1992 Fiscal Year Final Research Report Summary
Detection, activation mechanism and its clinical application of basic fibroblast growth factor in renal cell carcinoma.
| Project/Area Number |
03670741
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Urology
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| Research Institution | Hokkaido University |
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Principal Investigator |
NONOMURA Katsuya Hokkaido Univ. School of Med., Associate Professor, 医学部, 助教授 (60113750)
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| Co-Investigator(Kenkyū-buntansha) |
SEKI Toshimori Hokkaido Univ. Medical Hospital,Lecture, 医学部附属病院, 講師 (70196947)
TOGASHI Masaki Hokkaido Univ.School of Med., Associate Professor, 医学部, 助教授 (50041843)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Renal cell carcinoma / Basic fibroblast growth factor (bFGF) / von Hippel-Lindau (VHL) disease / Collagenase activity |
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| Research Abstract |
Von Hippel-Lindau (VHL) disease which is manifested by cerebellar hemangioblastomas, retinal angiomas and cysts of the pancreas,kidney and epididymis is well known to be highly associated with renal cell carcinoma (RCC). Sporadic RCC is also known to be one of highly vascularized tumors. These clinical evidence supposes us an intimate association between the growth and proliferation of RCC and tumor angiogenesis. Although endothelial cells of blood vessels generally have a very slow turnover time, basic fibroblast growth factor (bFGF) is said to stimulate the endothelial cells and to induce the formation of new capillaries which ultimately sustain the growth of a solid tumor.
bFGF activity was assayed and compared among 12 specimens (10 were sporadic and 2 were with VHL disease) of RCC and their corresponding autologous normal renal tissue. bFGFs in sporadic RCC and normal renal tissue were 98.2*38.68 and 143.2*31.16 fmol/mg. protein (Mean*SD, n=10), respectively. bFGF activity in malignant tissue was significantly lower than that in the corresponding autologous normal tissue. Otherwise, bFGF activities of RCC and non-malignant renal tissue in 2 case with VHL disease were 137, 632 and 82, 44 fmol/mg. protein, respectively.
In general, bFGF as an inert form exists in the extracellular matrix. The collagenase activity might have an important role in terms of disruption of the extracellular matrix and of mobilization of endothelial cells by bFGF. Collagenese activities in the renal tissues irrespetive of malignancy were quite low in our assay system using by Collageno kit CLN-100.
These data suggest that bFGF activity may acularate growth and proliferation of RCC at least in VHL disease.
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