ITGB2 (Integrin Subunit Beta 2)

A prognostic model constructed from CAPG + Mac signature genes effectively stratified HCC patients into high- and low-risk groups and demonstrated stable predictive performance in external validation. This study reveals that CAPG + Mac putatively modulate ferroptosis signaling to influence immune homeostasis, highlighting them as a key target for HCC progression and immunotherapy responsiveness.

Our results indicate that the mechanisms of action of ZQD involve impeding neutrophil recruitment and activation, as well as reducing the levels of NETs-related markers. These suggest the potential of ZQD in suppressing NETs formation or release, inhibiting NSCLC progression and metastasis.

Furthermore, following phagocytosis, CAR-monocytes induced antigen-specific CD8+ T cell activation via antigen presentation. Collectively, these findings highlight CD32a-based and combinatorial ICD designs as a framework for functionally tuned CAR-M platform for solid tumor immunotherapy and anti-viral applications.

The findings revealed that the PLR regulatory network is associated with HER2⁺/ER-/PR- lapatinib resistance through multiple mechanisms, including interferon signaling silencing, T cell exhaustion, and the fostering of an immunosuppressive niche. These insights pave the way for interventions aimed at overcoming lapatinib resistance in HER2⁺ breast cancer.

This review was registered in PROSPERO (CRD420251070874) and supported by FCT/MCTES UIDP/05608/2020 and UIDB/05608/2020. Institutional.

Our data indicate that Myo1f regulates monocyte adhesion and contributes to the pathogenesis of atherosclerosis by recruiting EPLINα, which stabilizes F-actin. This stabilization enhances MRTFA nuclear translocation, thereby promoting ITGB2 transcription.

Furthermore, risk models incorporating specific protein signatures effectively stratified patients by platinum sensitivity/resistance (9-protein panel: ILK, CDCP1, CD86, CLDN4, CLEC1B, CDHR5, CLDN11, JAM2, FOLH1), lymph node metastasis status (7-protein panel: APOE, CD28, CLDN4, FOLH1, ITGAL, JAML, ULBP3), and post-surgical residual disease burden (4-protein panel: CD44, CLMP, ITGA4, AMIGO1), with Cluster 13 (ITGB1-high) also significantly associated with residual disease. This work demonstrates the power of single-EV proteomics combined with machine learning for non-invasive diagnosis and clinical outcome assessment in advanced ovarian cancer, though the absence of early-stage patients limits its applicability for early detection.

B-cell chronic lymphocytic leukemia (B-CLL) was diagnosed, which in cats is much less frequent than T-CLL. There was a favorable response to alkylating therapy, and the cat survived for 19 months.

We treated parental and GemR cell lines with gemcitabine in combination with a CXCR2 antagonist, Navarixin. In conclusion, these findings highlight the critical role of the CXCR2 axis in PDAC therapy resistance. Targeting CXCR2 enhances gemcitabine efficacy, offering a potential therapeutic strategy to overcome resistance in PDAC.

These findings reveal the complexity of immune cell marker expression in the peripheral blood of felines and support the broader application of flow cytometry in feline immunological and diagnostic research. The establishment of these baseline immunophenotypic profiles in healthy cats is crucial for improving the diagnosis and monitoring of feline hematopoietic diseases, ultimately contributing to better clinical management and therapeutic strategies.

VNPs displayed significant antimicrobial and biofilm disruption activity against C. albicans and strong anticancer potential against T3M-4 and CD18/HPAF pancreatic cancer cell lines, with IC50 ∼ 4 µg mL-1. These results underscore fungal-mediated synthesis as a viable approach for generating multifunctional, biocompatible nanomaterials for antifungal and anticancer therapy.