Takahashi T, Ueda R, Takahashi T
Laboratory of Ultrastructure Research, Aichi Cancer Center Research Institute, Nagoya, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1995 Dec;33 Suppl:29-32.
Lung cancer is associated with a number of cytogenetic abnormalities, such as chromosomal deletions on 3p, 12q, and 17p, which suggest the involvement of multiple tumor suppressor genes. These findings led to the discovery of the inactivation of the Rb and p53 genes in lung cancer. Recent remarkable progress in molecular biology should add a number of genes to the list of tumor suppressor gene involved in the pathogenesis of lung cancer. In addition, dominant oncogenes as well growth factors and their receptors have been shown to be involved in this process. Our understanding of the molecular pathogenesis of this fatal disease will now allow us to design new strategies to better diagnose and treat lung cancer. In this symposium, we discuss how the molecular oncological approach can be used to reduce the rapidly increasing rates of death due to lung cancer.
肺癌与许多细胞遗传学异常有关，例如3号染色体短臂、12号染色体长臂和17号染色体短臂上的染色体缺失，这表明多个肿瘤抑制基因参与其中。这些发现导致了肺癌中Rb和p53基因失活的发现。分子生物学最近的显著进展应该会使参与肺癌发病机制的肿瘤抑制基因名单增加许多。此外，显性癌基因以及生长因子及其受体也已被证明参与了这一过程。我们对这种致命疾病分子发病机制的理解现在将使我们能够设计新的策略，以更好地诊断和治疗肺癌。在本次研讨会上，我们将讨论如何利用分子肿瘤学方法来降低因肺癌导致的迅速上升的死亡率。
