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Shifting treatment goals in myeloproliferative neoplasms: focusing on polycythemia vera. 骨髓增生性肿瘤治疗目标的转变:聚焦真性红细胞增多症。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-30 DOI: 10.1007/s12185-025-04119-5
Keita Kirito

JAK2V617F is the major driver mutation in polycythemia vera, and detection of this mutation is one of the most important keys for the diagnosis of this disease. In addition, JAK2V617F mutation is highlighted as a molecular marker for monitoring treatment. Clinical studies of the JAK inhibitor ruxolitinib and two recently introduced new forms of alfa interferon, pegylated interferon alfa 2b and ropeginterferon alfa 2b, demonstrated that treatment with these agents induced a molecular response, defined as a more than 50% reduction in the JAK2V617F allele burden from baseline, in approximately 60% of patients. In addition, some patients achieved a complete molecular response, defined as the disappearance of the mutation. More importantly, achievement of a molecular response was positively correlated with improved thrombosis-free and progression-free survival in PV patients. To date, controlling hematological parameters, especially maintaining hematocrit levels below 45%, has been the gold standard surrogate endpoint in PV treatment. With new treatment options and knowledge, molecular response should be incorporated as a new therapeutic surrogate endpoint in the management of PV.

JAK2V617F是真性红细胞增多症的主要驱动突变,该突变的检测是真性红细胞增多症诊断的最重要关键之一。此外,JAK2V617F突变被强调为监测治疗的分子标记。JAK抑制剂ruxolitinib和最近推出的两种新形式的α干扰素(聚乙二醇干扰素α 2b和ropeg干扰素α 2b)的临床研究表明,使用这些药物治疗可诱导分子反应,定义为在大约60%的患者中,JAK2V617F等位基因负担较基线降低50%以上。此外,一些患者实现了完全的分子反应,定义为突变消失。更重要的是,分子反应的实现与PV患者无血栓形成和无进展生存期的改善呈正相关。到目前为止,控制血液学参数,特别是将血细胞比容水平维持在45%以下,一直是PV治疗的金标准替代终点。有了新的治疗选择和知识,分子反应应该被纳入PV管理的一个新的治疗替代终点。
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引用次数: 0
A phase 2 study of ibrutinib with venetoclax in Japanese patients with untreated CLL and SLL. 伊鲁替尼联合venetoclax治疗日本未治疗的CLL和SLL患者的2期研究。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-28 DOI: 10.1007/s12185-025-04114-w
Jun Takizawa, Isao Yoshida, Yoshiaki Ogawa, Tomomi Toubai, Shigeru Kusumoto, Mitsumasa Watanabe, Natsumi Ogawa, Natsuko Satomi, Yasuko Nishimura, Hideyuki Honda, Brenda Chyla, Koji Izutsu

The development of effective and safe therapies for chronic lymphocytic leukemia (CLL)/small lymphocytic lymphoma (SLL) in Japan remains a key focus of research. We conducted a phase 2, open-label, multicenter, non-comparative study to evaluate the safety and efficacy of fixed-duration venetoclax plus ibrutinib in 10 patients with previously untreated CLL/SLL (7 CLL/3 SLL). The primary endpoint was the rate of complete remission (CR)/CR with incomplete marrow recovery (CRi) assessed by the independent review committee (IRC). The median age was 72.5 (range 61-77) years. The IRC-assessed CR/CRi rate was 60.0% (95% confidence interval: 26.2-87.8%), exceeding the pre-specified efficacy threshold of 10% and meeting the primary endpoint. The median venetoclax treatment duration was 11.0 (range 2.1-17.7) months. At a median follow-up of 20.6 months, the secondary endpoints of median progression-free and overall survival were not estimated. The overall undetectable measurable residual disease rate was 60.0%. All patients experienced treatment-emergent adverse events (TEAEs), including 7 (70.0%) with grade 3/4 and 2 (20.0%) with serious TEAEs, respectively, and 1 discontinued venetoclax because of a TEAE (increased blood creatine phosphokinase). These findings suggest that venetoclax plus ibrutinib has a favorable benefit-risk profile with high efficacy and manageable safety.

