Blood Advances血液进展
Blood Advances(英文缩写 BLOOD ADV),ISSN 2473-9529,eISSN 2473-9537,中文译名:血液进展 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 7.642 | Q1 |
| 2022 | 7.500 | Q1 |
| 2023 | 7.400 | Q1 |
| 2024 | 7.100 | Q1 |
| 2025 | 7.700 | Q1 |
Blood Advances 最新收录文献
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1. Phase 1/2 study of favezelimab plus pembrolizumab in anti-PD-1-naive relapsed or refractory classical Hodgkin lymphoma.
1. favezelimab联合帕博利珠单抗在抗PD-1初治复发或难治性经典型霍奇金淋巴瘤中的1/2期研究PMID:日期:2026-10-02The phase 1/2 MK-4280-003 study evaluated favezelimab plus pembrolizumab for relapsed or refractory (R/R) hematologic malignancies. We report results in anti-PD-1-naive R/R classical Hodgkin lymphoma (cHL; cohort 1). The study comprised a safety lead-in (across 4 cohorts) to establish the recommended phase 2 dose (RP2D) of favezelimab plus pembrolizumab and an efficacy expansion phase (pembrolizumab 200 mg plus favezelimab at RP2D intravenously [IV] every 3 weeks [Q3W]). Adults with anti-PD-1-naive R/R cHL were enrolled in cohort 1. Primary end point was safety (dose-limiting toxicity [DLT], adverse events [AEs], and AEs leading to discontinuation) to establish RP2D. Objective response rate (ORR) was secondary. Duration of response (DOR), progression-free survival (PFS), and overall survival (OS) were exploratory. RP2D was favezelimab 800 mg plus pembrolizumab 200 mg IV Q3W. DLT occurred in 1 of 21 participants in the safety lead-in (grade 4 autoimmune hepatitis). Cohort 1 enrolled 30 participants. Treatment-related AEs occurred in 27 participants (90%; grade 3 or 4 in 7 participants [23%]; no grade 5), and 5 participants (17%) discontinued treatment. ORR was 83% (95% CI, 65-94); complete response rate was 37% (95% CI, 20-56). Median DOR was 17.0 months (range, 2.6-33.3+); an estimated 44% of responders continued to have responses after ≥24 months. Median PFS was 19.4 months (95% CI, 9.5-28.5); 24-month PFS rate was 46%. Median OS was not reached (NR; 95% CI, 46.9-NR); 24-month OS rate was 93%. Favezelimab plus pembrolizumab showed antitumor activity and manageable safety in participants with anti-PD-1-naive R/R cHL. This trial was registered at www.ClinicalTrials.gov as NCT03598608.
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2. An Electronic Frailty Index Is Associated with Outcomes in Older Adults Receiving CAR-T Therapy.
2. 电子衰弱指数与接受CAR-T治疗的老年人的预后相关PMID:日期:2026-10-02Predicting outcomes for older adults undergoing Chimeric Antigen Receptor T-cell (CAR-T) therapy is critical. Frailty is associated with poor outcomes, but can be difficult to measure in clinical practice. We retrospectively analyzed patients age ≥65 years receiving commercial CAR-T at Mass General Brigham for multiple myeloma and B-cell non-Hodgkin lymphoma. We calculated an electronic frailty index (eFI), a validated, automated frailty score (<0.1=robust, 0.1-0.2=pre-frail, 0.2-0.3=frail, and >0.3=very frail). We evaluated associations of eFI (robust/prefrail vs frail vs very frail) with overall survival (OS), event-free (death, progression, or new treatment) survival (EFS), toxicity (cytokine release syndrome (CRS) and/or immune effector cell-associated neurotoxicity syndrome (ICANS)), and days alive and out of hospital in the first 30 days (DAOH) using regression models controlling for confounders. Among 260 patients (median age: 73 years [range 65-91]), 10% were robust, 25% prefrail, 28% frail, and 37% very frail. In multivariable analyses, being frail was not associated with OS (hazard ratio [HR] 1.22, p=0.45) or EFS (HR=1.39, p=0.14), but very frail patients had significantly worse OS (HR=1.64, p<0.05) and EFS (HR=2.02, p<0.01). Both frail and very frail patients, respectively, had higher odds of grade 3+ toxicity (odds ratio [OR]=3.28, p<0.05; OR=4.84, p<0.01) and fewer DAOH (β= -2.37, p = 0.03; β= -3.79, p<0.01). The eFI identifies frail and very frail patients with higher risk for grade 3+ CRS/ICANS and increased healthcare utilization. Very frail patients are especially high-risk with poor OS and EFS. The eFI holds promise as an automated CAR-T risk-stratification tool.
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3. Brief Cognitive Assessment in Sickle Cell Care: Psychometric Properties of the RUDAS Across Two Languages.
