| Project/Area Number |
13671398
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Thoracic surgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
YAMAKAWA Yosuke (2002) Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (40148284)
梶 政洋 (2001) 名古屋市立大学, 医学部, 助手 (30326144)
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| Co-Investigator(Kenkyū-buntansha) |
FUJII Yoshitaka Nagoya City University, Graduate School of Medical Sciences, Professor and Chair, 大学院・医学研究科, 教授 (40156831)
山川 洋右 名古屋市立大学, 医学部, 助教授 (40148284)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | CDKN2 / p16^<INK4a> / p14^<ARF> / lung cancer / p16 / p14 / pRb / p53 |
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| Research Abstract |
The CDKN2 gene on the short arm of chromosome 9p encodes two different cell cycle regulatory proteins, p16^<INK4a> and ARF. P16^<INK4a> and p14^<ARF> play an important role in independent cell cycle regulatory pathways, the retinoblastoma pathway and the p53 pathway, respectively. We have examined the expression of p16^<INK4a> and p14^<ARF> using competitive RT-PCR in 60 NSCLCs and matching normal lung tissues. The intensities of bands for p16^<INK4a> and p14^<ARF> were nearly equal or the intensity of p16^<INK4a> band slightly exceeded that of p14^<ARF> in the normal lung tissues (n=60). In 38 tumors the intensity of p16^<INK4a> band was similar to or slightly weaker than that of p14^<ARF>. In 6 tumors the intensity of p16^<INK4a> band was weaker than that of p14^<ARF>. In 15 tumors the intensity of p14^<ARP> band was very strong and p16^<INK4a> band was barely visible. In only one tumor the intensity of p16^<INK4a> band was very strong, while the band of p14^<ARF> was barely visible. The ratio of the intensity of p16^<INK4a> to p14^<ARF> band had an interesting correlation with the tumor's clinicopathological characteristics. The p stage II-IV tumors had significantly lower p16^<INK4a> to p14^<ARF> ratios than the p stage I tumors (p=0.036). The T2-4 tumors had significantly lower p16^<INK4a> to p14^<ARF> ratios than the T1 tumors (p=0.005). The N1-3 tumors had significantly lower p16^<INK4a> to p14^<ARF> ratios than the N0 tumors (p=0.014). Our results suggest that the ratio of expression of p16^<INK4a> to p14^<ARF> tends to decrease during the progression of NSCLC.
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