Establishment of a large cell lung cancer cell line (Y-ML-1B) producing granulocyte colony-stimulating factor
Establishment of a large cell lung cancer cell line (Y-ML-1B) producing granulocyte colony-stimulating factor
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DOI：
10.1016/s0165-4608(02)00536-8
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发表时间：
2002-08-01
影响因子：
--
通讯作者：
Shimokata, K
中科院分区：
文献类型：
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作者：
Sekido, Y;Sato, M;Shimokata, K
我们建立了一个新的肺癌细胞系，命名为Y-ML-1B，从一个70岁的日本男性肺癌白细胞增多症和血小板增多症。手术切除前，白色细胞和血小板计数分别升高至34，400/mm（3）和668，000/mm（3），血清中粒细胞集落刺激因子（G-CSF）水平升高至141 pg/mL。原发性肿瘤表现出未分化的形态与大细胞，并诱导广泛增厚的胸膜在右半胸。Y-ML-1B细胞作为单层生长，倍增时间为19小时，并且在裸鼠中具有致瘤性，其显示出与异种移植物中的原发性肿瘤相似的形态学。对Y-ML-1B细胞培养基上清液的分析显示，G-CSF和其他细胞因子（如白细胞介素（IL）-6，IL-8和粒细胞-巨噬细胞集落刺激因子（GM-CSF））水平升高，与患者血清中检测到的高水平一致。细胞遗传学分析显示，非整倍体大于56中期与许多结构异常。肿瘤抑制基因的突变分析表明，Y-ML-1B在TP 53和RASSF 1A中失活，但在p14（ARF）、p16（INK 4A）或RB中不失活。既没有检测到KRAS或NRAS的激活突变，也没有检测到MYC或MDM 2的扩增。Y-ML-1B表达N-cadherin，不表达E-cadherin。这一新建立的细胞系可能作为一个有用的模型，为研究大细胞肺癌的分子发病机制，表达高水平的细胞因子。(C)2002年爱思唯尔科学公司All rights reserved.
We established a new lung cancer cell line, designated Y-ML-1B, from a lung cancer of a 70-year-old Japanese man with leukocytosis and thrombocytosis. Before surgical resection, the white blood cell and platelet counts were elevated to 34,400/mm(3) and 668,000/mm(3), respectively, and the granulocyte colony-stimulating factor (G-CSF) level in the serum was increased at 141 pg/mL. The primary tumor showed an undifferentiated morphology with large cells and induced extensive thickening of the pleura in the right hemithorax. The Y-ML-1B cells grow as a monolayer, with a doubling time of 19 hours, and are tumorigenic in nude mice, which showed a morphology similar to the primary tumor in xenografts. Analysis of the supernatant of cell culture medium of Y-ML-1B showed elevated levels of G-CSF and other cytokines such as interleukin (IL)-6, IL-8, and granulocyte-macrophage colony-stimulating factor (GM-CSF), consistent with the high levels detected in the patient's serum. Cytogenetic analysis revealed aneuploidy of greater than 56 in metaphases with many structural abnormalities. Mutation analysis of the tumor suppressor genes showed that Y-ML-1B is inactivated in TP53 and RASSF1A, but not in p14(ARF), p16(INK4A), or RB. Neither activating mutations of KRAS or NRAS nor amplification of MYC or MDM2 were detected. Y-ML-1B expressed N-cadherin but not E-cadherin. This newly established cell line might serve as a useful model for studying the molecular pathogenesis for large cell cancers of the lung which express high levels of cytokines. (C) 2002 Elsevier Science Inc. All rights reserved.