Interleukin-17A Modulates Circulating Tumor Cells in Tumor Draining Vein of Colorectal Cancers and Affects Metastases

Tseng, Ju Yu; Yang, Chung‐May; Liang, Shu Ching; Liu, Ru‐Shi; Yang, Shung Haur; Lin, Jen Kou; Chen, Yuh Min; Wu, Yu Chung; Jiang, Jeng Kai; Lin, Chi

doi:10.1158/1078-0432.ccr-13-2162

Cited by 49 publications

(54 citation statements)

References 52 publications

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“…However, IL17A is associated with protumorigenic effects. Elimination of IL17A in a colon cancer mouse model reduced tumor development and the number of circulating tumor cells, it prevented metastases and decreased the expression of several inflammatory cytokines, such as IL6, IL1b, and COX2 (51,52). Treatment of colon cancer cells with IL17A increased the expression of MMP9 and tumor cell mobility (52).…”

Section: Il17mentioning

confidence: 99%

“…IL6 is additionally associated with increased tumor size, tumor stage, metastases, and decreased survival (39). IL17A levels also positively correlate with tumor size (70), the percentage of circulating tumor cells, and risk of recurrence (52). IL17F is, however, not detected in the serum of patients with colorectal cancer (70), whereas higher serum levels of IL8 are observed in patients with stage IV colorectal cancer compared with stage II and stage III patients (28,47).…”

Section: Inflammation and Vitamin D In Patients With Colorectal Cancermentioning

confidence: 99%

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Vitamin D, Inflammation, and Colorectal Cancer Progression: A Review of Mechanistic Studies and Future Directions for Epidemiological Studies

Harten-Gerritsen

Balvers

Witkamp

et al. 2015

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Survival from colorectal cancer is positively associated with vitamin D status. However, whether this association is causal remains unclear. Inflammatory processes may link vitamin D to colorectal cancer survival, and therefore investigating inflammatory markers as potential mediators may be a valuable next step. This review starts with an overview of inflammatory processes suggested to be involved in colorectal cancer progression and regulated by vitamin D. Next, we provide recommendations on how to study inflammatory markers in future epidemiologic studies on vitamin D and colorectal cancer survival. Mechanistic studies have shown that calcitriol-active form of vitamin Dinfluences inflammatory processes involved in cancer progression, including the enzyme cyclooxygenase 2, the NF-kB pathway, and the expression of the cytokines TNFa, IL1b, IL6, IL8, IL17, and TGFb1. Based on this and taking into account methodologic issues, we recommend to include analysis of specific soluble peptides and proteins, such as cytokines, in future epidemiologic studies on this issue. Vitamin D and the markers should preferably be measured at multiple time points during disease progression or recovery and analyzed using mediation analysis. Including these markers in epidemiologic studies may help answer whether inflammation mediates a causal relationship between vitamin D and colorectal cancer survival. Cancer Epidemiol Biomarkers Prev; 24(12); 1820-8. Ó2015 AACR.

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Section: Il17mentioning

confidence: 99%

Section: Inflammation and Vitamin D In Patients With Colorectal Cancermentioning

confidence: 99%

Vitamin D, Inflammation, and Colorectal Cancer Progression: A Review of Mechanistic Studies and Future Directions for Epidemiological Studies

Harten-Gerritsen

Balvers

Witkamp

et al. 2015

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Potential risks of bias identified in categorizing IL-17 or Th17 expression were optimal cut-off values chosen arbitrarily 15,16 or using a minimum p value, 17-23 receiver operating characteristic (ROC) curve [24][25][26][27] or regression tree analysis. 28 Furthermore, one study compared the six long (>3 y) vs. short (<1.5 y) surviving patients.…”

Section: Study Design and Selection Criteriamentioning

confidence: 99%

The correlations between IL-17 vs. Th17 cells and cancer patient survival: a systematic review

et al. 2015

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Both IL-17 and Th17 cells have been ascribed tumor promoting as well as tumor suppressing functions. We reviewed the literature on correlations between IL-17 versus Th17 cells and survival in human cancer, following the PRISMA guidelines. Serum, formalin-fixed, paraffin-embedded (FFPE) tissue and peripheral blood samples were most frequently studied. High IL-17 quantities were correlated with poor prognosis, whereas high Th17 cell frequencies were correlated with improved prognosis. Since Th17 cells are a subpopulation of IL-17 cells and had a different correlation with prognosis than total IL-17, we substantiate that a distinction should be made between Th17 and other IL-17 cells.

