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Chemokine Expression in Melanoma Metastases Associated with CD8+ T-Cell Recruitment
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Abstract
Despite the frequent detection of circulating tumor antigen-specific T cells, either spontaneously or following active immunization or adoptive transfer, immune-mediated cancer regression occurs only in the minority of patients. One theoretical rate-limiting step is whether effector T cells successfully migrate into metastatic tumor sites. Affymetrix gene expression profiling done on a series of metastatic melanoma biopsies revealed a major segregation of samples based on the presence or absence of T-cell-associated transcripts. The presence of lymphocytes correlated with the expression of defined chemokine genes. A subset of six chemokines (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10) was confirmed by protein array and/or quantitative reverse transcription-PCR to be preferentially expressed in tumors that contained T cells. Corresponding chemokine receptors were found to be up-regulated on human CD8(+) effector T cells, and transwell migration assays confirmed the ability of each of these chemokines to promote migration of CD8(+) effector cells in vitro. Screening by chemokine protein array identified a subset of melanoma cell lines that produced a similar broad array of chemokines. These melanoma cells more effectively recruited human CD8(+) effector T cells when implanted as xenografts in nonobese diabetic/severe combined immunodeficient mice in vivo. Chemokine blockade with specific antibodies inhibited migration of CD8(+) T cells. Our results suggest that lack of critical chemokines in a subset of melanoma metastases may limit the migration of activated T cells, which in turn could limit the effectiveness of antitumor immunity.
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“Tumors from patients showing sustained treatment response predominately demonstrate a T cell-inflamed tumor microenvironment prior to, or early on, treatment.”
From Reimagining IDO Pathway Inhibition in Cancer Immunotherapy via Downstream Focus on the Tryptophan–Kynurenine–Aryl Hydrocarbon Axis (2019) · cites this paper as [6]
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“Tumor analysis from patients with metastatic melanoma receiving vaccine and cytokine therapies suggested a paradigm of two broad phenotypes characterized by the presence or absence a T cell-inflamed tumor.”
From Reimagining IDO Pathway Inhibition in Cancer Immunotherapy via Downstream Focus on the Tryptophan–Kynurenine–Aryl Hydrocarbon Axis (2019) · cites this paper as [6]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“an effector population shown to be a target of downstream STING signaling involving the IFN-β-CXCL9/10 axis.54–58”
From Functional tumor cell-intrinsic STING, not host STING, drives local and systemic antitumor immunity and therapy efficacy following cryoablation (2023) · cites this paper as [55]
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Citations
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Items 301–400 of 1,000
Primer on tumor immunology and cancer immunotherapy
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Immunotherapy-induced CD8+ T Cells Instigate Immune Suppression in the Tumor
McGray, A. R., Hallett, R. M., Bernard, D., Swift, S. L., Zhu, Z., Teoderascu, F., VanSeggelen, H., Hassell, J. A., Hurwitz, A. A., Wan, Y., et al. (2013) · Molecular Therapy · doi:10.1038/mt.2013.255 · Cited by 75
Gene-expression profiling in vaccine therapy and immunotherapy for cancer
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“In addition, multiple chemokines were associated with the recruitment of T cells into tumor nests [37], and the expression of appropriate chemokines in the TME was critical for effector T cell trafficking into tumor sites [38].”
BackgroundAn essential role for DNA methyltransferase 3a in melanoma tumorigenesis
Deng, T., Kuang, Y., Wang, L., Jiang, L., Wang, Z., & Fei, J. (2009) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2009.07.093 · Cited by 74
Rational combinations of immunotherapeutics that target discrete pathways
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“The underlying mechanisms responsible for lack of a T cell-inflamed tumor microenvironment are not fully understood, but this phenotype correlates with absence of a type I IFN signature and poor chemokine production, suggesting defective innate immune activation and a deficient ability to recruit activated T cells [18…”
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“The increased levels of tumor-infiltrating CD8 T cells correlated with up-regulation of CD8 T cell-attracting chemokines CCL2, CCL3, CCL5, and T helper type 1-related CXCL9, CXCL10, IL-12, and Granzyme B (Figure 2f) (Harlin et al., 2009).”
