Factors regulating initiation, progression and submucosal invasion in gastric cancer.

调节胃癌发生、进展和粘膜下浸润的因素。

• 批准号: nhmrc : 299838
• 负责人: Dr Louise Judd
• 金额: $ 30.06万
• 依托单位: Murdoch Childrens Research Institute
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2004
• 资助国家: 澳大利亚
• 起止时间: 2004-01-01 至 2006-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/factors-regulating-initiation-gastric-cancer/94649
• 关键词: Factors; regulating; initiation; progression; submucosal

Gastric cancer is the second most common cause of death in humans. It is strongly associated with Helicobacter pylori, a common and easily transmitted bacterium which infects about half the world's population. Exactly how Helicobacter pylori (HP) causes cancer, and why it does so in only a small percentage of those infected is unknown. It is clear however that Helicobacter species that produce a strong inflammatory response in the host and possess a full complement of pathogenic (disease-associated) genes are more strongly associated with cancer development after long-term infection than others. We have recently developed a genetically modified mouse which has a minor defect in a regulatory pathway which controls some aspects of gut inflammation. Surprisingly 100% of these mice rapidly develop gastric cancer which has many similarities with the human disease, including inflammation, loss of structure of the stomach lining and penetration of cancerous cells into the muscle layers below. The objectives of this project are to work out whether HP induces similar changes in normal stomach cells as occurs in our defined mouse model of gastric cancer. Specifically we will determine if HP disturbs the way a particular mediator of inflammation works, and if so the way this impacts on certain stomach genes which detect cancerous cells and prevent tumor growth.

胃癌是人类第二大常见死因。它与幽门螺杆菌密切相关，幽门螺杆菌是一种常见且易于传播的细菌，感染了世界上大约一半的人口。幽门螺杆菌（HP）究竟是如何导致癌症的，以及为什么它只在一小部分感染者中发生，目前还不清楚。然而，很明显，在宿主中产生强烈炎症反应并具有完整的致病（疾病相关）基因的螺杆菌物种在长期感染后与癌症发展的相关性比其他更强。我们最近开发了一种转基因小鼠，它在控制肠道炎症某些方面的调节途径中有一个小缺陷。令人惊讶的是，100%的这些小鼠迅速发展胃癌，这与人类疾病有许多相似之处，包括炎症，胃粘膜结构的丧失和癌细胞渗透到下面的肌肉层。该项目的目标是确定HP是否会诱导正常胃细胞发生与我们定义的胃癌小鼠模型中发生的类似变化。具体来说，我们将确定HP是否会干扰炎症的特定介质的工作方式，如果是这样，它会影响某些检测癌细胞和防止肿瘤生长的胃基因。