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)

Bone scintigraphy is often performed to assess the response to systemic therapy of bone metastasis from prostate cancer. We examined the changes in bone scintigraphic findings and the agreement with AIP, AcP, or other tumor markers measured in the follow-up of patients with known bone metastasis after hormonal therapy. Out of 32 patients, 22 (69%) showed improved scintigraphic findings on the first follow-up bone scintigraphy after hormonal therapy. However, 7 out of 22 patients who showed improvement on the first follow-up scintigraphy, deteriorated thereafter. Changes in the scintigraphic findings were closely correlated with those in the measured tumor markers except for patients with small bone metastasis. Though there were no significant differences in the agreement ratios of the 6 tumor markers evaluated, AIP might be a practical and acceptable indicator. Bone X-ray findings did not change at all in almost half of the cases though the scintigraphic findings showed improvement or deterioration.
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PMID:Scintigraphic changes in bone metastasis from prostate cancer after hormonal therapy--comparison with tumor markers and bone X-ray. 753 50

Aberrant DNA methylation plays a significant role in nearly all human cancers and may contribute to disease progression to advanced phenotypes. Study of advanced prostate cancer phenotypes in the human disease is hampered by limited availability of tissues. We therefore took advantage of the Transgenic Adenocarcinoma of Mouse Prostate (TRAMP) model to study whether three different phenotypes of TRAMP tumors (PRIM, late-stage primary tumors; AIP, androgen-independent primary tumors; and MET, metastases) displayed specific patterns of CpG island hypermethylation using Restriction Landmark Genomic Scanning. Each tumor phenotype displayed numerous hypermethylation events, with the most homogeneous methylation pattern in AIP and the most heterogeneous pattern in MET. Several loci displayed a phenotype-specific methylation pattern; the most striking pattern being loci methylated at high frequency in PRIM and AIP but rarely in MET. Examination of the mRNA expression of three genes, BC058385, Goosecoid, and Neurexin 2, which exhibited nonpromoter methylation, revealed increased expression associated with downstream methylation. Only methylated samples showed mRNA expression, in which tumor phenotype was a key factor determining the level of expression. The CpG island in the human orthologue of BC058385 was methylated in human AIP but not in primary androgen-stimulated prostate cancer or benign prostate. The clinical data show a proof-of-principle that the TRAMP model can be used to identify targets of aberrant CpG island methylation relevant to human disease. In conclusion, phenotype-specific hypermethylation events were associated with the overexpression of different genes and may provide new markers of prostate tumorigenesis.
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PMID:Phenotype-specific CpG island methylation events in a murine model of prostate cancer. 1851 76