BackgroundSolid Tumor Immunotherapy with T Cell Engager‐Armed Oncolytic Viruses
Scott, E. M., Duffy, M. R., Freedman, J. D., Fisher, K. D., & Seymour, L. W. (2017) · Macromolecular Bioscience · doi:10.1002/mabi.201700187 · Cited by 76
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Risk factors for immune-related adverse events: what have we learned and what lies ahead?
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ENPP1 Immunobiology as a Therapeutic Target
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“Harlin et al described [6] 10 chemokine genes (CCL2, CCL3, CCL4, CCL5, CCL19, CCL21, CXCL9, CXCL10, CXCL11 and CXCL13) which were found to be expressed by melanoma cells, with some of their corresponding receptors expressed on tumor infiltrating CD8+ T-cells.”
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“In addition, tumors treated with CpG-NP MNs showed increased expression of leukocyte chemokines, including the monocyte chemoattractant protein 1 (MCP-1) and the C-X-C motif chemokine ligand 1 (CXCL1), and pro-inflammatory cytokines such as interleukin 1 beta (IL-1β) responsible for immune cell recruitment [50] (Figur…”
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“Other features of these hot tumors are their high levels of intratumoral chemokines (CCL5, CXCL9, CXCL10) favoring the recruitment of T cells into the tumor.(16) They express IFNγ supporting the functionality of T lymphocytes.”
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Cytosolic Delivery of Thiolated Mn‐cGAMP Nanovaccine to Enhance the Antitumor Immune Responses
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“promoted the survival and proliferation of tumor-specific T cells by upregulating the expression of survivin and Ifi202.(159)”
BackgroundEnhancing radiotherapy-induced anti-tumor immunity via nanoparticle-mediated STING agonist synergy
Zeng, Q., Liu, M., Wang, Z., Zhou, R., & Ai, K. (2025) · Molecular Cancer · doi:10.1186/s12943-025-02366-y · Cited by 90
“Type I IFN can induce DCs to express a range of ISGs, such as CXCL10, CXCL9, and CCL5, thereby further promoting T cell activation and proliferation [27, 157].”
Combination of radiotherapy and vaccination overcomes checkpoint blockade resistance
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“In addition to the lack of response to checkpoint inhibitors, non-T cell-inflamed melanomas are also characterized by the downregulation of chemokines and other immune markers [5].”
BackgroundCXCR5 guides migration and tumor eradication of anti-EGFR chimeric antigen receptor T cells
Li, G., Guo, J., Zheng, Y., Ding, W. Y., Han, Z., Qin, L., Mo, W., & Luo, M. (2021) · Molecular Therapy — Oncolytics · doi:10.1016/j.omto.2021.07.003 · Cited by 68
“One reason for insufficient recruitment of CAR-T cells to tumor is themismatching of chemokine-chemokine receptor pairs, especially the lack of CXCL9 andCXCL10, the two ligands of chemokine receptor CXCR3 typically expressed on activated T cells.(19,20)Given the criticality of chemokines in lymphocytemigration and hom…”
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“effector cell migration into inflamed tissues (17, 18).”
BackgroundAngiocrine endothelium: from physiology to cancer
Pasquier, J., Ghiabi, P., Chouchane, L., Razzouk, K., Rafii, S., & Rafii, A. (2020) · Journal of Translational Medicine · doi:10.1186/s12967-020-02244-9 · Cited by 68
“CCL2, CCL3, CCL4 CCL5, CXCR9 CXCR10 Tumor immune tolerance All types of tumors [190, 214, 215]”
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Growing tumors induce a local STING dependent Type I IFN response in dendritic cells
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cGAS/STING Pathway in Cancer: Jekyll and Hyde Story of Cancer Immune Response
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“In subset of melanoma metastasis, it was suggested that reduced critical chemokine expressions is a key factor in limiting activated T cell migration and, thereby, effective anti-cancer response [20].”
