MOLECULAR GENETIC EVENTS IN LUNG CANCER

A.本文回顾了263例肺癌患者的血清钠值 治疗的开始。 与此同时，130个非小 133例小细胞肺癌（NSCLC）患者中有21例（16%） 患者有低钠血症（p=0.0001）。21例患者中有11例 低钠血症组有9株肿瘤细胞表达ANFmRNA，7株表达ANFmRNA， 11个细胞株中有5个同时产生ANF和AVP mRNA。 所有11个细胞系均产生ANF mRNA、AVP mRNA或两者兼而有之。 从这些研究中，我们观察到所有研究的肿瘤细胞系， 低钠血症SCLC患者产生ANF mRNA或AVP mRNA，或 两者 心房利钠肽可能是先前假设的 第三因素，并发挥重要作用的发病机制 低钠血症在一些SIADH患者。 B。已在细胞表面检测到心房利钠因子A受体mRNA 小细胞肺癌细胞系cDNA的PCR分析 和RNA酶保护测定。 与碘化ANF的结合研究表明， 饱和结合，但位点数量太低，无法准确 估算 细胞对外源性心房利钠素有反应 细胞内cGMP增加的因素，类似于正常 受体。 因此，似乎有功能性心钠素受体上， 小细胞肺癌细胞的表面。 C. 86名不同个体的血清和尿降钙素值分别为 通过放射免疫分析研究，其中包括20名非吸烟者，17名吸烟者， 49例小细胞肺癌患者。 尿量最高 在这三组个体中存在差异（p小于0.00001）。 RNA酶保护试验（RPA）和RIA的11个肿瘤细胞系，从这些 小细胞肺癌的患者显示， 尿降钙素值，但没有异位降钙素生产， 他们的肿瘤细胞系。 因此降钙素升高 肺癌患者体内的水平可能来自于 肿瘤细胞

A. We reviewed the serum sodium values of 263 lung cancer patients before the initiation of treatment. In contrast to none of the 130 non-small cell lung cancer (NSCLC) patients, 21 of 133 (16%) small cell lung cancer patients had hyponatremia (p=0.0001). Eleven of 21 patients with hyponatremia had tumor cell lines available and 9 expressed ANF mRNA, 7 expressed AVP mRNA, and 5 of 11 cell lines produced both ANF and AVP mRNA. All of the 11 cell lines produced ANF mRNA, AVP mRNA, or both. From these studies we have observed that all tumor cell lines studied from SCLC patients with hyponatremia produce ANF mRNA or AVP mRNA, or both. Atrial natriuretic peptide may be the previously hypothesized third factor and play an important role in the pathogenesis of hyponatremia in some patients with SIADH. B. The atrial natriuretic factor A receptor mRNA has been detected on small cell lung cancer cells by PCR analysis of cDNA from the cell lines and RNase protection assay. Binding studies with iodinated ANF showed saturable binding but the number of sites were to low to accurately estimate. The cells respond to exogenously added atrial natriuretic factor with an increase in intracellular cGMP, similar to the normal receptors. Therefore, there appear to be functional ANF receptors on the surface of small cell lung cancer cells. C. The serum and urine calcitonin values of 86 different individuals were studied by radioimmunoassay which included 20 nonsmokers, 17 smokers, and 49 patients with small cell lung cancer. The urine values were the most different in these three groups of individuals (p is less than 0.00001). RNase protection assays (RPA) and RIAs of 11 tumor cell lines from these patients with small cell lung cancer showed some had elevated serum and urine calcitonin values but did not have ectopic calcitonin production in their tumor cell lines. Therefore it appears that elevated calcitonin levels in patients with lung cancer can come from a source other than the tumor cells.