ITGA1 (Integrin Subunit Alpha 1)

Additionally, we validate cTR-T's phenotypic changes following PD-1 blockade therapy in mouse tumor models with artificial antigen. These findings suggest that the phenotypic state and transition of cTR-Ts may reflect their functional potential after tumor infiltration and are associated with therapeutic outcomes of ICIs.

Upon 808 nm laser irradiation, NPs-H-I elicited potent photodynamic therapy (PDT), selectively eliminating HNRNPC-high tumor cells and ITGA1+ myCAFs, which robustly inhibited tumor growth and restored anti-tumor immunity in murine models. Our work not only delineates the HNRNPC-ITGA1 axis as a novel metabolic-immune checkpoint in OSCC but also establishes a versatile and translatable precision medicine platform capable of disrupting this pathway for effective combination therapy.

Notably, COL1A1 reconstitution rescues CAF-induced tumor progression, underscoring COL1A1 dependency. Collectively, our findings position BT as a first-in-class COL1A1 antagonist that exerts dual cytotoxic and microenvironment-normalizing effects, providing a rational therapeutic avenue for NSCLC.

We identified 131 protein-cancer-associations that reached statistical significance in the meta-analysis, of which some may be cancer markers and others may have aetiological roles, indicated by supporting genetic analyses, including ITGA11 and lung cancer. Our findings highlight the need for large, diverse, and mature prospective proteomic cohort studies of cancer risk to ensure the equity and generalisability of insights into cancer risk.

Thus, GEP-NETs are organized along a conserved neuronal-to-secretory axis defined by distinct epigenetic programs and spatially coupled to specific microenvironmental niches. This framework unifies NET heterogeneity across organ sites and identifies pathway-specific, microenvironment-linked vulnerabilities for therapeutic targeting.

In TLSs, TGF-β orchestrated BHLHE40 expression in TRM and effector TRM differentiation. Our findings identified an effector subset of TRM as CD49a+PD1hi CD8+ TRM, and highlighted a BHLHE40-orchestrated, resident immune component, rather than circulating cells, as a major contributor to allograft rejection.

By integrating this knowledge, we discuss strategies to manipulate these pathways with the goal of developing more effective vaccines and personalized therapies based on resident memory T cells. We also examine how these molecular signals and pathways, either independently or in combination, can be explored both in the fight against viral infections and cancer, and in identifying CD8+ TRM predictive biomarkers for response to anticancer immunotherapies across various tumor types.

However, challenges persist because of TME heterogeneity and persistent dysfunctional states. Understanding these adaptive mechanisms provides a framework for developing NK cell-based therapies that leverage plasticity to counteract tumour resistance.

We developed a predictive model for vascular issues in LIHC, identified important gene ITGA11 that can promote angiogenesis in LIHC and influence tumor progression in LIHC patients through the regulation of angiogenesis. We also found a small molecule medication called diosgenin that can target ITGA11's angiogenic effects.

Our study demonstrates the first successful expansion of adaptive NK cells with robust functional responses from donors with chronic viral infection. This approach creates opportunities for NK cell-based therapies alone or in combination with monoclonal antibodies contributing to HBV functional cure strategies and the treatment of HBV-driven cancers.

Our study defines COL6A3+ GAFs as a key feature of GBM, driving vascular dysfunction and hypoxi, and suggests COL6A3 as a promising therapeutic target for disrupting fibrosis-angiogenesis crosstalk in GBM.

Pharmacological inhibition of CTSL not only mitigates anti-PD-L1-induced muscle wasting but also further suppresses tumor growth, potentially via downregulation of BNIP3. Here, we show that CTSL is a dual-action target to uncouple anti-tumor efficacy from muscle-specific irAEs, offering a strategy to improve clinical outcomes of ICIs.