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Despite recent advances in cancer screening; new radiotherapy techniques; and chemotherapies, including targeted agents, metastasis is the primary cause of death in cancer patients [1]. Systemic inflammatory responses have gained attention as a prognostic indicator in cancer patients, and an increasing number of reports focusing on leukocytosis, neutrophilia, thrombocytosis, the neutrophil-lymphocyte ratio, or the platelet-lymphocyte ratio have been published in the past 10 years [2, 3]. Tumor-related leukocytosis (TRL) is a paraneoplastic syndrome, which is occasionally (10-15%) encountered in cancer patients, and it is associated with a poor prognosis [4, 5]. In studies of uterine cervical cancer, we have previously demonstrated that the granulocyte-colony stimulating factor (G-CSF) produced by tumor cells causes TRL and that myeloidderived suppressor cells (MDSC) are responsible for the rapidly growing and radio/chemo-resistant natures of TRL-positive cancer [4, 5]. MDSC, which are immature myeloid cells that exhibit immunosuppressive activity, are key components of the tumor microenvironment. Accumulating evidence suggests that MDSC promote cancer progression by suppressing anti-tumor immune responses and stimulating tumor cell proliferation, epithelial-mesenchymal transition, cancer stem cell formation, and angiogenesis [6]. Thus, MDSC are now regarded as an important therapeutic target for cancer treatment as well as a predictive biomarker of treatment outcomes. Although previous case series have highlighted the aggressive nature of TRL-positive cancer [7], the metastatic potential of TRL-positive cancer as well as the role of MDSC in the metastatic processes of gynecological cancers remain to be elucidated. Recently, we demonstrated, for the first time, that uterine cervical and endometrial cancers that display TRL or neutrophilia represent a distinct clinical entity with a highly metastatic nature [8]. Preclinical findings obtained in mouse models of cervical cancer and studies involving patient-derived samples have suggested that this highly metastatic nature might be the result of tumorderived G-CSF, G-CSF-induced MDSC, and MDSCmediated premetastatic niche formation. In the current study, to mimic the clinical setting found in cases of TRLpositive cancer, we employed a mouse model bearing G-CSF expressing cervical cancer cells and found that the MDSC in premetastatic lungs secreted Bv8, matrix metalloproteinase-9, and S100A8/A9. Moreover, we demonstrated that the MDSC in premetastatic lungs secreted the proinflammatory chemokine, chemokine (C-X-C motif) ligand 2 (CXCL2), which attracted C-X-C motif chemokine receptor 2 (CXCR2)-expressing cancer cells. This indicated that the MDSC induced by tumorderived G-CSF contribute to the metastatic process Editorial

Premetastatic niche and tumor-related leukocytosis: a close relationship that cannot be ignored in uterine cancer patients