Genetic analysis in early age of onset lung cancer patie

为了验证这一假设，我们分析了60例肺腺癌和邻近的非肿瘤组织，这些患者在诊断时年龄小于50岁，大于79岁，或在57-72岁之间，在5个常见的受累染色体臂（包括3 p，3q，9 p，17 p和19 p）中存在洛。这种方法导致人们将第3页上的一个小区域识别为与50岁以下肺癌患者关系最密切的区域。在过去的一年中，我们在这个区域确定了一小部分候选基因，作为早期发病患者肺肿瘤失活的潜在靶点。我们的数据是第一个提供直接证据，将极端年龄人群的肺癌易感性与人类基因组中的特定遗传改变联系起来。我们现在正在对原发性肿瘤和匹配的正常肺中的这些候选基因进行测序，以确定这些基因中的遗传改变是否可能导致肺癌的发展。其他研究也在进行中，以确定这些基因的细胞定位及其在细胞生长和肿瘤形成中的潜在分子功能。

To test this hypothesis, w analyzed paired 60 lung adenocarcinomas and adjacent non-tumor tissues from patients who were less than 50, older than 79, or between 57-72 years of age at the time of diagnosis for the presence of LOH in five commonly affected chromosome arms including 3p, 3q, 9p, 17p, and 19p. This approach led use to identify a small region on ch. 3p as the region most strongly associated with patients who had lung cancers younger than age 50. In the past year, we identified a small set of candidate genes in this region as potetial targets of inactivation in lung tumors of early age onset patients. Our data is the first to provide direct evidence linking lung cancer susceptibility in extreme-age populations to a specific genetic alteration in the human genome. We are now sequence these candidate genes in primary tumors and the matched normal lungs to determine if genetic alterations in these genes might contribute to lung cancer development. Additional studies are also underway to determine the cellular location of these genes and their potential molecular function in cell growth and tumor formation.