Effect of the lymphocyte-to-monocyte ratio on the clinical outcome of chemotherapy administration in advanced melanoma patients.
Skin cancer affects more individuals in the USA than any other malignancy and malignant melanoma is particularly deadly because of its metastatic potential. Melanoma has been recognized as one of the most immunogenic malignancies; therefore, understanding the mechanisms of tumor-immune interaction is key for developing more efficient treatments. As the tumor microenvironment shows an immunosuppressive action, immunotherapeutic agents promoting endogenous immune response to cancer have been tested (interleukin-2, anticytotoxic-T-lymphocyte-associated antigen 4, and antiprogrammed cell death protein 1 monoclonal antibodies) as well as combinations of cytotoxic chemotherapy agents and inhibitors of angiogenesis (taxol/carboplatin/avastin). However, clinical outcomes are variable, with only a minority of patients achieving durable complete responses. The variability of immune homeostasis, which may be more active or more tolerant at any given time, in cancer patients and the interaction of the immune system with the tumor could explain the inconsistency in clinical outcomes among these patients. Recently, the role of the lymphocyte-to-monocyte-ratio (LMR) in the peripheral blood has been investigated and has been proven to be an independent predictor of survival in different hematological malignancies and in solid tumors. In melanoma, our group has validated the significance of LMR as a predictor of relapse after resection of advanced melanoma. In this study, we examined the dynamics in the immune system of patients with advanced melanoma by performing serial multiday concentration measurements of cytokines and immune cell subsets in the peripheral blood. The analysis of outcomes of chemotherapy administration as related to LMR on the day of treatment initiation showed that progression-free survival was improved in the patients who received chemotherapy on the day when LMR was elevated.
aDepartment of Health Science Research, Division of Biomedical Statistics and Informatics bDepartment of Medical Oncology cDepartment of Hematology, Mayo Clinic, Rochester, Minnesota, USA.
Alexey A
AA
Leontovich
Roxana S
RS
Dronca
Wendy K
WK
Nevala
Michael A
MA
Thompson
Lisa A
LA
Kottschade
Leonid V
LV
Ivanov
Svetomir N
SN
Markovic
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000465:Algorithms; D018906:Antineoplastic Agents, Alkylating / Q000008:administration & dosage*; D039521:CD11c Antigen / Q000378:metabolism; D017252:CD3 Complex / Q000378:metabolism; D015704:CD4 Antigens / Q000378:metabolism; D003606:Dacarbazine / Q000008:administration & dosage / Q000031:analogs & derivatives*; D018572:Disease-Free Survival; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000378:metabolism; D018655:Lymphocyte Count; D008214:Lymphocytes / Q000378:metabolism; D008297:Male; D008545:Melanoma / Q000097:blood* / Q000188:drug therapy* / Q000276:immunology; D008875:Middle Aged; D009000:Monocytes; D012189:Retrospective Studies; D012878:Skin Neoplasms / Q000097:blood* / Q000188:drug therapy* / Q000276:immunology; D000077204:Temozolomide; D013997:Time Factors; D016896:Treatment Outcome
D018906:Antineoplastic Agents, Alkylating; D039521:CD11c Antigen; D017252:CD3 Complex; D015704:CD4 Antigens; D018950:Lipopolysaccharide Receptors; D003606:Dacarbazine; D000077204:Temozolomide