非小细胞肺癌肿瘤进展的副肿瘤样白血病反应

Caroline E. McCoach , Jessica G. Rogers , Denis M. Dwyre , Brian A. Jonas
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引用次数: 12

摘要

副肿瘤白血病反应(PLR)是一种描述良好的实体,其中白细胞计数扩大到大于50,000/mm3,与恶性肿瘤相关。它被认为发生在大约10-15%的癌症中。值得注意的是,已知PLR可预测预后不良。最近的研究表明,由肿瘤内粒细胞集落模拟因子(G-CSF)、RAS/RAF/MEK通路激活的PLR可能与肿瘤发生有关。具体来说,RAS/RAF/MEK通路的激活被认为可以调节G-CSF的产生,而G-CSF反过来又可以介导产生促进肿瘤转移因子的细胞的扩增和动员。方法/结果在本报告中,我们展示了非小细胞肺癌患者对治疗的PLR反应。此外,我们发现患者血清中G-CSF升高507 pg/ml (0-39.1 pg/ml),患者肿瘤组织中G-CSF免疫组化染色呈阳性。最后,我们描述了一种促进肿瘤扩散的可能途径。虽然G-CSF传统上被视为预后标志物,但在这里,我们提供的证据表明,它可能是一个有价值的标志物,可以在细胞水平上研究治疗反应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Paraneoplastic leukemoid reaction as a marker of tumor progression in non-small cell lung cancer

Background

Paraneoplastic leukemoid reaction (PLR) is a well-described entity in which the white blood cell count expands to greater than 50,000/mm3 in association with malignancy. It is thought to occur in approximately 10–15% of cancers. Notably, PLR is known to be predictive of a poor prognosis. Recent work has demonstrated that there may be a relationship between PLR activated by intratumoral production of granulocyte colony-simulating factor (G-CSF), the RAS/RAF/MEK pathway and tumorogenesis. Specifically, activation of the RAS/RAF/MEK pathway is thought to regulate G-CSF production, which in turn, mediates expansion and mobilization of cells that produce factors that promote tumor metastasis.

Methods/results

In this report we demonstrate the PLR response to treatment in a patient with non-small cell lung cancer. Additionally, we demonstrate elevated G-CSF in the patient׳s serum 507 pg/ml (0–39.1 pg/ml) and positive staining by immunohistochemistry of G-CSF in the patient׳s tumor tissue. Finally, we describe a possible pathway by which this promotes tumor spread.

Conclusion

Though G-CSF has been traditionally viewed as a prognostic marker, here we provide evidence that it may be a valuable marker to investigate for treatment response at a cellular level.

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