BackgroundCancer immune exclusion: breaking the barricade for a successful immunotherapy
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Antitumor Activity Mediated by CpG
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Nanoparticle formulation improves doxorubicin efficacy by enhancing host antitumor immunity
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“CCL2–5 and CXCL10, which all trended towards induction with CP-Dox, have been tied to CD8+ T cell recruitment [35].”
Harnessing the cDC1-NK Cross-Talk in the Tumor Microenvironment to Battle Cancer
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“TGF-b decreases chemokine secretion of CXCL2, CX3CL1, and CXCL1 which attract CD56 low and increases chemokine production, which recruit CD56high (CXCL9, CXCL10, CXCL11, and CCL5) (107, 110, 113).”
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Uveal Melanoma, Angiogenesis and Immunotherapy, Is There Any Hope?
Castet, F., García‐Mulero, S., Pamplona, R. S., Cuellar, A., Casanovas, O., Mitjana, J. M. C., & Piulats, J. M. (2019) · Cancers · doi:10.3390/cancers11060834 · Cited by 64
“Indeed, the co-expression of both molecules leads to a high CD8+ T-cell infiltration in cutaneous melanoma [179,180], and upregulation of both CCR5/CXCR3 is associated to greater response to different immunotherapies, including checkpoint inhibitors [181] and adoptive cell therapy [182].”
BackgroundBuilding on dendritic cell subsets to improve cancer vaccines
Palucka, K., Ueno, H., Zurawski, G., Fay, J. W., & Banchereau, J. (2010) · Current Opinion in Immunology · doi:10.1016/j.coi.2010.02.010 · Cited by 62
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“Previous studies by us [19] and others [10,20-25] have shown that intra-tumoral expression of chemokines regulate local levels of CTL infiltration, suggesting that T cell-targeting immunotherapies can benefit from modulating tumor-associated chemokine microenvironments in order to enhance local CTL infiltration.”
Recent advances in understanding antitumor immunity
Munhoz, R. R., & Postow, M. A. (2016) · F1000Research · doi:10.12688/f1000research.9356.1 · Cited by 70
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“significant proportion of melanoma tumors as a consequence of immune exclusion and/or immunologic ignorance (33).”
BackgroundVonderhaar, E. P., Barnekow, N. S., McAllister, D., McOlash, L., Eid, M. A., Riese, M. J., Tarakanova, V. L., Johnson, B. D., & Dwinell, M. B. (2021) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2021.01.018 · Cited by 61
Regulation of cGAS‐Mediated Immune Responses and Immunotherapy
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Radiotherapy to Enhance Chimeric Antigen Receptor T-Cell Therapeutic Efficacy in Solid Tumors
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“Activation of the cGAS / STING pathway and production of immunomodulatory molecules such as INF-α , IL-6, CXCL9 and CXCL10 were described to be involved in the enhanced migration of immune cells in cancer, particularly macrophages, and regulate anti-tumor immune response ( 40 ,41 ).”
BackgroundInfluentialVariation of Tumor-Infiltrating Lymphocytes in Human Cancers: Controversy on Clinical Significance
Sasada, T., & Suekane, S. (2011) · Immunotherapy · doi:10.2217/imt.11.106 · Cited by 60
Cytokines as potential combination agents with PD‐1/PD‐L1 blockade for cancer treatment
Mohammad, G. R. K. S., Ghahremanloo, A., Soltani, A., Fathi, E., & Hashemy, S. I. (2020) · Journal of Cellular Physiology · doi:10.1002/jcp.29491 · Cited by 60
Immune Checkpoint Ligand PD-L1 Is Upregulated in Pulmonary Lymphangioleiomyomatosis
Maisel, K., Merrilees, M. J., Atochina‐Vasserman, E. N., Lian, L., Obraztsova, K., Rue, R. W., Vasserman, A. N., Zuo, N., Angel, L. F., Gow, A. J., et al. (2018) · American Journal of Respiratory Cell and Molecular Biology · doi:10.1165/rcmb.2018-0123oc · Cited by 59
Cancer Immunosurveillance by T Cells
Rao, S., Gharib, K., & Han, A. S. (2018) · International review of cytology · doi:10.1016/bs.ircmb.2018.08.001 · Cited by 60
Choi, H., Kwon, J., Cho, M. S., Sun, Y., Zheng, X., Wang, J., Bouker, K. B., Casey, J. L., Atkins, M. B., Toretsky, J. A., et al. (2021) · Cancer Research · doi:10.1158/0008-5472.can-20-3790 · Cited by 60
“CCL5 is a known T-cell chemoattractant, and it also could recruit T cells to tumors (55).”
