well and poorly differentiated histologic grade respectively. Polymerase chain reaction (PCR) was used to amplify the K-RAS, N-RAS, and H-RAS 12, 13, 61 codons of these specimens and mutations were detected with mutation-specific oligonucleotide probe hybridization of southern and slot blots. No definite point mutations were detected. PCR's and hybridizations were performed three separate times by three investigators to confirm these results. PCR-generated mutation-specific positive controls and known negative controls were used and found to be important to interpret oligonucleotide hybridization assays. RAS gene mutations appear to be infrequent in clinical prostate carcinomas in American males.
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PMID:Infrequent RAS oncogene mutations in human prostate cancer. 160 59

Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) analysis of all of the ten exons of the WT1 gene and restriction fragment length polymorphism (RFLP) analysis of the WT1 locus were performed on primary urinary tract cancers: seven renal pelvic cancers, one ureteral cancer, 11 bladder cancers, and 22 renal cell cancers. Four human bladder cancer cell lines (T24, JTC30, JTC32, and HUB41) and three human prostate cancer cell lines (PC-3, DU145, and LNCaP) were also examined. None of the primary cancers showed any apparent mutations of the gene, whereas one base substitution of exon 5 was found in DU 145 and gross alteration of the gene was recognized in HUB41. Heterozygosity of polymorphic exon 7 was retained in all of the 12 informative cases, and none of 10 informative cases showed loss of heterozygosity at the WT1 locus in RFLP analysis. It is concluded that mutations of the WT1 gene may not be involved in the formation of malignant tumors of the adult urinary tract.
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PMID:Infrequent mutations of the WT1 gene in primary cancers of the adult urinary tract. 747 3

Occult micrometastases detected by immunohistochemistry have prognostic significance in patients with localized breast cancer. To determine the usefulness of this technique and of polymerase chain reaction in detecting occult prostate cancer, we evaluated the sensitivity and specificity of immunohistochemistry and polymerase chain reaction amplification of mRNA to detect prostate cancer cells in bone marrow samples. We used cells from an established prostate cancer cell line (LNCAP) mixed with lymphocytes at various dilutions from 10(5) cancer cells in 10(6) lymphocytes to 1:10(6). Both techniques had a 100% specificity and identified cancer cells at all dilutions. Polymerase chain reaction was more sensitive than immunohistochemistry at the lowest dilutions (10(-5) and 10(-6), p = 0.033). We have evaluated seven patients with prostate cancer for micrometastases. Both of the patients with known metastatic prostate cancer and one of the five patients with clinically localized tumors had micrometastases. Detection of micrometastases may be useful in the staging of prostate cancer.
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PMID:Sensitivity of immunohistochemistry and polymerase chain reaction in detecting prostate cancer cells in bone marrow. 751 Mar 19

The NM23 gene family (nm23-H1 and nm23-H2) has been reported as a measure of metastatic potential. The goal of this study was to discriminate nm23-H1 and nm23-H2 gene expression in benign and malignant human prostate tissue and to determine the relationship of their expression to tumor stages. Specimens included 5 benign prostatic hyperplasias (BPH), 11 primary prostate adenocarcinomas (CaP) (5 stage B, 5 stage C and 1 stage D1), 2 pelvic lymph nodes with metastases and 3 prostate cancer cell lines derived from metastatic lesions. Polymerase chain reaction analysis of mRNA (RNA/PCR) was used to amplify transcripts of both NM23 genes and a normalizing gene (c-N-ras) to determine the relative levels of expression. A significant difference was shown between the BPH specimens and the cell lines from metastatic prostate cancer for nm23-H2 expression (p = 0.037) and the nm23-H1/nm23-H2 gene expression ratio (p = 0.037). The nm23-H1/nm23-H2 ratio increased significantly (p = 0.026, tau-b = 0.377) from BPH, through the CaP stages, to the cell lines. The expression of nm23-H2 decreased significantly (p = 0.002, tau-b = -0.517) from BPH, through the CaP stages, to the cell lines. Thus, while nm23-H2 appears to be significant for characterizing stages of CaP, an understanding of the metastatic phenotype will require further analysis of both NM23 genes.
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PMID:Quantitation of NM23 expression in human prostate tissues. 751 52

A study was made of the incidence of p53 mutations in Japanese males with prostate cancer or benign prostatic hyperplasia. Polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) was used as a primary screening technique with gene sequencing being carried out in positive cases. Two out of 21 prostate cancers (9.5%) were found to have p53 mutations. These were stage B2 and D2 prostate cancers. No abnormalities were found in the remaining cases or benign prostatic hyperplasia. Mutations of the p53 gene would thus appear infrequent in the tumourigenesis of primary prostate cancer.
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PMID:Infrequent involvement of p53 gene mutations in the tumourigenesis of Japanese prostate cancer. 769 Nov 45

