Oshika Y, Nakamura M, Abe Y, Fukuchi Y, Yoshimura M, Itoh M, Ohnishi Y, Tokunaga T, Fukushima Y, Hatanaka H, Kijima H, Yamazaki H, Tamaoki N, Ueyama Y
Department of Pathology, Tokai University School of Medicine, Kanagawa, Japan.
Eur J Cancer. 1998 Nov;34(12):1958-61. doi: 10.1016/s0959-8049(98)00236-6.
Granulocyte-macrophage colony-stimulating factor (GM-CSF) has been suggested to be 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.
粒细胞-巨噬细胞集落刺激因子（GM-CSF）已被认为通过自分泌或旁分泌机制参与某些类型肿瘤的致癌过程。我们检测了20个人类非小细胞肺癌（NSCLC）异种移植物中GM-CSF/GM-CSF受体（GM-CSFR）基因的表达。使用产生大量人GM-CSF的GM-CSF转基因严重联合免疫缺陷（SCID）小鼠（GM-Tg-SCID）检测GM-CSF的刺激作用。一种NSCLC异种移植物（LC11-JCK）表达GM-CSFR但不表达GM-CSF，并且在GM-Tg-SCID小鼠中比非GM-CSF转基因SCID小鼠（非Tg-SCID）生长更快。在90例原发性NSCLC人类标本中的48例（53%）检测到GM-CSF基因表达，在42例标本（47%）中检测到GM-CSFR基因表达。在30例鳞状细胞癌标本中的13例（43%）检测到GM-CSF表达，在10例标本（33%）中检测到GM-CSFR表达。同时表达GM-CSF和GM-CSFR的鳞状细胞癌患者的预后明显比既不表达GM-CSF也不表达GM-CSFR的患者差（P < 0.05，Cox-Mantel检验）。这些结果表明GM-CSF对某些NSCLC可能具有刺激作用。