BackgroundShah, S. J., Ward, J. E., Bao, R., Hall, C. R., Brockstein, B., & Luke, J. J. (2016) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-16-0087 · Cited by 58
“A more robust approach to tumor microenvironmental evaluation may thus be facilitated by gene expression profiling where an active antitumor immune environment has been coined the "T cell–inflamed tumor microenvironment" (10).”
BackgroundTumor inhibition or tumor promotion? The duplicity of CXCR3 in cancer
Russo, E., Santoni, A., & Bernardini, G. (2020) · Journal of Leukocyte Biology · doi:10.1002/jlb.5mr0320-205r · Cited by 59
Meng, J., Peng, J., Feng, J., Maurer, J., Li, X., Li, Y., Yao, S., Chu, R., Pan, X., Li, J., et al. (2021) · Journal of Translational Medicine · doi:10.1186/s12967-021-03073-0 · Cited by 58
Tumor-infiltrating lymphocytes: apparently good for melanoma patients. But why?
Cipponi, A., Wieërs, G., van Baren, N., & Coulie, P. G. (2011) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-011-1026-2 · Cited by 56
“Gajewski and colleagues identiWed a subset of melanoma cell lines secreting these chemokines and found that these chemokine genes were expressed, together with T-cell genes, in the metastases of vaccinated patients who had a favorable clinical outcome [51].”
BackgroundZhu, Y., Wang, X., Zhang, Y., Xu, D., Dong, J., Zhang, Z., Yi, C., Jia, H., & Yang, X. L. (2018) · Cancer Management and Research · doi:10.2147/cmar.s172719 · Cited by 57
“Accumulating evidence suggests that the presence of antitumor tumor-infiltrating lymphocytes is important for the activity of immunotherapies, including checkpoint blockade.(11,12) Early research showed that a high degree of CD8+ T-cell infiltration in ICC correlated with better prognosis after curative resection, sug…”
Development of adaptive immune effector therapies in solid tumors
Comoli, P., Chabannon, C., Koehl, U., Lanza, F., Urbano-Ispizúa, Á., Hudecek, M., Ruggeri, A., Secondino, S., Bonini, C., & Pedrazzoli, P. (2019) · Annals of Oncology · doi:10.1093/annonc/mdz285 · Cited by 57
Sridaran, D., Chouhan, S., Mahajan, K. N., Renganathan, A., Weimholt, C., Bhagwat, S., Reimers, M. A., Kim, E. H., Thakur, M. K., Saeed, M. A., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-34724-5 · Cited by 59
Tumor Immunogenic Cell Death as a Mediator of Intratumor CD8 T-Cell Recruitment
Roussot, N., Ghiringhelli, F., & Rébé, C. (2022) · Cells · doi:10.3390/cells11223672 · Cited by 55
Sapoznik, S., Ortenberg, R., Galore-Haskel, G., Kozlovski, S., Levy, D., Avivi, C., Barshack, I., Cohen, C. J., Besser, M. J., Schachter, J., et al. (2012) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-012-1245-1 · Cited by 56
“, high expression of CXCR3, moderate CCR5 levels [2, 39, 40], low CCR7 expression confined to naı̈ve cells [2, 40], and low CCR4 and CXCR1, confined to small subsets of antigen-experienced CD8? T cells [40].”