3. 镰状细胞病护理中的简要认知评估：RUDAS量表在两种语言中的心理测量学特性PMID:日期:2026-10-02Neurocognitive disorders (NCD) are frequent yet underrecognized in adults with sickle cell disease (SCD), and practical strategies for routine cognitive assessment remain limited. We evaluated the psychometric properties of the Rowland Universal Dementia Assessment Scale (RUDAS) in the cognitive evaluation of adults with SCD.Between 2018 and 2023, adults with SCD were recruited from three comprehensive centers in Canada and France. Participants completed either the French or English version of the RUDAS. A prespecified subset underwent comprehensive multidisciplinary neurocognitive evaluation to establish a clinical diagnosis of minor or major NCD. The diagnostic performance of clinically relevant RUDAS cutoffs was assessed against a multidisciplinary reference diagnosis of minor or major NCD.A total of 440 adults with SCD were included (median age, 34 years; 56.4% female). The median RUDAS score was 26 (range, 16-30). A RUDAS cutoff score <27 demonstrated a specificity of 83% for detecting NCD. Adjustment for educational attainment increased specificity to 89%, with corresponding reduction in sensitivity from 50% to 45%. Latent class analysis identified two distinct cognitive profiles; individuals in the lower-performing group were older and more likely to have a history of prior stroke, vascular risk factors, impaired kidney function, lower educational attainment, and unemployment.In adults with SCD, the RUDAS provides a pragmatic and accessible approach to support brief cognitive assessment in routine clinical care. While its role in isolation is limited by moderate sensitivity, its high specificity may facilitate targeted referral for comprehensive neurocognitive evaluation and interventions.
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4. Platelet GPVI drives fibrotic lung remodeling.
4. 血小板GPVI驱动纤维化肺重塑PMID:日期:2026-10-02Platelets are a major reservoir of bioactive mediators, including growth factors such as transforming growth factor β1 (TGF-β1), that regulate vascular repair and tissue remodeling. Beyond these classical functions, platelets also participate in inflammatory hemostasis through activation pathways that differ from those engaged during hemostatic thrombus formation. However, the platelet mechanisms linking inflammatory vascular activation to chronic fibrotic remodeling remain poorly defined. Here, we identify the immunoreceptor tyrosine-based activation motif (ITAM)-coupled platelet receptor glycoprotein VI (GPVI) as a critical driver of fibrotic lung remodeling. We observed that platelets accumulated within fibrotic regions of lungs from patients with idiopathic pulmonary fibrosis and from mice with bleomycin-induced lung injury and displayed a preactivated phenotype characterized by P-selectin exposure and integrin αIIbβ3 activation. Using genetic mouse models, we demonstrate that platelet aggregation mediated by integrin β3 is dispensable for the development of lung fibrosis. Similarly, signaling through the ADP receptor P2Y12 was also dispensable. In contrast both genetic deletion and pharmacological inhibition of GPVI protected mice from bleomycin-induced mortality and markedly reduced lung fibrosis. Mechanistically, both GPVI deficiency and pharmacological GPVI inhibition reduced the early release of the platelet chemokine PF4 into bronchoalveolar lavage fluid, whereas TGF-β1 levels were unaffected. Consistently, PF4-deficient mice were protected from bleomycin-induced fibrosis, and PF4 directly promoted fibroblast differentiation and collagen gene expression in vitro. Together, these findings identify GPVI as a critical upstream regulator of platelet-driven fibrotic lung remodeling and support a model in which GPVI-dependent PF4 release contributes to pulmonary fibrosis independently of platelet aggregation.
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7. Novel KIR2DS4:HLA-B*35 interaction predicts HLA-B*35 positive patient survival post hematopoietic stem cell transplant.
7. 新型KIR2DS4:HLA-B*35相互作用预测HLA-B*35阳性患者造血干细胞移植后的生存率PMID:日期:2026-09-30Haplo-identical hematopoietic cell transplantation (haploHCT) is an integral treatment paradigm for patients with leukemia. While overall survival (OS) post-haploHCT has steadily improved, relapse-free survival (RFS) remains relatively stagnant. Upon the discovery of killer immunoglobulin-like receptors (KIRs) on natural killer (NK) cells and their cognate human leukocyte antigen (HLA) ligands, algorithms have been developed to enhance graft versus leukemia effects. However, these algorithms fail to yield consistent predictions in patient outcomes. We utilized a combination of in silico protein folding and interactions to determine KIR:HLA reactivity in conjunction with in vitro acoustic force microscopy to measure cell avidity (CA) as a readout for KIR signal strength. CA was determined using monoallelic HLA expressing K562 cell lines, monoallelic KIR Jurkat cells, and peripheral blood NK cells. We extended the CA results and performed standard cytotoxicity assays as well. We discovered that HLA-B*35 interacts with KIR2DS4. We applied the newly discovered interaction to predict outcomes for HCT patients. Stratifying patients based on their HLA-B*35 positivity and donor KIR2DS4 status, we delineated a correlation to survival (P=0.061) when donors only had full-length KIR2DS4. Patients who received a haploHCT and NK cell addback from donors with only full-length KIR2DS4 had a significantly improved RFS (P=0.001) and OS (P=0.016) compared to truncated (KIR1D) and full-length KIR2DS4 donors. This was independently validated in a diverse 10/10 HLA matched European cohort with RFS (P=0.0255) and OS (P=0.0388). Thus, the identified novel KIR2DS4:HLA-B*35 interaction axis predicts patient survival, in both haplo-identical and fully matched, HCT and highlights that our current understanding of the KIR:HLA interactome is incomplete and requires remapping for enhanced therapeutic applications.
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8. Democratizing cancer risk testing in children before alloHCT.
8. 在异基因造血干细胞移植前实现儿童癌症风险检测的普及化PMID:日期:2026-09-25该文献暂无摘要。
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10. Beyond hemolysis: redefining pediatric AIHA.
10. 超越溶血：重新定义儿童自身免疫性溶血性贫血PMID:日期:2026-09-24该文献暂无摘要。