Growth stimulation of non-small cell lung cancer xenografts by granulocyte-macrophage colony-stimulating factor (GM-CSF)
Growth stimulation of non-small cell lung cancer xenografts by granulocyte-macrophage colony-stimulating factor (GM-CSF)
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DOI：
10.1016/s0959-8049(98)00236-6
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发表时间：
1998-11-01
影响因子：
8.4
通讯作者：
Ueyama, Y
中科院分区：
文献类型：
--
作者：
Oshika, Y;Nakamura, M;Ueyama, Y
粒细胞-巨噬细胞集落刺激因子（GM-GSF）通过自分泌或旁分泌机制参与某些类型肿瘤的发生。我们检测了20例人非小细胞肺癌（NSCLC）异种移植瘤中GM-CSF/GM-CSF受体（GM-CSFR）基因的表达。使用产生丰富的人GM-CSF的GM-CSF转基因：严重联合免疫缺陷（SCID）小鼠（GM-Tg-SCID）检查GM-CSF的刺激作用。NSCLC异种移植物（LC 11-JCK）表达GM-CSFR但不表达GM-CSF，并且在GM-Tg-SCID中显示出比非GM-CSF转基因SCID小鼠（非Tg-SCID）更快的生长。在90例原发性NSCLC人类标本中，48例（53%）检测到GM-CSF基因表达，42例（47%）检测到GM-CSFR基因表达。30例鳞状细胞癌中13例（43%）表达GM-CSF，10例（33%）表达GM-CSFR。GM-CSF和GM-CSFR共表达的鳞癌患者的预后显著低于GM-CSF和GM-CSFR均不表达的鳞癌患者（P < 0.05）。这些结果表明GM-CSF对某些NSCLC有刺激作用，（C）1998 Elsevier Science Ltd.保留所有权利。
Granulocyte-macrophage colony-stimulating factor (GM-GSF) has been suggested to involved in the carcinogenesis of some types of tumours by autocrine or paracrine mechanisms. We examined GM-CSF/GM-CSF receptor (GM-CSFR) gene expression in 20 human non-small cell lung cancer (NSCLC) xenografts. The stimulatory effects of GM-CSF were examined using GM-CSF transgenic: severe combined immunodeficient (SCID) mice (GM-Tg-SCID), which produce abundant human GM-CSF. A NSCLC xenograft (LC11-JCK), expressed GM-CSFR but not GM-CSF, and showed more rapid growth in GM-Tg-SCID than non-GM-CSF transgenic SCID mice (non-Tg-SCID). GM-CSF gene expression was detected in 48 of 90 (53%) primary NSCLC human specimens and GM-CSFR gene expression was detected in 42 specimens (47%). GM-CSF expression was detected in 13 of 30 squamous cell carcinoma specimens (43%) and GM-CSFR expression was detected in 10 specimens (33%). Patients with squamous cell carcinoma coexpressing GM-CSF and GM-CSFR showed significantly poorer prognosis than those expressing neither GM-CSF nor GM-CSFR (P < 0.05, Cox-Mantel test). These results suggest that GM-CSF can have a stimulatory effect on some NSCLC, (C) 1998 Elsevier Science Ltd. All rights reserved.