Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Barrett's esophagus, currently defined as endoscopically apparent columnar metaplasia of the esophagus with histologic documentation of goblet cells, is the precursor to esophageal adenocarcinoma. However, not all patients with this disorder require intensive surveillance. Pathologic diagnosis and grading of dysplasia in mucosal biopsies remains the best and most widely used method of determining which patients are at highest risk for neoplastic progression. The task of diagnosing dysplasia suffers from considerable interobserver variability. Therefore, consultation with expert gastrointestinal pathologists to confirm the diagnosis of dysplasia before definitive management is highly advisable. Adjunctive methods to improve reproducibility, such as immunostaining for alpha-methylacyl-CoA racemase, show promise but require confirmation in larger studies. This article focuses on dysplasia in Barrett's esophagus in terms of its classification, pathologic diagnostic criteria, limitations, natural history, and treatment.
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PMID:Neoplastic precursor lesions in Barrett's esophagus. 1799 90

Androgen-independent prostate cancer eventually develops metastasis, and radical treatment may not be possible for patients at this stage. In this study, we examined the gene-expression profiles of two prostate cancer cell lines, LNCaP (androgen-dependent) and C4-2 (androgen-independent), using cDNA-microarray hybridization. We focused on the expression of alpha-methylacyl-CoA racemase (AMACR), whose expression is much higher in C4-2 than in LNCaP, and investigated its biological role in acquisition of androgen-independent cancer growth. Immunohistochemistry and Western blot analysis of subcellular fractions revealed that AMACR expression was much stronger in C4-2 than in LNCaP. Inhibition of AMACR expression using AMACR-siRNA induced an increase in the expression of androgen receptor (AR) and B-cell translocation gene 1, along with a decrease in the expression of genes associated with cancer progression, including insulin-like growth factor I and platelet-derived growth factor alpha, in C4-2 with compared to non-treated C4-2. BrdU analysis and MTT assay demonstrated that AMACR inhibition induced a significant decrease of cell viability in C4-2 when cultured in androgen-depleted serum, becoming consistent with that of LNCaP, suggesting that AMACR inhibition may induce an increase in the expression of AR and characteristic conversion of prostate cancer cells from hormone independency to hormone dependency. We suggest that AMACR inhibition may be a new strategy for treatment of patients with hormone-refractory prostate cancer.
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PMID:Conversion of prostate cancer from hormone independency to dependency due to AMACR inhibition: involvement of increased AR expression and decreased IGF1 expression. 1959 19