BackgroundMethodInfluentialChimeric antigen receptor T cells in solid tumors: a war against the tumor microenvironment
Zhao, Z., Xiao, X., Saw, P. E., Wu, W., Huang, H., Chen, J., & Nie, Y. (2019) · Science China Life Sciences · doi:10.1007/s11427-019-9665-8 · Cited by 56
The Next Challenge in Cancer Immunotherapy: Controlling T-Cell Traffic to the Tumor
Abastado, J. (2012) · Cancer Research · doi:10.1158/0008-5472.can-11-3538 · Cited by 55
A comprehensive analysis of immune infiltration in the tumor microenvironment of osteosarcoma
Yang, H., Zhao, L., Zhang, Y., & Li, F. (2021) · Cancer Medicine · doi:10.1002/cam4.4117 · Cited by 52
Car T Cells in Solid Tumors: Overcoming Obstacles
Rojas, J., Diaz, M. P., Palmar, J., Galán‐Freyle, N. J., Morillo, V., Escalona, D., González-Torres, H. J., Torres, W., Quiroz, E. N., Rivera-Porras, D., et al. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25084170 · Cited by 57
“In these studies, CAR T cells were more effectively delivered to different kinds of solid tumors, including melanomas [186], neuroblastomas [187], ovarian cancer [188], renal cancer [189], prostate cancer [190], and mesotheliomas [191].”
BackgroundCancer Biomarker Discovery: The Entropic Hallmark
Berretta, R. E., & Moscato, P. (2010) · PLoS ONE · doi:10.1371/journal.pone.0012262 · Cited by 55
“Again using GATHER [155] on the first 44 genes recognized by the software, and again using Gene Ontology, we observe as most important common function that of cell motility (CCL3, CXCL10, FPRL1, SEMA6A, SPP1), p-value = 0.0002, Bayes Factor 5, and chemotaxis (CCL3, CKLFSF7, CXCL10, FPRL1, SPP1), p-value,0.0001, Bayes…”
BackgroundInfluentialImmune surveillance in melanoma: From immune attack to melanoma escape and even counterattack
Mahmoud, F. A., Shields, B. D., Makhoul, I., Avaritt, N. L., Wong, H. K., Hutchins, L. F., Shalin, S. C., & Tackett, A. J. (2017) · Cancer Biology & Therapy · doi:10.1080/15384047.2017.1323596 · Cited by 57
“the vascular endothelium will enable homing of the activated T cells to the tumor microenvironment.(15,16) Murine models of”
BackgroundXiao, P., Guo, Y. L., Zhang, H., Zhang, X., Cheng, H., Cao, Q., & Ke, Y. (2018) · Oncogene · doi:10.1038/s41388-018-0337-6 · Cited by 54
The anticancer peptide RT53 induces immunogenic cell death
Pasquereau-Kotula, E., Habault, J., Kroemer, G., & Poyet, J. (2018) · PLoS ONE · doi:10.1371/journal.pone.0201220 · Cited by 57
Methylation of immune synapse genes modulates tumor immunogenicity
Berglund, A., Mills, M. N., Putney, R. M., Hamaidi, I., Mulé, J. J., & Kim, S. (2019) · Journal of Clinical Investigation · doi:10.1172/jci131234 · Cited by 54
“Interestingly, key chemokines that drive T cell recruitment and trafficking in melanoma (16), CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10, were elevated in PC1Low patients (Figure 4G).”
