Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-11066
Weber, A; Kristiansen, I; Johannsen, M; Oelrich, B; Scholmann, K; Gunia, S; May, M; Meyer, H A; Behnke, S; Moch, H; Kristiansen, G (2008). The FUSE binding proteins FBP1 and FBP3 are potential c-myc regulators in renal, but not in prostate and bladder cancer. BMC Cancer, 8:369:1-11.
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BACKGROUND: The three far-upstream element (FUSE) binding proteins (FBP1, FBP2, and FBP3) belong to an ancient family of single-stranded DNA binding proteins which are required for proper regulation of the c-myc proto-oncogene. Whereas it is known that c-myc alterations play a completely different role in various carcinomas of the urogenital tract, the relevance of FBPs is unclear. Methods: FBP1, FBP3 and c-myc expression was studied in 105 renal cell, 95 prostate and 112 urinary bladder carcinomas by immunohistochemistry using tissue microarrays. High rates of FBP1 and FBP3 expression were observed in all cancer types. RESULTS: There was a concomitant up-regulation of FBP1 and FBP3 in renal cell and prostate carcinomas (p<0.001 both). C-myc expression was detectable in 21% of prostate, 30% of renal and 34% of urothelial carcinomas. Interestingly, strong FBP1 and FBP3 expression was associated with c-myc up-regulation in clear cell renal cell carcinomas (p<0.001 and 0.05 resp.), but not in bladder or prostate cancer. CONCLUSIONS: The correlation between FBP1/FBP3, c-myc and high proliferation rate in renal cell carcinoma provides strong in vivo support for the suggested role of FBP1 and FBP3 as activators of c-myc. The frequent up-regulation of FBP1 and FBP3 in urothelial and prostate carcinoma suggests that FBPs also have an important function in gene regulation of these tumors.
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|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Surgical Pathology|
|Dewey Decimal Classification:||610 Medicine & health|
|Deposited On:||30 Jan 2009 07:27|
|Last Modified:||28 Nov 2013 01:29|
|Additional Information:||Free full text article|
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