<p>Dynamic impact of inflammation-based indices in colorectal cancer patients receiving FOLFOX-based chemotherapy</p>

Abstract

Background: Inflammatory cellular response is implicated in the pathogenesis of colorectal cancer (CRC). Nevertheless, the dynamic effects of inflammatory index coNLR (neutrophil-to-lymphocyte ratio)-PLR (platelet-to-lymphocyte ratio) during chemotherapy remain elusive. Methods: The baseline clinical data and laboratory parameters of 480 CRC patients who received palliative resection of primary tumors and FOLFOX-based chemotherapy from January 2007 to January 2013 were retrospectively analyzed. Receiver operating characteristic curves were plotted to obtain the predictive NLR and PLR values, and to calculate the coNLR-PLR score. The Kaplan–Meier method was used to estimate the rates of recurrence-free survival (RFS) and overall survival (OS), and the Cox proportional hazards model was employed for analysis. Results: The dynamic cut-off values of NLR during four periods of chemotherapy were 3.029, 2.466, 2.102 and 1.795, respectively, and those of PLR were 216.438, 187.572, 169.027 and 174.368, respectively. A higher coNLR-PLR was significantly associated with lower rates of RFS and OS ( P <0.05). Both univariate and multivariate analyses showed that coNLR-PLR was a significant independent prognostic factor for RFS and OS ( P <0.05). Conclusions: CoNLR-PLR was a significant prognostic predictor for CRC patients who received FOLFOX-based chemotherapy. Evaluating this index can accurately predict the clinical treatment outcomes after chemotherapy.

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“…Inflammation is involved in multiple different stages of tumor development, including the initiation, promotion and migration (40,41). In previous studies, the expression levels of COX-2 were reported to be significantly overexpressed in patients with glioma, positively correlated with glioma malignancy and negatively correlated with prognosis (19,20).…”

A novel molecular subtypes and risk model based on inflammatory response-related lncrnas for bladder cancer

“…Unfortunately, continuous inflammatory stimulation can lead to chronic inflammation, poor tissue regeneration, tumorigenesis, and metastasis [5]. Pro-inflammatory cytokines are released by tumor-associated inflammatory cells, such as IL-1, IL-6, TNF, and VEGF, which further influences the tumor progression and metastasis [6,7]. Besides, inflammation has an osculating link with the development and malignant progression of most cancers by regulating DNA damage and repair, p53 mutation, chemokines, and soon [8].…”