Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0007097 (carcinoma)
 152,788 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of parenterally given polyestradiol phosphate (80 or 160 mg i.m. monthly) and bilateral subcapsular orchiectomy on blood coagulation and fibrinolytic parameters were compared in 11 patients with prostatic carcinoma. Estrogen therapy lowered antithrombin III, plasminogen and plasminogen activator inhibitor activities, whereas these parameters remained unchanged in orchiectomized patients. There were no significant changes in platelet count, fibrinogen, factor VII, protein C and alpha 2-antiplasmin in either group. Estrogen had unfavorable effects on hemostatic laboratory parameters in the direction of a hypercoagulable state. However, no thromboembolic complications were encountered.
 ...
PMID:The effect of parenteral estrogen versus orchiectomy on blood coagulation and fibrinolysis in prostatic cancer patients. 217 41

Sixteen patients with clinically localized breast carcinoma who had been receiving tamoxifen 20 mg twice daily for between 3 and 38 months (median, 14 months) were studied. Several parameters of coagulation (antithrombin III, protein C, fibrinopeptide A and in vitro monocyte procoagulant activity) were investigated in this group and compared to a group of 15 patients with clinically localised breast carcinoma not given tamoxifen. Tamoxifen did not induce significant changes in these parameters to account for the reported thromboembolic events associated with this therapy. The reduced antithrombin III activity previously described in patients receiving tamoxifen for metastatic breast cancer may reflect disease activity rather than a direct effect of tamoxifen on blood coagulation.
 ...
PMID:Effects of tamoxifen on blood coagulation. 334 87

Germline mutations of the tumor suppressor gene APC cause familial adenomatous polyposis. Somatic APC alterations are involved in several sporadic neoplasms, including colorectal, duodenal, gastric, and esophageal carcinoma. The APC mRNA is encoded by 15 exons. Additional transcripts have been reported, due to alternative splicing of coding as well as noncoding regions. Two mRNA isoforms occur due to a deletion of exon 7 or a partial deletion of exon 9. We have identified a novel exon, flanked by APC exons 10 and 11, which is expressed as an alternatively transcribed product of the gene. Further, we have shown that the novel exon consists of a heptad repeat motif and is conserved across species.
 ...
PMID:Evidence for a novel exon in the coding region of the adenomatous polyposis coli (APC) gene. 749 Jan 1

The aim of this study was to develop a method for quantitation of APC mRNA and to measure APC mRNA levels in human tissues. This was done using a competitive reverse transcription PCR with a synthetic RNA control. APC mRNA (pg/microgram total RNA) was quantitated in the following tissues: normal colon 133.6 +/- 69.0; normal duodenum 16.6 +/- 15.7; normal thyroid 30.4 +/- 20.3; normal esophagus 65.2 +/- 58.8; colonic carcinoma 66.5 +/- 30.3; esophageal carcinoma 54.7 +/- 26.5; papillary thyroid carcinoma 55.8 +/- 32.9 and colonic adenomas from patients with familial adenomatous polyposis 46 +/- 15. APC mRNA levels were significantly lower in the duodenum and thyroid than in the colon and esophagus. The quantity of APC mRNA was lower in colonic adenomas from FAP patients than in normal colonic mucosa (p < 0.05).
 ...
PMID:Quantitation of APC mRNA in human tissues. 750 12

We present a restriction fragment length polymorphism (RFLP) analysis of 29 benign and 30 malignant prostatic tumors, using polymorphic DNA probes to the putative tumor suppressor genes DCC (Deleted in Colorectal Carcinoma; chromosome 18q21.3), nm23-H1 (17q21.3), APC (Adenomatous Polyposis Coli; 5q21) and p53 (17p13). Six of 23 evaluable cancers (26%) showed loss of heterozygosity (LOH) at DCC; 5 were advanced stage and one was clinically localized (p < 0.05). Mapping 18q deletions, another (advanced) cancer showed LOH at a locus distal to DCC (18q22), but no LOH at DCC. Three of 15 evaluable cancers (20%), all advanced, showed LOH at APC. Three of eight (38%) cancers, of which 2 were advanced, showed LOH at p53. One high grade/stage cancer of 21 (5%) showed LOH at nm23-H1 (and also at DCC). Combining data, allelic losses at either DCC, APC, or p53 genes were seen in 13% of localized cancers, but in 71% of advanced cancers (p < 0.002). Allelic loss involving nm23-H1 is rare in prostatic carcinoma. We suggest that loss of tumor suppressor genes DCC and/or an unidentified gene located distally on chromosome 18q, APC, or p53 may influence progression in prostatic carcinoma.
 ...
PMID:Somatic allelic loss at the DCC, APC, nm23-H1 and p53 tumor suppressor gene loci in human prostatic carcinoma. 751 Mar 45

