The expression of miR-382 and programmed cell death ligand 1 (PD-L1) were determined in CRC cell lines by quantitative real-time polymerase chain reaction and western blot, respectively.
B7-H3, B7-H1, and CA-50 expressions were higher in patients with CRC than those in healthy controls and the patients with benign gastrointestinal diseases.
Immunohistochemistry was conducted to assess the densities of intraepithelial and stromal CD3+, CD8+, CD45RO+, and FOXP3+ TILs, and to estimate PD-L1 expression in tumor cells for 168 patients with stage II CRC.
Remarkably, promoter methylation status of LAG-3, TIGIT and PD-L1 was in concordance with transcriptomic expression in CRC: the more the hypomethylation, the higher the expression.
This study aimed to establish the clinicopathologic importance of the Immunoscore (IS) in CRC and to clarify the relationships between the IS, programmed death-ligand 1 (PD-L1) expression, and tumor-associated macrophages.
Average PD-1/PD-L1 lymphocytic expression was 1.1/1.0, 1.2/2.9, 4.8/6.9, and 12.4/15.2 in SSA, SSA-LD, SSA-HD, and CRC, respectively, compared with 0.5/0 in normal crypts (P < .0001).
Whilst CTCs are well documented in other tumor streams such as breast, colorectal cancer and prostate cancers, the data and clinical utility in HNSCC remains limited.<b>Areas covered</b>: Here we summarize the recent advances of CTCs and applications in HNSCC.<b>Expert opinion</b>: CTC enumeration can be prognostic in HNSCC; further studies are warranted to investigate the role of CTC clusters in HNSCC; CTC culture (<i>in vivo</i>/<i>ex vivo</i>) may present a possibility to expand these rare cells to a critical mass for functional testing; PD-L1 expression of HNSCC CTCs may present a means by which to determine patients likely to respond to therapy; a HNSCC CTC-specific marker is warranted.
These data reveal that the CRC microenvironment promotes the coexistence of seemingly antagonistic suppressive and pro-inflammatory immune responses and might provide an explanation why a blockade of the PD1/PD-L1 axis is ineffective in CRC.
In conclusion, our data support a regulatory mechanism of PD-L1 expression on tumor cells and immune suppression via miR-148a-3p downregulation in colorectal cancer.
Triple blockade of EGFR, MEK and PD-L1 has antitumor activity in colorectal cancer models with constitutive activation of MAPK signaling and PD-L1 overexpression.
Obesity was all over significantly associated with risk of CRC with low density of FoxP3<sup>+</sup> T cells and low programmed cell-death protein 1 (PD-L1) expression on tumor cells, but with high density of CD8<sup>+</sup> T cells and CD20<sup>+</sup> B cells.
Correction to: The Immunoscore is a Superior Prognostic Tool in Stages II and III Colorectal Cancer and is Significantly Correlated with Programmed Death-Ligand 1 (PD-L1) Expression on Tumor-Infiltrating Mononuclear Cells.
We demonstrate regulation of PD-L1 by oncogenic BRAF<sup>V600E</sup> and investigated its ability to influence apoptotic susceptibility in colorectal cancer (CRC) cells.
The results obtained in the current study suggested that a subpopulation of patients with MSI-L/MSS-CRC and pMMR-CRC with upregulated IFN-γ and CD8 T effector gene signatures may benefit from immunotherapy with antibodies against PD-1 and PD-L1.