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“…Moreover, the CRC cell lines currently available cannot represent the vast heterogeneity of CRC. Therefore, we require experimental models which mimic human CRC distant metastases as end-points [24]. This further demonstrates the predictive value and practicability of the model.…”

Section: Colorectal Cancermentioning

confidence: 88%

Mouse Models of Colorectal Cancer-Derived Circulating Tumor Cells

Nanduri¹,

García²

2016

Med chem (Los Angeles)

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Metastasis is the major cause of death in colorectal cancer (CRC) patients. Circulating tumor cells (CTCs) are the biologic correlate of metastasis. Despite the clinical relevance of CTCs, there has been little progress in understanding their biology in detail; particularly the phenotype of CTCs with metastasis-forming capacities is still unknown. In this article we discuss the benefits and limitations of mouse models of CRC-derived CTCs. Keywords: Colorectal cancer; Tumor cells; Metastasis; Primary tumor Colorectal CancerColorectal cancer (CRC) is one of the most common tumor diseases [1] and has high mortality and morbidity rates especially in metastatic stages [2]. The vast majority of CRC-related deaths are due to distant metastases, most prominently to the liver, rather than the primary tumor [2]. Metastasis is a multi-step process during which the cells develop a migratory phenotype and detach from the primary tumor, invade the local vasculature and survive in circulation, extravasate into distant organs and finally outgrow to manifest metastatic lesions [3,4]. The presence of circulating tumor cells (CTCs) in the blood stream of the patients indicates metastatic activity and is a negative prognostic factor in all stages of CRC [5][6][7][8][9][10].Metastatic dissemination is a dynamic process requiring dramatic phenotypic alterations in order for the tumor cells to survive the challenges posed in circulation and by the microenvironment at the distant metastatic sites. Hence, CTCs require a considerable degree of plasticity in order to successfully complete the process of metastasis. As distant metastases are generally phenotypically similar to the primary tumor [11], most of these phenotypic changes must be reversible. Prominent examples of this plasticity are epithelial-to-mesenchymal transition (EMT), which CTCs undergo to gain a migratory phenotype by down-regulation of epithelial markers (E-cadherin, EpCAM) and upregulation of mesenchymal markers (N-cadherin, vimentin); and mesenchymal-to-epithelial transition (MET) in the target organ, ultimately resulting in epithelial metastases [12][13][14][15][16][17].Although tumors shed millions of CTCs into circulation [18], in most patients only a few metastases arise during the course of the disease. Therefore, it is conceivable that only a very small fraction of CTCs is actually capable of forming distant metastases. It is these few CTCs with metastasis-forming capacities which must be identified and characterized in order to conceive novel anti-metastatic therapeutics. The phenotype of metastasis-forming CTCs has already been narrowed down in breast cancer-derived CTCs [19]; however, tens of thousands of cells had to be screened and thousands of metastasis-forming CTCs had to be injected into mice in order to induce metastases in these animals. As CTCs are a much rarer event in CRC than in breast cancer, such an approach seems hardly possible in CRC. Additionally, the still rather large amount of CTCs needed to induce tumors in mice indicates the ...

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Interleukin-17A Modulates Circulating Tumor Cells in Tumor Draining Vein of Colorectal Cancers and Affects Metastases

Cited by 49 publications

References 52 publications

Vitamin D, Inflammation, and Colorectal Cancer Progression: A Review of Mechanistic Studies and Future Directions for Epidemiological Studies

Vitamin D, Inflammation, and Colorectal Cancer Progression: A Review of Mechanistic Studies and Future Directions for Epidemiological Studies

The correlations between IL-17 vs. Th17 cells and cancer patient survival: a systematic review

Mouse Models of Colorectal Cancer-Derived Circulating Tumor Cells

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