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- Prostate Cancer DNA Methylation PCR Array
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- 2026年02月11日
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Prostate Cancer DNA Methylation PCR Array
- 提供商：
SAB
Calcium Channel Signaling: EDNRB.
Caveolae Protein: CAV1.
Cell Cycle, Growth, Differentiation & Development: APC, CCNA1, CDKN2A, DLC1, RARB, RASSF1.
Cell Adhesion & Migration: APC, CDH1, DLC1, TIMP2.
Cytokine: TNFRSF10D.
Drug Metabolism: GPX3, GSTP1, SLC5A8.
DNA Methyltransferase: MGMT (AGT).
Extracellular Matrix Remodeling: TIMP2.
Inflammation: PTGS2 (COX2).
Mitogenesis: PTGS2 (COX2).
Nuclear Receptors: AR, RARB.
Oncogene: CAV1.
Protease Inhibitor: TIMP2.
Retinoid Acid Signaling: RARB.
Solute Carrier Family: SLC5A8.
Transcription Factors & Cofactors: MSX1, PDLIM4 (RIL).
Tumor Suppressor Gene Candidates: APC, CAV1, CDKN2A, RASSF1, SLC5A8, ZNF185.
WNT Signaling Pathway: APC, DKK3, SFRP1.
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文献和实验DNA Methylation Changes in Prostate Cancer
Epigenetic alterations contribute significantly to the development and progression of prostate cancer, the most prevalent malignant tumor in males of Western industrialized countries. Here, we review recent research on DNA methylation
DNA Methylation in Promoter Region as Biomarkers in Prostate Cancer
The prostate gland is the most common site of cancer and the second leading cause of cancer death in American men. Recent emerging molecular biological technologies help us to know that epigenetic alterations such as DNA methylation
清楚。除上述复合物外，MBD还与几种与转录抑制有关的蛋白有一定关系，如c-ski,N-CoR。二、DNA甲基化与肿瘤形成（一）、CPG岛的高度甲基化肿瘤细胞呈现两种绝然相反的甲基化模式：即整体基因组甲基化不足和CPG岛超甲基化。这两种甲基化模式在肿瘤形成中均起重要作用。现对CPG岛内甲基化的研究比较透彻，其在肿瘤形成中的作用也更加明确。1、候补基因(candidante gene)的分析1986年首先报道[1]人类肿瘤CPG岛超甲基化，直到1996年[2],基于PCR的甲基化技术的出现，对CPG岛甲基
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