LY9 (Lymphocyte Antigen 9)

By integrating germline (GWAS-based) and somatic evidence, this study provides a comprehensive view of HCC pathogenesis. This integrated strategy successfully identified a core set of genes and proteins with potential causal links to HCC, elucidating their functional convergence in cancer biology. These findings offer novel molecular insights and candidate targets for precise diagnosis, prognostic assessment, and targeted therapy of HCC, laying a solid foundation for future translational research.

Recent analyses of their T cell receptor repertoire, thymic differentiation, and mechanism of suppression are summarized. Identification of the human homolog of these cells has suggested new strategies for CD8+ Treg-dependent immunotherapy for autoimmune disease and cancers.

The inactivation of the CXCR4/PI3K/Akt/HIF-1 pathway played a pivotal role in mediating the capacity of erinacine S to inhibit chemoresistant CRC growth while enhancing tumor apoptosis. Thus, erinacine S demonstrates notable inhibitive effects, both in vitro and in vivo, through the inhibition of invasion, migration, and proliferation in human chemoresistant cell lines, and holds promise as a natural agent for clinical therapy of patients with CRC.

Our study identified 37 potential lymphoma drug targets, emphasizing FCRL3 and LY9 as valuable therapeutic candidates, and amiodarone and chrysin in clinical translational application.

For therapeutic applications, we develop a liposome-based nanoparticle system that delivers the LY96 inhibitor L6H21 to tumor cells and effectively suppresses HCC progression through a combination of in vivo and in vitro studies. Taken together, the current observations identify LY96 as a promising diagnostic indicator and a viable intervention for therapeutic modulation to improve HCC treatment.

In vivo, ZJH-1 (20 mg/kg, i.p.) significantly attenuated tumor growth in PC3 xenograft models (75% volume reduction vs. controls) with no obvious weight loss or overt toxic side effects observed. These findings suggest that ZJH-1, a selective HDAC1 inhibitor, merits further investigation as a potential treatment for PCa.

PML also occurs as a serious adverse event for a subset of immunosuppressive therapies (e.g., natalizumab and rituximab) used to treat patients with immune disorders (e.g., multiple sclerosis and hematological malignancies). Interestingly, of the 4 genes with a PML risk variant, 2 (LY9 and STXBP2) cause or are linked to HLH. The aim of our review is two-fold: (1) raise awareness among researchers and clinicians (e.g., neurologists, oncologists, and rheumatologists) that patient genetics are a key risk factor for PML, and (2) further reinforce the rationale for screening at-risk patients for PML risk variants before prescribing a PML-linked drug.

The immune pressure exerted by anti-CD229 CAR-T cells led to the loss of the CD229 antigen expression in some instances. In summary, this work underscores the potential utility of CD229 alone or in combination with BCMA, as an immunotherapeutic target in multiple myeloma, especially in cases marked by diminished or absent BCMA expression.

Both proteins may be potential targets for sepsis. This study identified several protein biomarkers associated with the risk of sepsis, provided novel insights into the etiology of sepsis, and identified promising targets (CD33 and LY9) for the development of therapeutic drugs for sepsis.

Expression of Ly49A alone on an H-2Dd background restored missing-self target cell rejection, NK cell licensing, and NK cell KLRG1 expression. Thus, a single inhibitory Ly49 receptor is sufficient to license NK cells and mediate missing-self in vivo.

By performing analyses of HNSCC tumor samples from The Cancer Genome Atlas (TCGA) database, we discovered that decreased expression of these genes, both as single genes and as a 5-gene signature (5-GS), was significantly correlated with worse overall survival (OS). Our data show that the levels of expression of the 5-GS represent an immune profile predicting OS in patients with HNSCC.

The expression levels of SOD1 in tumor tissues of DLBCL patients were significantly increased. As a SOD1 inhibitor, LCS-1 can significantly inhibit the viability and proliferation of DLBCL cell lines OCI-Ly18 and OCI-Ly19, and promote cell apoptosis, which provides a new idea for the treatment of DLBCL.