TY - JOUR
T1 - Paraneoplastic leukemoid reaction as a marker of tumor progression in non-small cell lung cancer
AU - McCoach, Caroline E.
AU - Rogers, Jessica G.
AU - Dwyre, Denis M
AU - Jonas, Brian
PY - 2015
Y1 - 2015
N2 - 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[U+05F3]s serum 507. pg/ml (0-39.1. pg/ml) and positive staining by immunohistochemistry of G-CSF in the patient[U+05F3]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.
AB - 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[U+05F3]s serum 507. pg/ml (0-39.1. pg/ml) and positive staining by immunohistochemistry of G-CSF in the patient[U+05F3]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.
KW - G-CSF
KW - Lung cancer
KW - Paraneoplastic leukemoid reaction
KW - RAS/RAF/MEK
KW - Tumorigenesis
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U2 - 10.1016/j.ctrc.2015.03.003
DO - 10.1016/j.ctrc.2015.03.003
M3 - Article
AN - SCOPUS:84947918818
VL - 4
SP - 15
EP - 18
JO - Cancer Treatment and Research Communications
JF - Cancer Treatment and Research Communications
SN - 2213-0896
ER -