Caroline E. McCoach , Jessica G. Rogers , Denis M. Dwyre , Brian A. Jonas
{"title":"非小细胞肺癌肿瘤进展的副肿瘤样白血病反应","authors":"Caroline E. McCoach , Jessica G. Rogers , Denis M. Dwyre , Brian A. Jonas","doi":"10.1016/j.ctrc.2015.03.003","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Paraneoplastic leukemoid reaction (PLR) is a well-described entity in which the white blood cell count expands to greater than 50,000/mm<sup>3</sup> 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.</p></div><div><h3>Methods/results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>","PeriodicalId":90461,"journal":{"name":"Cancer treatment communications","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.ctrc.2015.03.003","citationCount":"12","resultStr":"{\"title\":\"Paraneoplastic leukemoid reaction as a marker of tumor progression in non-small cell lung cancer\",\"authors\":\"Caroline E. McCoach , Jessica G. Rogers , Denis M. Dwyre , Brian A. Jonas\",\"doi\":\"10.1016/j.ctrc.2015.03.003\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><h3>Background</h3><p>Paraneoplastic leukemoid reaction (PLR) is a well-described entity in which the white blood cell count expands to greater than 50,000/mm<sup>3</sup> 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.</p></div><div><h3>Methods/results</h3><p>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.</p></div><div><h3>Conclusion</h3><p>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.</p></div>\",\"PeriodicalId\":90461,\"journal\":{\"name\":\"Cancer treatment communications\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2015-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1016/j.ctrc.2015.03.003\",\"citationCount\":\"12\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer treatment communications\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S2213089615000109\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer treatment communications","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2213089615000109","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.