HLA-B (Major Histocompatibility Complex, Class I, B)

In particular, HLA-B leader matched patients had a higher CD57 expression of total NK and NKG2A+KIR- NK cells, with enhanced NKG2A+KIR- NK cell cytotoxicity (CD107a expression) and IFN-γ secretion at 1, 3, and 6 months post-transplantation (all false discovery rate-adjusted P <0.05). These findings identify HLA-B leader matching status as a disease-specific prognostic biomarker, suggesting its potential relevance for personalized donor selection considerations in haplo-HSCT settings.

Additionally, we reveal multiple biomarkers associated with nICT efficacy, including SBS19, HLA-B∗15:02, FDXR expression, and FGFR pathway activity, and provide a multi-omic stratification model for treatment response-based patient stratification. This study provides mechanistic insights into nICT in GC, informs therapeutic decisions, and reveals potential targets.

These data suggest that KIR AA individuals possess strong inhibitory interactions of KIR alleles and HLA, arming KIR AA + NK cells to meditate stronger alloreactivity and cytotoxicity against leukemia cells with lowered HLA expression. Our findings may provide valuable insights into leukemia pathogenesis and better understanding of the immune mechanisms.

Instead, novel alleles emerge: HLA-C*03:04:01 correlating strongly with anti-infliximab ADAs and HLA-B*15:18:01 with anti-adalimumab ADAs. This letter aimed to contextualize these findings within the broader literature and to lay the ground for further analysis of ethnic variations and the implications for personalized medicine in inflammatory bowel disease. This divergence may suggest how genetic architecture shapes immunogenicity risk across ethnicities.

These findings suggest an important role of HLA class I and II molecules in the genetic susceptibility of MM compared with MGUS, suggesting alterations in peptide-binding capabilities may impair immune recognition of malignant cells. Further studies are needed to validate our findings and elucidate the biological mechanisms.

P1, N=28, Recruiting, Massachusetts General Hospital | Not yet recruiting --> Recruiting

P1, N=20, Suspended, Fred Hutchinson Cancer Center | Recruiting --> Suspended

Chemosensitivity analysis showed that the high-risk group had increased sensitivity to four drugs, including Axitinib, but decreased sensitivity to 21 drugs, including Cisplatin...Molecular docking revealed that five compounds, including Oseltamivir, could bind directly to NEU1. Knockdown of NEU1 significantly reduced proliferation, migration, and invasion of LIHC cells, and slowed LIHC tumor growth. We constructed a histone acetylation-based risk model for LIHC diagnosis, prognosis, and therapy, identifying NEU1 as a key biomarker and potential therapeutic target.

Employing Micro-C, a micrococcal nuclease-based 3D genome mapping technique, we show that EZH1/2 inhibition with Valemetostat induced significant changes at multiple genome organizational levels (compartment, topological associated domain, and chromatin loop) without incurring cell death in NE SCLC...Notably, EZH1/2 inhibition reactivated Class I MHC expression by facilitating enhancer-promoter looping. Our results demonstrate that repression of a subset of EZH2 targets including Class I MHC genes is affected through modulation of 3D genome structure to the level of chromatin looping and further support clinical investigation of EZH2 inhibition in boosting therapeutic efficacy of ICI in SCLC patients.

P2, N=313, Active, not recruiting, Center for International Blood and Marrow Transplant Research | Recruiting --> Active, not recruiting

Class II alleles, especially those within DQA1 and DPB1, are important genetic factors influencing AML susceptibility in the Kazakhstani population.

B1.23.2 treatment of the human KLM-1 pancreatic cancer model in humanized (NSG-IL15) mice provides evidence of suppression of tumor growth. Such anti-MHC-I mAb that block inhibitory KIR/HLA interactions may prove useful for tumor immunotherapy.