Altogether, KYA1797K inhibits the β-catenin/STT3 signaling pathway to reduce the stability of PD-L1, thus further inhibiting immune evasion and inducing apoptosis of colon CSCs, which contributes to the development of immunotherapy for colon cancer.
Results reveal that expression of EpCAM and PD-L1 on CD4<sup>+</sup> T cells significantly increased in patients with CC, compared with age- and sex- matching healthy controls and patients with colonic polyps.
We used ErNPs functionalized with cross-linked hydrophilic polymer layers attached to anti-PD-L1 (programmed cell death-1 ligand-1) antibody for molecular imaging of PD-L1 in a mouse model of colon cancer and achieved tumor-to-normal tissue signal ratios of ~40.
Low miR200c expression in tumor budding of invasive front predicts worse survival in patients with localized colon cancer and is related to PD-L1 overexpression.
In this study, the effects of sole and dual CTLA-4 and PD-L1 blockade were investigated in a microsatellite stable highly aggressive orthotopic mouse model of colon cancer.
In conclusion, targeting CBP/β-catenin, combined with PD-1/PD-L1 immune checkpoint blockade, shows potential as a new therapeutic strategy for treating liver metastasis during colon cancer.
PD-L1 expression was significantly increased in BRAF<sup>V600E</sup> human colon cancers, and patients whose tumors had high vs. low PD-L1 had significantly better survival.
Compared with antitumor effects of single silencing of PD-1 or PD-L1 alone, cosilencing of PD-1 and PD-L1 showed more significant tumor growth suppression and long-term tumor inhibition in colon cancer.
More importantly, the CA<sub>cluster</sub><i>in vivo</i> improved the tumor response to the PD1/PD-L1 immune checkpoint blockade in melanoma and colon cancer.
The pooled odds ratios (ORs) showed that PD-L1 expression was associated with poor differentiation (OR = 3.47, 95% CI 1.37-8.77, <i>P</i> = 0.008) and right colon cancer (OR = 2.38, 95% CI 1.57-3.60, <i>P</i> < 0.0001).
While only a small part of colon cancer cells express PD-L1, we sought to evaluate the differential impact of stromal and epithelial PD-L1 expression of primary tumors and liver metastasis on overall survival (OS) in colon cancer patients.
In this study, we demonstrated that blockade of RANKL improves anti-metastatic activity of antibodies targeting PD1/PD-L1 and improves subcutaneous growth suppression in mouse models of melanoma, prostate and colon cancer.
Serial sections of MSI-H colon cancer tissue were stained with haematoxylin and eosin (H&E) and Masson trichrome stains; immunohistochemical analysis of PD-L1, CD8, D2-40 and CD31 was performed.
Collectively, our data showed that tumor-associated stromal cells support T-cell suppression by PD-L1 induction, which is dependent on colon cancer inflammatory signaling.
The purpose of this study was to test if IL-17 and TNF-α may synergistically induce PD-L1 expression in human prostate cancer LNCaP and human colon cancer HCT116 cell lines.
Our results suggest that breast and colon cancers may be sensitive to PD1/PD-L1 immunotherapy and thus warrant further investigations of CSC targeted PD1/PD-L1 therapy.
We evaluated tumour CD274 expression by immunohistochemistry in 823 rectal and colon cancer cases within the Nurses' Health Study and Health Professionals Follow-up Study.
The prognostic value of the SOX2 cancer stem-like cell marker in colon cancer is modified by expression of immune-cell related factors FoxP3 and PD-L1.
Patients and Methods Using data from 617 patients with rectal and colon cancer in the Nurses' Health Study and the Health Professionals Follow-Up Study, we examined the association of postdiagnosis aspirin use with patient survival in strata of tumor CD274 expression status measured by immunohistochemistry.