| Project/Area Number |
17591770
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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 |
Obstetrics and gynecology
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| Research Institution | Japanese Foundation For Cancer Research |
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Principal Investigator |
HIRAI Yasuo Japanese Foundation For Cancer Research, CANCER INSTITUTE, RESEARCH FELLOW (00260076)
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| Project Period (FY) |
2005 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,730,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥330,000)
Fiscal Year 2007: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Endocervical adenocarcinoma / Endometrial adenocarcinoma / DCC(18q21.3) / array-based CGH / genetic instability / PTEN / LRP 1B(2q 21.2) / DAB2(5n13) / 子宮頸部腺癌 / DAB2(5p13) / conventional CGH / P-cadherin / MLH1 |
|---|
| Research Abstract |
In our institute, rare clinical materials from both endocervical and endometrial adenocarcinomas are available for several investigations. We investigated new diagno-therapeutic procedures of human uterine cancer based on molecular cytogenetic study. The array-based CGH analysis of endocervical adenocarcinomas revealed decreasing copy numbers in LRP1B (2q21.2) DAB2 (5p13), and DCC (18q21.3). These genetic changes are presumably specific to the endocervical adenocarcinomas, which may be engaged in the carcinogenesis. As the chemotherapy for uterine cancers is usually effective, surgical or radiation therapy combined with neoadjuvant and/or adjuvant chemotherapy is expected to improve significantly over all survival of the patients. Therefore, any prediction of chemotherapeutic sensitivity may be helpful for therapeutic decisions associated with switching from surgery to radiation therapy and so forth.
Recently, a high rate of endometrial cancer has been reported in women with hereditary nonpolyposis colorectal cancer (HNPCC), suggesting a relation between familial endometrial cancers and HNPCC. Familial endometrial cancers constitute only about 0.5% of all endometrial carcinomas and it is essential to examine family histories in detail. We performed a mutational analysis of three DNA mismatch repair (MMR) genes (hMLH1, hMSH2 and hMSH6) in patients with endometrial cancer who meet our criteria for familial predisposition to HNPCC-associated endometrial cancers.
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