Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Although N-803 plus vaccine induced peripheral CD8<sup>+</sup> T-cell activation and cytokine production, there was no reduction in tumor burden and poor tumor infiltration of CD8<sup>+</sup> T cells with minimal levels of granzyme B.
|
31645354 |
2020 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The antitumor immunity in IL-1β-deficient mice includes activated CD8<sup>+</sup> lymphocytes expressing IFN-γ, TNF-α, and granzyme B; these cells infiltrate tumors and induce regression.
|
30545915 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Type I interferon suppresses tumor growth through activating the STAT3-granzyme B pathway in tumor-infiltrating cytotoxic T lymphocytes.
|
31228946 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Taken together, our results suggest that GzmB expression in MDSCs is another means to promote tumor growth and warrants further investigation to unravel the exact underlying mechanism.
|
31212684 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In immunocompetent mouse 4T1 breast tumor model, intratumoral delivery of rAd.sT inhibited both tumor growth and lung metastases. rAd.sT downregulated the expression of several transforming growth factor β (TGFβ) target genes involved in tumor growth and metastases, inhibited Th2 cytokine expression, and induced Th1 cytokines and chemokines, and granzyme B and perforin expression. rAd.sT treatment also increased the percentage of CD8<sup>+</sup> T lymphocytes, promoted the generation of CD4<sup>+</sup> T memory cells, reduced regulatory T lymphocytes (Tregs), and reduced bone marrow-derived suppressor cells.
|
31126191 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Accordingly, mice treated with niclosamide and PD-L1 antibody showed significant delay in tumor growth and increased survival which were associated with the increase of tumor infiltrating T cells and granzyme B release.
|
31511071 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Tumor-educated MAIT cells significantly upregulated inhibitory molecules like PD-1, CTLA-4, TIM-3, secreted significantly less IFNγ and IL17, and produced minimal granzyme B and perforin while shifting to produce tumor-promoting cytokines like IL8.
|
30723143 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In 14 patients, the association between necrosis and MMVR and tumour immune contexture were analysed by multiple immunofluorescent (IF) staining for CD8, PD-1, granzyme B (GrzB) and NFATC2.
|
31214790 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In p50<sup>-/-</sup> mice, total tumor CD4 T cells are threefold more abundant, whereas CD8 T-cell numbers are unchanged, and both produce increased IFNγ and Granzyme B. Naïve splenic p50<sup>-/-</sup> CD8 T cells manifest increased activation, whereas naïve p50<sup>-/-</sup> and WT CD4 T cells show similar Th1, Th2, and Th17 polarization.
|
30030559 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, the activation/suppression marker values of the lymphocytes (i.e., such as PD-1, ICOS, Granzyme B and the PD-1/CD8 ratio) in the primary tumor were correlated with values in the metastatic tumor.
|
29614981 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
More importantly, NK-92-S3KD immunotherapy increases the production of not only IFNγ, but also granzyme B and perforin in tumors; therefore, inhibiting cancer progression in two xenograft mouse models with human hepatoma (HepG2) and melanoma (A375).
|
29915022 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
QIF is used to simultaneously measure the level of CD3+ tumor infiltrating lymphocytes (TILs), in situ T-cell proliferation (Ki-67 in CD3) and effector capacity (Granzyme-B in CD3).
|
30097571 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Combined efficacy was CD8<sup>+</sup> T cell dependent and associated with increased granzyme B expression; however, TIM-3 expression was predominantly localized to myeloid cells in both human and murine tumors.
|
29316433 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In NK cells and CTLs the levels of active cathepsin C and of granzyme B are dependent on the concentration of monomeric, active cystatin F. In tumour microenvironment, inactive dimeric cystatin F can be secreted from tumour cells or immune cells and further taken up by the cytotoxic cells.
|
29748898 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The combination also promoted IFNg, IL12 and granzyme B production in the tumor microenvironment and decreased the formation of liver metastasis in a very early phase of tumor development, enabling 90% survival.
|
30356111 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Similarly, there was robust granzyme B staining localizing to the tumors; affirming the presence of cytotoxic immune cells within the tumor.
|
29930558 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Taken together, we found a subset of PD-1 therapy-responsive CD8+ T cells that were capable of withstanding chemotherapy and executing tumor rejection with their unique abilities of drug efflux (ABCB1), cytolytic activity (granzyme B and perforin), and migration to and retention (CX3CR1 and CD11a) at tumor sites.
|
29669928 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
T cell cytotoxicity was mediated via granzyme B release and mediated enhanced tumor control <i>in vivo</i>.
|
30214445 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, the prognosis of CRC patients was positively associated with the frequency of TDLN CD8<sup>+</sup>CXCR5<sup>+</sup> T cells, and with the expression of IFNG, PRF1, and GZMB expression by tumor and TDLN CD8<sup>+</sup>CXCR5<sup>+</sup> T cells.
|
29544815 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In addition, an increased number of CD3<sup>+</sup> T cells in the circulation and tumors and increased granzyme B levels and decreased Ki67 expression levels in the tumors were observed in the mice treated with GPC3-28Z-sPD1 T cells.
|
30078052 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Tumor cell resistance to granzyme B and how this alters NK cell killing is not clearly defined.
|
29925431 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Dendritic cells transfected with DNA vaccine constructs were found to stimulate both tumor cytotoxicity mediated by autologous lymphocytes and granzyme B production by CD8+ T-cells, and pMEL-A0201 was found to be the most efficient.
|
30421674 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, a limited number of T cells (CD3+) was present in the tumor microenvironment, with a higher number of regulatory T cells (Foxp3+) and macrophages (Cd11b+) as compared to a low infiltration of activated cytotoxic T cells (CD8+/ Granzyme B+).
|
30458852 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Tumour-infiltrating lymphocytes (TILs) and Granzyme B play crucial roles in immune reactions against colorectal carcinoma (CRCa).
|
29970545 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, after the gene electrotransfer of plasmids with constitutive promoters, granzyme B-positive cells were detected in the tumor and spleen, indicating a systemic effect of the therapy.
|
29593358 |
2018 |