BackgroundEmerging Strategies in TCR-Engineered T Cells
Fang, W., Cheng, X., Xue, J. Z., & Xue, S. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.850358 · Cited by 58
Inhibition of the Wnt/β-catenin pathway enhances antitumor immunity in ovarian cancer
Doo, D. W., Meza‐Perez, S., Londoño, A. I., Goldsberry, W. N., Katre, A. A., Boone, J. D., Moore, D. J., Hudson, C. T., Betella, I., McCaw, T. R., et al. (2020) · Therapeutic Advances in Medical Oncology · doi:10.1177/1758835920913798 · Cited by 52
Rutihinda, C., Haroun, R., Saidi, N. E., Ordoñez, J. P., Naasri, S., Lévesque, D., Boisvert, F., Fortier, P., Belzile, M., Fradet, L., et al. (2022) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-022-03313-2 · Cited by 54
Palucka, K., Ueno, H., Roberts, L. K., Fay, J. W., & Banchereau, J. (2010) · The Cancer Journal · doi:10.1097/ppo.0b013e3181eaca83 · Cited by 54
Cooperativity of adaptive and innate immunity: implications for cancer therapy
Shanker, A., & Marincola, F. M. (2011) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-011-1053-z · Cited by 53
Tumor microenvironment as the “regulator” and “target” for gene therapy
Wu, J., Chen, J., Feng, Y., Tian, H., & Chen, X. (2019) · The Journal of Gene Medicine · doi:10.1002/jgm.3088 · Cited by 54
Modeling CAR T-Cell Therapy with Patient Preconditioning
Owens, K., & Božić, I. (2021) · Bulletin of Mathematical Biology · doi:10.1007/s11538-021-00869-5 · Cited by 54
Neoadjuvant Intravenous Oncolytic Vaccinia Virus Therapy Promotes Anticancer Immunity in Patients
Samson, A., West, E. J., Carmichael, J., Scott, K. J., Turnbull, S. J., Kuszlewicz, B., Dave, R., Peckham-Cooper, A., Tidswell, E. L., Kingston, J. L. T., et al. (2022) · Cancer Immunology Research · doi:10.1158/2326-6066.cir-21-0171 · Cited by 51
“IP-10 is a chemokine known to play an important role in recruiting activated T cells into sites of tissue inflammation and associates with the presence ofCD8þTcells in tumors (36, 37).”
BackgroundThakur, A. B., Schalk, D. L., Sarkar, S. H., Al-Khadimi, Z., Sarkar, F. H., & Lum, L. G. (2011) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-011-1116-1 · Cited by 52
“Lack of critical chemokines (CCL2, CXCL9 and CXCL10) in melanoma metastases aggravated disease due to blockage in activated T-cell migration and anti-tumor immunity [36].”
Immunotherapy in Cancer: A Combat between Tumors and the Immune System; You Win Some, You Lose Some
Rowdo, F. P. M., Barón, A., Urrutia, M., & Mordoh, J. (2015) · Frontiers in Immunology · doi:10.3389/fimmu.2015.00127 · Cited by 51
“These observations could be explained by the fact that some tumors express chemokines that mediate the recruitment of activated T cells into metastatic sites, while others do not (126).”
BackgroundImproving homing in T cell therapy
Vignali, D., & Kallikourdis, M. (2017) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2017.06.009 · Cited by 51
Innate immune sensing of cancer: clues from an identified role for type I IFNs
Gajewski, T. F., Fuertes, M. B., & Woo, S. (2012) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-012-1305-6 · Cited by 52
“This includes clinical benefit to several cancer vaccines, the anti-CTLA-4 mAb ipilimumab, and IL-2 [6–11].”
BackgroundCD40 controls CXCR5-induced recruitment of myeloid-derived suppressor cells to gastric cancer
Ding, Y., Shen, J., Zhang, G., Chen, X., Wu, J., & Chen, W. (2015) · Oncotarget · doi:10.18632/oncotarget.5644 · Cited by 50
“Studies have shown that effector T cells lacking critical chemokines exhibit deficient migration and activation, and that this results in compromised anti-tumor T cell activity and enhanced tumor invasiveness and metastasis [21].”
BackgroundMauldin, I. S., Wages, N. A., Stowman, A. M., Wang, E., Smolkin, M. E., Olson, W. C., Deacon, D. H., Smith, K. T., Galeassi, N., Chianese‐Bullock, K. A., et al. (2016) · Cancer Immunology Immunotherapy · doi:10.1007/s00262-016-1881-y · Cited by 51
Tarhini, A. A., Lin, Y., Lin, H.-M., Vallabhaneni, P., Sander, C., LaFramboise, W. A., & Hamieh, L. (2016) · OncoImmunology · doi:10.1080/2162402x.2016.1231291 · Cited by 45
“observed a major segregation of tumor samples based on the differential expression of T-cell-associated genes.(15) More importantly, the expression of defined chemokine genes was significantly associated with the presence of tumor-infiltrating lymphocytes.”
