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2022 Fiscal Year Final Research Report

Elucidation of heterozygous deletion mechanism of MEN1 gene in multiple endocrine neoplasia type 1

Research Project

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Project/Area Number 20K08901
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 54040:Metabolism and endocrinology-related
Research InstitutionGunma University

Principal Investigator

Ozawa Atsushi  群馬大学, 大学院保健学研究科, 教授 (10573496)

Project Period (FY) 2020-04-01 – 2023-03-31
Keywords遺伝子 / 腫瘍症候群 / マウス
Outline of Final Research Achievements

MEN1, the causative gene of multiple endocrine neoplasia type 1 (MEN type 1), is considered to be a tumor suppressor gene.
We investigated the significance of LOH (loss of heterozygosity) in the process of tumorigenesis in endocrine glands. In target endocrine glands in MEN1, the genetic profile before LOH was significantly different from that after tumorigenesis. In endocrine tumorigenesis, the occurrence of LOH of the MEN1 gene is not uniform even in the same individual tumor site, and there is no correlation between the degree of LOH and the malignancy of the tumor or gain of function (hormone hypersecretion).

Free Research Field

内分泌代謝学

Academic Significance and Societal Importance of the Research Achievements

これまでMEN1型の腫瘍発症機構の研究としては、癌抑制遺伝子の機能破綻後の、すなわちLOHが生じた後の腫瘍組織を用いてMEN1の機能不全が腫瘍増殖に及ぼす影響について論ぜられた研究が主であったが、今回、私達は、MEN1型におけるLOH発症前の標的内分泌腺における遺伝子変動に着目して研究を遂行した。今後研究を発展させることでp53遺伝子、Rb遺伝子、APC遺伝子など他の癌抑制遺伝子にも共通するLOHの機構の解明につながる可能性がある。また、膵内分泌腫瘍化に関わる新規因子群や経路の詳細が解明されれば、膵内分泌腫瘍の診断、治療における新たな分子マーカーや、創薬のターゲットとなることが期待される。

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Published: 2024-01-30  

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