Neoplastic progression of colorectal epithelial cells from benign adenomas to malignant carcinomas appears to result from a series of genetic alterations involving both oncogenes and tumor suppressor genes. This progression was recently found to be associated with expression of splice variant isoforms of CD44, a cell surface hyaluronate receptor implicated in carcinogenesis. In this study we examined the relationship of CD44 expression to somatic genetic events in the adenoma-carcinoma sequence: point mutation of K-ras in codons 12 and 13 and overexpression of p53 protein as a marker of gene mutation. Among 22 small adenomas, CD44 was present in 9 (41%), of which only 1 contained a K-ras mutation. CD44 was absent in the other 2 small adenomas positive for K-ras mutation or p53 overexpression. In contrast to the early expression of CD44 in small adenomas, mutations of K-ras and p53 were detected preferentially in large adenomas and late-stage adenomas containing carcinoma. The frequent expression of CD44 prior to K-ras and p53 gene alterations in colorectal neoplasia suggests that activation of CD44 gene expression is related to earlier events in the adenoma-carcinoma sequence, possibly cell activation and proliferation following APC gene mutation or alteration of DNA methylation.
 ...
PMID:CD44 expression in colorectal adenomas is an early event occurring prior to K-ras and p53 gene mutation. 751 84

Focal neoplastic change occurs frequently within the colorectum. Yet, of the several hundreds of microadenomas that are likely to be present within an individual colorectum, only one or two will develop into a clinically diagnosable adenoma. In turn, only a fraction of adenomas will progress to malignancy. The risk that a particular microadenoma will end its natural history as a carcinoma varies according to clinical context. The risk is very low in familial adenomatous polyposis (FAP), but relatively high in hereditary non-polyposis colorectal cancer (HNPCC). This variation is governed by the timing and ordering of the underlying mutational events. In FAP, inactivation of the wild-type APC gene occurs early, whereas K-ras mutations are late events. The converse appears to apply in the case of sporadic adenomas. In flat adenomas, which are known to be relatively aggressive, K-ras mutations may not occur at all. In HNPCC, mutational events are accelerated as a result of defective DNA mismatch repair. The evolution of colorectal adenoma occurs through a variety of quite distinct genetic pathways.
 ...
PMID:Colorectal adenoma progression and genetic change: is there a link? 754 18

Colorectal cancer affect the 15% of general population in developed countries. Cancer is a multistep process in which multiple genetic alterations must usually occur in several years. The premalignant step consists of one or multiple aberrant crypts due to hyperproliferation of cells and its shift from the deep third of the crypt to its surface. It has been suggested that abnormality in the APC gene is responsible for this. Furthermore, there exists DNA hypometilation, activation of the gene K-ras and ornithine decarboxylase activity. There is also a loss of MCC gene, that seems to interact with the APC gene. Entire alterations described make possible the Class I adenoma formation. This adenoma, needs the loss of the DCC gene (late stage in the carcinogenesis process), to become a Class II adenoma. The following alteration is deleted and mutation of the p53 gene. There is also an activation of the c-myc oncogene. These two genes are important mechanisms for the conversion of a benign adenoma to a malignant one, adenoma with in situ carcinoma or Class III adenoma. This type of adenoma becomes carcinoma and metastatic stage, throughout inactivation of several tumor suppressor genes. Besides the hereditary APC alteration and other acquired genetic changes as described above there are other associated genetics, antigenics, and enzymes that have an important role in the adenoma-carcinoma sequence. Several carcinogenic factors have been described which also contribute in the adenoma and carcinoma formation: ulcerative colitis, acromegaly, familial history of colonic neoplasia, certain professions, smoking and drinking, consumption of red or processed meat, etc.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Etiology of colorectal cancer]. 755 83

The APC (adenomatous polyposis coli) gene was isolated as a gene responsible for familial polyposis coli, an autosomal-dominant disease, characterized by development of hundreds to thousands of adenomatous polyps in the colon and rectum. However, recent studies revealed that inactivation of the APC gene also plays a significant role in development of sporadic forms of colorectal adenoma and carcinoma. Furthermore, somatic mutations have also been detected in pancreatic carcinomas as well as some type of gastric carcinomas, suggesting that APC has a critical function in regulation of cell growth in digestive tissues.
 ...
PMID:The adenomatous polyposis coli gene and human cancers. 755 32

Results of epidemiological studies have shown that nitrosamine-induced carcinogensis is involved in esophageal cancer in China. In order to demonstrate the mechanism at molecular level, Multiple tumor suppressor genes Rb, p53, APC and MCC in human fetus esophageal epithelium treated with NMBzA (in vitro) for 24 hours or three weeks and esophageal carcinoma induced by NMBzA were analyzed with PCR amplification and direct sequencing. In PCR amplification analysis. Rb, p53, APC and MCC deletions in esophageal carcinoma of human fetus induced by NMBzA were found, but no deletions of these genes was demonstrated in NMBzA-treated human fetal esophageal epithelium. PCR direct sequencing analysis revealed mutation of p53, Rb and MCC genes in human fetal esophageal epithelium treated with NMBzA for three weeks. The results first confirmed (in vitro) that nitrosamine can cause mutations and deletions of multiple tumor suppressor genes in human esophageal epithelium. The mutations of tumor suppressor genes in nitrosamine-induced esophageal carcinoma may occur in the early stage, while deletions in late stage of carcinogenesis.
 ...
PMID:[Multiple tumor suppressor genes in esophageal carcinoma induced in human fetus esophageal epithelium by NMBzA]. 765 18


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>