BackgroundSingle-cell spatial analysis of tumor immune architecture in diffuse large B-cell lymphoma
Colombo, A., Hav, M., Singh, M. P., Xu, A. M., Gamboa, A., Lemos, T., Gerdtsson, E., Chen, D., Houldsworth, J., Shaknovich, R., et al. (2022) · Blood Advances · doi:10.1182/bloodadvances.2022007493 · Cited by 51
“Age, mean ± SD (range) 49 ± 15 (20-82) Mutation status 22 (67%) Sex TP53 8 (24%) F 9 (27%) BCL2 3 (9%) M 24 (73%) BCL6 2 (6%) Ethnicity CD79b 6 (18%) Black 1 (3%) SGK1 1 (3%) Asian 5 (15%) MYD88.”
Wang, Z., Han, J., Cui, Y., Zhou, X., & Fan, K. (2013) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2013.08.072 · Cited by 49
Liposomal Formulations to Modulate the Tumour Microenvironment and Antitumour Immune Response
Gilabert‐Oriol, R., Ryan, G. M., Leung, A. W. Y., Firmino, N. S., Bennewith, K. L., & Bally, M. B. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19102922 · Cited by 53
“Several chemokines produced by both cancer and stroma cells (CCL2, CCL3, CCL4, CCL5, CXCL9, and CXCL10) also serve as chemoattractants to lymphocytes [39].”
BackgroundTumor Microenvironment and Immunotherapy Response in Head and Neck Cancer
Economopoulou, P., Kotsantis, I., & Psyrri, A. K. (2020) · Cancers · doi:10.3390/cancers12113377 · Cited by 48
Non-coding RNAs and macrophage interaction in tumor progression
Entezari, M., Sadrkhanloo, M., Rashidi, M., Asnaf, S. E., Taheriazam, A., Hashemi, M., Ashrafizadeh, M., Zarrabi, A., Rabiee, N., Hushmandi, K., et al. (2022) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2022.103680 · Cited by 50
Innate Immune Cells and Their Contribution to T-Cell-Based Immunotherapy
Ginefra, P., Lorusso, G., & Vannini, N. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21124441 · Cited by 48
“T cell recruitment in the tumor microenvironment is orchestrated by a large set of chemokines and cytokines [25] especially produced by myeloid lineages component of the innate immunity such as DCs [26] and macrophages [23].”
Background
Metadata
- Authors
- Harlin, H., Meng, Y., Peterson, A. C., Zha, Y., Tretiakova, M., Slingluff, C., McKee, M., & Gajewski, T. F.
- Affiliations
- 1Department of Pathology,
- 2Department of Medicine, Section of Hematology/Oncology, and
- University of Virginia (US)
- University of Chicago (US)
- Venue
- Cancer Research
- Published
- 2009-04-01
- Volume
- 69
- Issue
- 7
- Pages
- 3077-3085
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC3886718
- OpenAlex
- W2162222767
- Cited by
- 1,121
- References
- 29
- Citations by year
- 2026: 40 · 2025: 58 · 2024: 89 · 2023: 95 · 2022: 118 · 2021: 121 · 2020: 105 · 2019: 87 · 2018: 69 · 2017: 77 · 2016: 51 · 2015: 42 · 2014: 29 · 2013: 37 · 2012: 28
- FWCI
- 17.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Burroughs Wellcome Fund
- University of Chicago
- National Cancer Institute (P01CA97296, R01 CA90575, R01CA090575, P01CA097296, P30CA044579)
- Topics
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- melanoma metastasis, chemokines, CD8+ T cell recruitment, T cell migration, MCP-1, CCL3, carbon tetrachloride, RANTES, CXCL9, CXCL10, chemokine receptors, tumor immune microenvironment, chemokine blockade, antitumor immunity, melanoma cell lines, xenografts
- MeSH terms
- Cell Movement, Multigene Family, Humans, Melanoma, Gene Expression, CD8-Positive T-Lymphocytes, Chemokines, Protein Array Analysis, Cell Line, Tumor
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