PD-L1 (Programmed death ligand 1)

Specific genomic alterations may help stratify immunotherapy outcomes in recurrent or metastatic cervical cancer. The proposed genomic risk model remains exploratory and requires validation in larger, independent cervical cancer cohorts.

This article provides a target-oriented synthesis of HCC-related CAR-T-cell therapy, summarizes registered clinical studies according to antigen target, CAR design, trial phase, administration route, and available outcomes, and discusses how CAR structural evolution may influence therapeutic development in HCC. This article aims to review recent advances in CAR-T-cell therapy for hepatocellular carcinoma.

Meanwhile, MT3-KN035 conjugated multiple aldoxorubicin (hereafter, these conjugates are referred to as MT3-KN035-DOX) via an acidic cleavable linker; MT3-KN035-DOXHigh induced tumor apoptosis and exhibited significant antitumor efficacy via facilitating immune cell infiltrations. This work provides a novel therapeutic strategy via nanobody-mediated target engagement and internalization that achieves synergistic therapeutic efficacy between chemotherapy and immune checkpoint blockade therapy.

In cases of nonresectable or metastatic disease platinum-etoposide-based regimens are the standard treatment. Definitive chemoradiotherapy represents an equivalent alternative for inoperable advanced cases. Due to the lack of prospective data all therapeutic recommendations must be considered an expert consensus.

Our findings suggest a novel mitochondrial-related gene signature for the TIME that could be used as a reliable prognostic biomarker for patients with glioma.

In 2025, Australia's Pharmaceutical Benefits Advisory Committee adopted a novel broad cancer listing on the Pharmaceutical Benefits Schedule for nivolumab, ipilimumab and pembrolizumab. We suggest that while a broad listing represents a pragmatic response to the growing prevalence of multi-indication medicines, it entails important trade-offs between access, transparency and value alignment. These design considerations are likely to be relevant for other jurisdictions considering similar reimbursement reforms.

Pharmacologically inhibiting kinases that phosphorylate Cdh1 increased STING abundance and STING-mediated type 1 interferon signaling in ccRCC cells, presumably by promoting the formation of APC/C-Cdh1-STING complexes. These findings reveal a Cdh1-STING axis in ccRCC that might be therapeutically exploited to potentiate antitumor innate immunity.

Emerging technologies such as CSC‑targeted nanoparticles and engineered cellular therapies are also discussed as hypothesis‑generating approaches. We conclude that while current data are promising, rigorous, biomarker‑driven trials are needed to determine whether targeting the CSC‑associated niche can durably improve anti‑tumor immunity in tumors where CSC-mediated immune evasion predominates.

LVSI+ EECs exhibited marked epithelial reprogramming, transitioning from differentiated ciliated epithelium to hyperproliferative and metabolically remodelled phenotypes, and contained TC4, a metastatic epithelial subset characterized by hypoxia, partial epithelial-mesenchymal transition, immunosuppression, and progesterone resistance...Using spatial multiplex immunofluorescence, we confirmed hypoxic tumour epithelial cells at the invasive front coexisting with an immunosuppressive microenvironment, and revealed spatial colocalization of PD-L1+ tumour cells, PD-L1+ macrophages, and PD-1+ T cells within LVSI thrombi. Our comprehensive study provides deeper insights into LVSI as an actively coordinated multicellular process, potentially improving LVSI risk prediction, supporting treatment decision-making, and informing new therapies targeting the tumour microenvironment.

irAEs are not uniformly associated with improved survival. Favorable outcomes are driven by thyroid-related and skin-related, non-steroid-requiring irAEs, suggesting shared biological mechanisms underlying organ-specific autoimmunity and antitumor immune response.

We highlight that TGF-β-driven immune suppression and immune exclusion are often spatially organized within stromal niches, vary across indications, and are not always the dominant barrier even when PD-L1 is expressed. SHR-1701's approval provides proof of principle in a defined context and supports mechanism-aligned development using biomarker-driven selection, rational combinations and sequencing, and pharmacodynamic endpoints that directly test these assumptions.

Importantly, combining EFHD2 knockdown with immune checkpoint blockade synergistically enhanced radiosensitivity and restored antitumor T cell responses. Collectively, these findings demonstrate that EFHD2 drives lactate-mediated immunosuppression and DNA repair to promote radioresistance in CRC, suggesting that targeting the EFHD2 axis may restore antitumor immunity and improve therapeutic outcomes.