PD-L1 overexpression

In this Middle Eastern cohort, no consistent molecular or clinical disparities across most parameters. These findings suggest the timing of metastasis may not independently influence prognosis and highlight the relevance of individualized, biology-driven management strategies.

In a cell-derived xenograft (CDX) mouse model, PDL1-CAR-γδT cells effectively suppressed GBM growth. These results suggest that PDL1-CAR-γδT cells represent a novel and promising therapeutic strategy for GBM.

Variations in PD-L1 expression were associated with the mean DNA index values exceeding 2.5 among the top 20 tumor cells analyzed. Compared with the non-expression group, the low-expression PD-L1 group demonstrated greater tumor cell invasiveness.

Our findings unveil a novel IFN-γ-nuclear PD-L1/POLR2A-LY6E signaling axis critical for TNBC lung metastasis. This immune-independent mechanism, driven by nuclear PD-L1 transcriptional activity, provides a mechanistic basis for the limited efficacy of anti-PD-L1 antibodies against metastasis and nominates nuclear PD-L1 complexes and LY6E as potential therapeutic targets to overcome metastatic resistance in TNBC.

Stereological quantification of specific immune cells in melanoma metastases, such as T-lymphocytes (CD3), cytotoxic T-lymphocytes (CD8), dendritic cells (CD1a) and PD-L1-positive cells, may predict ICIs treatment efficacy or the risk of irAEs. High infiltration of metastatic tissue by CD8-positive T cells is important for long-term favorable therapeutic response to ICIs.

This real-world study suggests that MET overexpression, as assessed by IHC, is associated with better survival in advanced NSCLC patients treated with ICIs, independent of PD-L1 level. These results suggest the potential of MET expression as a predictive marker for ICI efficacy in advanced NSCLC patients and support the combination of MET-targeted agents with anti-PD1/PD-L1 ICIs as a promising strategy for NSCLC patients with MET overexpression.

This case study provides an opportunity to better understand H-FLAC, whose genetic alterations have not been well characterized, and to identify valuable molecular markers for potential targeted therapies. We conducted gene sequencing and PD-L1 expression testing, which are helpful for H-FLAC research.

In the low inflammation population, PFS and OS were significantly improved in the combination chemoimmunotherapy group compared to the pembrolizumab group [median PFS: 8.8 vs. 16.0 months, hazard ratio (HR) =0.69, P=0.04; median OS: 29.4 vs. not reached (NR), HR =0.55, P=0.007]. In patients with advanced, driver gene mutation-negative NSCLC, high PD-L1 expression (≥50%), and low systemic inflammation, combination chemoimmunotherapy significantly improved PFS and OS compared to pembrolizumab monotherapy.

The patient with EML4::ALK fusion was treated with alectinib with partial response...These finding further suggest that SMARCA4d-UT and carcinomas with SMARCA4 loss may be on the same spectrum of disease, and accurate histologic distinction between these lesions may be challenging. A unified terminology may be beneficial for appropriate diagnosis and treatment.

The patient received combined dabrafenib, trametinib, and pembrolizumab with close safety monitoring, achieving rapid tumor control and complete remission by six months with manageable toxicity. This case suggests that early integration of PD-1 blockade with BRAF/MEK inhibition treatment may benefit selected patients and underscores the value of comprehensive molecular and immunohistochemical assessment to guide individualized therapy.

Furthermore, linarin treatment significantly inhibited colorectal cancer tumor growth in vivo. In conclusion, linarin could inhibit the proliferative, migratory, and invasive capacity, but enhance the apoptotic ability in colorectal cancer cells through repressing the HIF-1α/PD-L1 axis.

The combination of chemotherapy and immune checkpoint blockade therapy shows great potential in tumor treatment, but their integration remains a great challenge. Meanwhile‌, overexpression of programmed cell death ligand 1 (PD-L1) is suppressed by JQ1, thereby reversing PD-L1-mediated immune resistance to synergistically promote adaptive antitumor immune response. This hypoxia-sensitive versatile nanoplatform provides an elegant paradigm for precise tumor therapy.