Evaluation of CXCL10 as a novel serum marker for predicting liver metastasis and prognosis in colorectal cancer

Toiyama, Yuji; Fujikawa, Hiroyuki; Kawamura, Mikio; Matsushita, Kohei; Saigusa, Susumu; Inoue, Yasuhiro; Uchida, Keiji; Mohri, Yasuhiko; Kusunoki, Masato

doi:10.3892/ijo.2011.1247

Cited by 52 publications

(51 citation statements)

References 35 publications

(40 reference statements)

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“…IP-10 featured in all disease comparison panels for diagnosis, consisitent with a previous small study in PDAC [32] and a study in colorectal cancer [33]. Increased expression of IP-10 and its receptor CXCR3 have also been associated with several advanced human cancers, including ovarian cancer, malignant melanoma, mutliple myeloma and basal cell carcinoma [34].…”

Section: Discussionmentioning

confidence: 61%

Serum cytokine biomarker panels for discriminating pancreatic cancer from benign pancreatic disease

et al. 2014

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BackgroundWe investigated whether combinations of serum cytokines, used with logistic disease predictor models, could facilitate the detection of pancreatic ductal adenocarcinoma (PDAC).MethodsThe serum levels of 27 cytokines were measured in 241 subjects, 127 with PDAC, 49 with chronic pancreatitis, 20 with benign biliary obstruction and 45 healthy controls. Samples were split randomly into independent training and test sets. Cytokine biomarker panels were selected by identifying the top performing cytokines in best fit logistic regression models during multiple rounds of resampling from the training dataset. Disease prediction by logistic models, built using the resulting cytokine panels, was evaluated with training and test sets and further examined using resampled performance evaluation.ResultsFor the discrimination of PDAC patients from patients with benign disease, a panel of IP-10, IL-6, PDGF plus CA19-9 offered improved diagnostic performance over CA19-9 alone in the training (AUC 0.838 vs. 0.678) and independent test set (AUC 0.884 vs. 0.798). For the discrimination of PDAC from CP, a panel of IL-8, CA19-9, IL-6 and IP-10 offered improved diagnostic performance over CA19-9 alone with the training (AUC 0.880 vs. 0.758) and test set (AUC 0.912 vs. 0.848). Finally, for the discrimination of PDAC in the presence of jaundice from benign controls with jaundice, a panel of IP-10, IL-8, IL-1b and PDGF demonstrated improvement over CA19-9 in the training (AUC 0.810 vs. 0.614) and test set (AUC 0.857 vs. 0.659).ConclusionsThese findings support the potential role for cytokine panels in the discrimination of PDAC from patients with benign pancreatic diseases and warrant additional study.

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Section: Discussionmentioning

confidence: 61%

Serum cytokine biomarker panels for discriminating pancreatic cancer from benign pancreatic disease

et al. 2014

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“…Previous studies reported tumour-promoting as well as antimalignant functions of CXCL10 (5,12–14,19). However, the expression profile of CXCL10 in CRC patients has not been fully evaluated.…”

Section: Discussionmentioning

confidence: 90%

Protein expression and gene polymorphism of CXCL10 in patients with colorectal cancer

et al. 2014

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Chemokines (chemotactic cytokines) promote leukocyte attraction to sites of inflammation and cancer. Certain chemokines promote and regulate neoplastic progression, including metastasis and angiogenesis. One such chemokine, CXCL10, was found to be expressed in colorectal cancer (CRC) tissue. To gain insight into the prognostic significance of CXCL10, we investigated whether the levels of this chemokine were altered in the colorectal tissue or plasma of CRC patients. Using Luminex technology for protein analyses, we observed a significantly higher CXCL10 protein level in cancer tissue compared to that in paired normal tissue. Moreover, significantly higher plasma levels of CXCL10 were detected in patients compared to those in control subjects and the plasma levels of CXCL10 in disseminated disease were found to be significantly higher compared to those in localized disease. The single-nucleotide polymorphism rs8878, which has been described in exon 4 in the 3′-untranslated region of the CXCL10 gene, was investigated using a TaqMan system. There were significant differences in genotype distribution and allelic frequencies between CRC patients and control subjects. In conclusion, altered CXCL10 protein concentrations in CRC tissues or plasma and the rs8878 genotype variant of CXCL10 may contribute to the prediction of clinical outcome.

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“…This is not surprising because our sample size is relatively small and accumulating evidence has shown complex effects of cytokines in the tumor microenvironment, ranging from support to inhibition of tumor growth (23,45). IL1 and TNFα can be highly inflammatory in the tumor microenvironment and facilitate tumor growth, angiogenesis, and metastasis (27).…”

Section: Discussionmentioning

confidence: 93%

VEGF Neutralization Plus CTLA-4 Blockade Alters Soluble and Cellular Factors Associated with Enhancing Lymphocyte Infiltration and Humoral Recognition in Melanoma

Giobbie‐Hurder

Liao

et al. 2016

Cancer Immunology Research

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Immune recognition of tumor targets by specific cytotoxic lymphocytes is essential for the effective rejection of tumors. A phase I clinical trial of ipilimumab (an antibody that blocks CTLA-4 function) in combination with bevacizumab (an antibody that inhibits angiogenesis) in patients with metastatic melanoma found favorable clinical outcomes were associated with increased tumor endothelial activation and lymphocyte infiltration. To better understand the underlying mechanisms, we sought features and factors that changed as a function of treatment in patients. Ipilimumab plus bevacizumab (Ipi-Bev) increased tumor vascular expression of ICAM-1 and VCAM-1. Treatment also altered concentrations of many circulating cytokines and chemokines, including increases of IP-10, IL1α, TNFα, GRO, IFNα2, and IL8, with decreases in VEGF-A in most patients. IL1α and TNFα induced expression of E-selectin, ICAM-1, and VCAM-1 on melanoma tumor-associated endothelial cells (TEC) in vitro and promoted adhesion of activated T cells onto TEC. VEGF-A inhibited TNFα-induced expression of ICAM-1 and VCAM-1 and T-cell adhesion, which was blocked by bevacizumab. IP-10 promoted T-cell migration across TEC in vitro, was frequently expressed by melanoma cells, and was upregulated in a subset of tumors in treated patients. Robust upregulation of IP-10 in tumors was accompanied by increased T-cell infiltration. Ipi-Bev also augmented humoral immune responses recognizing targets in melanoma, tumor endothelial, and tumor mesenchymal stem cells. Our findings suggest that Ipi-Bev therapy augments immune recognition in the tumor microenvironment through enhancing lymphocyte infiltration and antibody responses. IL1α, TNFα, and IP-10, together with VEGF neutralization, contribute to Ipi-Bev–induced melanoma immune recognition.

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Evaluation of CXCL10 as a novel serum marker for predicting liver metastasis and prognosis in colorectal cancer

Cited by 52 publications

References 35 publications

Serum cytokine biomarker panels for discriminating pancreatic cancer from benign pancreatic disease

Serum cytokine biomarker panels for discriminating pancreatic cancer from benign pancreatic disease

Protein expression and gene polymorphism of CXCL10 in patients with colorectal cancer

VEGF Neutralization Plus CTLA-4 Blockade Alters Soluble and Cellular Factors Associated with Enhancing Lymphocyte Infiltration and Humoral Recognition in Melanoma

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