Mutations in the p53 tumour-suppressor gene are among the most common genetic alterations in human cancers. In the present study we analysed the mutations in the p53 tumor-suppressor gene in 25 primary and 20 metastatic human prostate cancer specimens. DNA extracted from the paraffin-embedded sections was amplified by hot-start polymerase chain reaction, and p53 gene mutations in the conserved mid-region (exons 4-9) were examined using single-strand conformation polymorphism (SSCP) analysis and immunohistochemistry. In the present study, we used a novel hot-start PCR-SSCP technique using DNA Taq polymerase antibody, which eliminates primer-dimers and non-specific products. Because of this new technique, the results of PCR-SSCP showed very high resolution. Polymerase chain reaction products were sequenced directly for point mutations for the p53 gene. Mutations were found in 2 out of 25 primary prostate cancers (8%) and 4 out of 20 metastatic cancers (20%). Mutations were observed exclusively in exon 7 and not in exons 4, 5, 6, 8 or 9. Nuclear accumulation of p53 protein, determined by immunohistochemistry, correlated with the degree of metastasis in prostatic cancer.
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PMID:P53 tumour-suppressor gene mutations are mainly localised on exon 7 in human primary and metastatic prostate cancer. 868 33

Recently published protocols using Reverse Transcriptase Polymerase Chain reaction (RT-PCR) for prostate specific antigen (PSA) provide a sensitive means for detecting circulating prostate cancer cells. Attempts to use these assays for staging of prostate cancer have produced conflicting results. As a first step towards rectifying these discrepancies, a modified immunobead-RT-PCR assay capable of detecting as few as 10 prostate cancer cells in 8cc of blood was developed. This 10 fold increase in sensitivity was achieved in part by introducing two target cell enrichment steps. As a model system to assess sensitivity of the modified assay, template RNA was extracted from PSA positive human carcinoma cells suspended in human blood and isolated with immunomagnetic beads following incubation with an epithelium specific antibody. After 45 cycles of PCR, product from as few as 10 target cells could be readily detected when displayed on a 2% agarose gel stained with SYBR Green fluorescent dye. The identity of amplified DNA fragments was confirmed by Southern blot hybridization. When applied to blood samples from patients with proven metastatic disease, the immuno-bead RT-PCR assay was successful in detecting circulating PSA positive epithelial cells, suggesting this assay may be useful for assessment of disease progression or recurrence.
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PMID:Application of immunomagnetic beads in combination with RT-PCR for the detection of circulating prostate cancer cells. 940 55

Breast and gynecological cancer-associated antigens RAK p120, p42 and p25 exhibit molecular, immunological and genetic homology to HIV-1 proteins. Normal tissues, including the majority of tissues adjacent to cancer, do not express these unique cancer markers. Antigens RAK are now detected in 100% of prostate cancer and in the majority of prostate benign hyperplasia (BPH) cases. Polymerase chain reaction (PCR) with HIV-1 gp41-derived primers revealed prostate cancer-associated DNA fragments of similar size (140 bp) as in HIV-1 genome. Ninety-five percent of BPH samples obtained from prostate cancer patients tested PCR-positive. For comparison, only 61.9% of BPH samples obtained from cancer-free patients tested PCR-positive. The DNA fragments amplified in prostate cancer and in BPH showed more than 90% homology to the HIV-1 gene for gp41. The obtained results strongly suggest that a retrovirus related to HIV-1 may be associated with cancers of the reproductive system.
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PMID:Prostate, breast and gynecological cancer markers RAK with homology to HIV-1. 950 Feb 13

To identify whether alterations of the p16 tumor suppressor gene are a common event in localized prostate cancer, we examined the frequency of p16 gene mutations in 30 primary tumors. Only two tumors demonstrated altered single-strand conformation polymorphism patterns for exon 2 of p16. In both cases, sequencing revealed a missense at codon 148, a G-->A transition that resulted in the replacement of the alanine by threonine. Polymerase chain reaction-single-strand conformation polymorphism analysis of matched blood samples revealed the same abnormal band shifts as the tumor samples, suggesting that these base changes are polymorphic. In addition, transcriptional inactivation by means of CpG island methylation has also been reported as a possible means of p16 gene inactivation. To address this point, we determined the pattern of DNA methylation at the Smal site for 21 of 30 samples for which DNA was available. Only one sample had an altered methylation pattern at the Smal site downstream of exon 1 of the p16 gene, which is outside the CpG island and is not normally associated with transcriptional inactivation. However, two samples did have deletions proximal to or within the p16 gene. These results indicate that mutations in p16 may not be a dominant pathway for p16 loss of function or that inactivation of p16 by DNA methylation may not be necessary for the transformation and progression of prostate cancer.
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PMID:Analysis of the p16 tumor suppressor gene in early-stage prostate cancer. 953 47


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