|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
IL-33 treatment also facilitates the production of CCL5 in the lung by eosinophils and CD8<sup>+</sup> T cells, which mediates the recruitment of NK cells to the tumor microenvironment.
|
31709531 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The "education" of mesenchymal stromal cells by tumor cell-conditioned medium enhanced mesenchymal stromal cells' proliferation and CCL5 secretion.
|
30309853 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Silencing CCL5 expression in PGRN-deficient tumor reduces NK cell recruitment and restores tumor growth to the control level.
|
31491449 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our findings suggest that within the tumor microenvironment, CD9 is responsible for the crosstalk between BMMSCs and HCC1806 breast cancer cells (via CCL5, CCR5, and CXCR12) which contributes to chemoresistance.
|
31191817 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CCL5 may contribute to promoting tumor growth, and CCL5 is a promising target that may help in understanding the pathogenesis of CRC.
|
30871911 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Despite the abundance of Th1 chemokines RANTES (CCL5) and MIP-1α (CCL3) in OAC tumour, enrichments of intratumoural T cells expressing corresponding receptors were not observed.
|
30834503 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The present study demonstrated that the positive expression of CCL5 was associated with lymph node status and tumor‑node‑metastasis stage.
|
31578575 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Genetic variants of CCL5 and CCR5 SNPs may predict outcomes in mCRC patients receiving cetuximab-based treatment depending on tumour location.
|
30554073 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Mechanistically, the current study demonstrated that this is achieved by promoting a pro-tumor microenvironment, with increased cancer-associated fibroblasts and macrophage infiltration, and by modulating the CCL5-CCR5 and CXCL12-CXCR4 chemokine axes in the primary tumor.
|
31705019 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The cooperation between tumor-derived CCL5 and IFN-γ-inducible CXCR3 ligands secreted by myeloid cells is key for orchestrating T cell infiltration in immunoreactive and immunoresponsive tumors.
|
31185212 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
GBE1 blockade promotes the secretion of CCL5 and CXCL10 to recruit CD8<sup>+</sup> T lymphocytes to the tumor microenvironment via the IFN-I/STING signaling pathway, accompanied by upregulation of PD-L1 in LUAD cells, suggesting that GBE1 could be a promising target for achieving tumor regression through cancer immunotherapy in LUAD.
|
31221150 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Our results suggest that a crosstalk between the tumor and its microenvironment plays a key role in the invasive nature of AIP-mutation-positive tumors and the CCL5/CCR5 pathway is a novel potential therapeutic target.
|
30867568 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Ovarian cancer stem cells promote tumour immune privilege and invasion via CCL5 and regulatory T cells.
|
28868628 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Unexpectedly, Δ3C-infected tumors had increased T-cell infiltration, increased expression of T-cell chemokines (CCL5, CCL20 and CCL22) and enhanced type I interferon response in comparison to WT tumors.
|
30125329 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
G-MDSC and M-MDSC from the peripheral blood and tumor parenchyma were analyzed by flow cytometry.CCR5 ligand CCL5 was detected by ELISA.
|
29303012 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
TILs were correlated with residual tumor size after neoadjuvant chemotherapy (NAC) and CCL5 expression.
|
29559701 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These findings collectively indicate that TGF-β regulates CCL2 and CCL5 expression in a stage-dependent manner during BCa progression, which in turn, determines Th1-Th2 balance within the tumor microenvironment.
|
29107385 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Mechanically, the results of RNA-sequencing, in vitro coculture system and hypoxia measurements demonstrated that knockdown of CCL5 could result in the metabolic disorders in CD11b<sup>hi</sup>F4/80<sup>low</sup> TAMs and suppress the expression of S100a9 to promote the migration of CD8<sup>+</sup> T cells in the tumor microenvironment.
|
29991744 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Clinically, we reported a strong positive correlation between the expression of NK cell marker and CCL5 in human melanoma tumors and more importantly, a significant increased survival is found in melanoma patients expressing a high level of CCL5.
|
29368981 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Because their tumor tissues displayed increased expression of C-C chemokine ligand 5 (CCL5), we hypothesized CCL5 might participate in cancer progression in such patients.
|
29872080 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our findings revealed the effective integration of tumor CCL5 and collagen IV, and a new method for predicting the prognosis of luminal B (HER2-) has been developed.
|
29988769 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Existing data suggest that the macrophage inflammatory protein (MIP)-1 family and related proteins, consisting of CCL3 (MIP-1α), CCL4 (MIP-1β), and CCL5 (RANTES), can be major determinant of immune cellular infiltration in certain tumors through their direct recruitment of antigen presenting cells, including dendritic cells (DCs) to the tumor site.
|
29399390 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Inhibiting DNMT1 activity with procainamide, inhibiting DNA methylation with 5-AZA, or inhibiting CCL5/CCR5 signaling with maraviroc reduced tumor growth <i>in vivo</i> In conclusion, upregulation of DNMT1 by CCL5/CCR5/STAT3 signaling is critical for TAM-mediated <i>GSN</i> silencing in gastric cancer.
|
28835422 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, kumatakenin was found to reduce the expressions of MCP-1 and RANTES, which are major determinants of macrophage recruitment at tumor sites in ovarian cancer cells.
|
28763204 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
IFN-β treatment enhanced CD8<sup>+</sup> T-cell infiltration into tumors and CCL5 and CXCR3 ligand expression.
|
28624449 |
2017 |