全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

Circulating CCL5 Levels in Patients with Breast Cancer: Is There a Correlation with Lymph Node Metastasis?

DOI: 10.1155/2013/453561

Full-Text   Cite this paper   Add to My Lib

Abstract:

CC-chemokine ligand 5 (CCL5) was measured in plasma of 238 patients with breast cancer and in serum of 149 of these patients. Mean circulating CCL5 levels tended to be higher in patients with lymph-node-positive breast cancer, larger tumour sizes, the presence of lymphovascular invasion, and multifocal tumours. Additionally, circulating CCL5 levels were higher in the order of stages III, II, and I. The addition of circulating CCL5 concentration to known clinicopathological predictors for lymph node involvement did not allow more precise prediction of the lymph node status. These results suggest that CCL5 is a biomarker for tumour load rather than for lymph node involvement. As such, it might be helpful to identify patients with escape from immunosurveillance who will benefit from therapies to restore immune function. 1. Introduction CC-chemokine ligand 5 (CCL5), previously called RANTES (Regulated on Activation, Normal T cell Expressed and Secreted), belongs to the family of the CC chemokines. The major role of chemokines is to act as chemoattractants to guide the migration of cells. Some chemokines control cells of the immune system during processes of immune surveillance. Others are inflammatory and mainly attract leukocytes to sites of inflammation and/or infection. Their release is stimulated by pro-inflammatory cytokines. Thus, chemokines coordinate intricate leukocyte trafficking patterns that regulate immune responses against cancer. These are multistep processes that involve localization of immune effectors to appropriate sites, antigen presentation, and optimal triggering of specific T cells. It is increasingly clear that cancer-mediated modulation of the host immune response contributes to tumour progression and correlates with patient outcome [1]. Indeed, tumours can evade immunosurveillance through altering the properties and functions of host stromal and/or immune cells. They polarize the tumour microenvironment towards chronic inflammatory states, leading to impaired tumor cell killing and to tumour escape. The exact functions of CCL5 in tumour biology are still unclear. On the one hand, CCL5 is important to trigger and amplify the anti-tumour host response. Besides its role as a potent chemoattractant, CCL5 plays an important role in T-cell responses. Therefore, production of CCL5 is important for inducing proper immune responses against tumours [2]. On the other hand, it has been reported that CCL5 is associated with cancer progression and metastasis because it promotes tumour cell survival, proliferation, and invasion [3]. CCL5 can be

References

[1]  N. S. Zuckerman, H. Yu, D. L. Simons, et al., “Altered local and systemic immune profiles underlie lymph node metastasis in breast cancer patients,” International Journal of Cancer, vol. 132, no. 11, pp. 2537–2547, 2013.
[2]  Y. Nesbeth, U. Scarlett, J. Cubillos-Ruiz et al., “CCL5-mediated endogenous antitumor immunity elicited by adoptively transferred lymphocytes and dendritic cell depletion,” Cancer Research, vol. 69, no. 15, pp. 6331–6338, 2009.
[3]  N. Lapteva and X. F. Huang, “CCL5 as an adjuvant for cancer immunotherapy,” Expert Opinion on Biological Therapy, vol. 10, no. 5, pp. 725–733, 2010.
[4]  M. Velasco-Velazquez, X. Jiao, M. de la Fuente, et al., “CCR5 antagonist blocks metastasis of basal breast cancer cells,” Cancer Research, vol. 72, no. 15, pp. 3839–3850, 2012.
[5]  Y. Niwa, H. Akamatsu, H. Niwa, H. Sumi, Y. Ozaki, and A. Abe, “Correlation of tissue and plasma RANTES levels with disease course in patients with breast or cervical cancer,” Clinical Cancer Research, vol. 7, no. 2, pp. 285–289, 2001.
[6]  H. K. Kim, K. S. Song, Y. S. Park et al., “Elevated levels of circulating platelet microparticles, VEGF, IL-6 and RANTES in patients with gastric cancer: possible role of a metastasis predictor,” European Journal of Cancer, vol. 39, no. 2, pp. 184–191, 2003.
[7]  S. Tsukishiro, N. Suzumori, H. Nishikawa, A. Arakawa, and K. Suzumori, “Elevated serum RANTES levels in patients with ovarian cancer correlate with the extent of the disorder,” Gynecologic Oncology, vol. 102, no. 3, pp. 542–545, 2006.
[8]  S. Lin, S. Wan, L. Sun, et al., “Chemokine C-C motif receptor 5 and C-C motif ligand 5 promote cancer cell migration under hypoxia,” Cancer Science, vol. 103, no. 5, pp. 904–912, 2012.
[9]  G. Luboshits, S. Shina, O. Kaplan et al., “Elevated expression of the CC chemokine regulated on activation, normal T cell expressed and secreted (RANTES) in advanced breast carcinoma,” Cancer Research, vol. 59, no. 18, pp. 4681–4687, 1999.
[10]  Y. Zhang, F. Yao, X. Yao et al., “Role of CCL5 in invasion, proliferation and proportion of CD44+/CD24- phenotype of MCF-7 cells and correlation of CCL5 and CCR5 expression with breast cancer progression,” Oncology Reports, vol. 21, no. 4, pp. 1113–1121, 2009.
[11]  N. Yaal-Hahoshen, S. Shina, L. Leider-Trejo et al., “The chemokine CCL5 as a potential prognostic factor predicting disease progression in stage II breast cancer patients,” Clinical Cancer Research, vol. 12, no. 15, pp. 4474–4480, 2006.
[12]  E. J. Duell, D. P. Casella, R. D. Burk, K. T. Kelsey, and E. A. Holly, “Inflammation, genetic polymorphisms in proinflammatory genes TNF-A, RANTES, and CCR5, and risk of pancreatic adenocarcinoma,” Cancer Epidemiology Biomarkers and Prevention, vol. 15, no. 4, pp. 726–731, 2006.
[13]  L. Y. Chang, Y. C. Lin, J. Mahalingam, et al., “Tumor-derived chemokine CCL5 enhances TGF-beta-mediated killing of CD8(+) T cells in colon cancer by T-regulatory cells,” Cancer Research, vol. 72, no. 5, pp. 1092–1102, 2012.
[14]  B. Cambien, P. Richard-Fiardo, B. F. Karimdjee, et al., “CCL5 neutralization restricts cancer growth and potentiates the targeting of PDGFRbeta in colorectal carcinoma,” PLoS One, vol. 6, no. 12, article e28842, 2011.
[15]  G. G. Vaday, D. M. Peehl, P. A. Kadam, and D. M. Lawrence, “Expression of CCL5 (RANTES) and CCR5 in prostate cancer,” Prostate, vol. 66, no. 2, pp. 124–134, 2006.
[16]  J. Y. Chuang, W. H. Yang, H. T. Chen et al., “CCL5/CCR5 axis promotes the motility of human oral cancer cells,” Journal of Cellular Physiology, vol. 220, no. 2, pp. 418–426, 2009.
[17]  J. Kanterman, M. Sade-Feldman, and M. Baniyash, “New insights into chronic inflammation-induced immunosuppression,” Seminars in Cancer Biology, vol. 22, no. 4, pp. 307–318, 2012.
[18]  M. Dougan and G. Dranoff, “Immune therapy for cancer,” Annual Review of Immunology, vol. 27, pp. 83–117, 2009.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133