在日本,开发有效和安全的治疗慢性淋巴细胞白血病(CLL)/小淋巴细胞淋巴瘤(SLL)的方法仍然是研究的重点。我们进行了一项2期、开放标签、多中心、非比较研究,以评估10例既往未治疗的CLL/SLL(7例CLL/3例SLL)患者的固定时间venetoclax + ibrutinib的安全性和有效性。主要终点是由独立审查委员会(IRC)评估的完全缓解(CR)/CR伴骨髓不完全恢复(CRi)率。中位年龄为72.5岁(61-77岁)。irc评估的CR/CRi率为60.0%(95%可信区间:26.2-87.8%),超过了预定的10%的疗效阈值,达到了主要终点。中位venetoclax治疗持续时间为11.0(2.1-17.7)个月。在中位20.6个月的随访中,没有估计中位无进展和总生存期的次要终点。总体不可检测的可测残留病率为60.0%。所有患者均出现治疗后出现的不良事件(TEAE),其中7例(70.0%)为3/4级,2例(20.0%)为严重TEAE, 1例因TEAE(血肌酸磷酸激酶升高)停用venetoclax。这些研究结果表明,venetoclax联合伊鲁替尼具有良好的获益-风险特征,具有高疗效和可管理的安全性。
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引用次数: 0
Comprehensive anticoagulant effect of heparinoid in blood samples from patients with hemophilia. 血友病患者血标本中类肝素的综合抗凝作用。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-26 DOI: 10.1007/s12185-025-04121-x
Tomoya Miyatake, Masahiro Takeyama, Kaoru Horiuchi, Shoko Furukawa, Kenichi Ogiwara, Keiji Nogami

Background: Heparinoid (Hirudoid®), a topical heparin-like agent, is labeled as contraindicated in bleeding disorders, yet its propensity for clinically relevant systemic anticoagulation remains uncertain.

Aim: To assess heparinoid's anticoagulant potential in blood from healthy individuals and people with hemophilia (PwH).

Methods: In normal plasma exposed to heparinoid (≤ 6.5 μg/mL) or heparin, and in plasma from PwH supplemented with FVIII or FIX (0-50 IU/dL), we quantified activated partial thromboplastin time (APTT) and adjusted maximum coagulation velocity (Ad|min1|) by clot waveform analysis. In heparinoid-treated whole blood from healthy volunteers (≤ 9 μg/mL), clotting time (CT) and clot formation time (CFT) were assessed by rotational thromboelastometry.

Results: In normal plasma, heparinoid dose-dependently prolonged APTT and reduced Ad|min1|; at the estimated Cmax (2.5 μg/mL), APTT increased ~ 1.2-fold and Ad|min1| approximated the effect of ~ 0.2 IU/mL heparin. In FVIII- or FIX-supplemented plasma from PwH, Ad|min1| showed a mild, factor-level-dependent decrease (~ 85% of control). In whole blood, CT + CFT changed minimally at therapeutic concentrations. Heparin controls provided an internal benchmark for assay sensitivity.

Conclusion: At therapeutic levels, heparinoid exerts only mild anticoagulant effects in both normal and hemophilic matrices, supporting the view that topical use is unlikely to pose systemic bleeding risk in PwH.

背景:类肝素(喜疗妥®)是一种外用类肝素药物,被标记为出血性疾病的禁忌症,但其在临床相关全身抗凝方面的倾向仍不确定。目的:评价健康人与血友病(PwH)患者血液中类肝素的抗凝潜能。方法:对暴露于类肝素(≤6.5 μg/mL)或肝素的正常血浆,以及添加FVIII或FIX (0-50 IU/dL)的PwH血浆,通过血块波形分析定量活化部分凝血活素时间(APTT)和调节最大凝血速度(Ad|min1|)。对健康志愿者经肝素处理的全血(≤9 μg/mL),采用旋转血栓弹性测量法评估凝血时间(CT)和凝块形成时间(CFT)。结果:在正常血浆中,肝素剂量依赖性地延长APTT,降低Ad|;在估计的Cmax (2.5 μg/mL)下,APTT增加了~ 1.2倍,Ad|min1|接近~ 0.2 IU/mL肝素的作用。在来自PwH的FVIII或fix补充的血浆中,Ad|min1|显示出轻微的因子水平依赖性下降(约为对照组的85%)。在全血中,治疗浓度下CT + CFT变化最小。肝素对照提供了测定灵敏度的内部基准。结论:在治疗水平上,肝素素在正常和血友病基质中仅发挥轻微的抗凝作用,支持局部使用不太可能造成PwH全体性出血风险的观点。
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引用次数: 0
Genome-epigenome crosstalk in T-cell lymphomas: from maps to mechanisms. t细胞淋巴瘤的基因组-表观基因组串扰:从图谱到机制。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-26 DOI: 10.1007/s12185-025-04115-9
Makoto Yamagishi

T-cell lymphomas are clinically and biologically heterogeneous malignancies that comprise ~ 10% of non-Hodgkin lymphomas. Outcomes with first-line chemotherapy remain poor. Over the past decade, integrative genomic and epigenomic studies have defined recurrent abnormalities converging on proximal T-cell antigen receptor/costimulatory signaling to the NF-κB/NFAT, JAK/STAT, PI3K/AKT/mTOR, and NOTCH pathways, alongside pervasive alterations in chromatin modifiers and the DNA methylation machinery. In this review, we frame the biology of peripheral T-cell lymphoma as two interdependent layers, including genetic events that establish constitutive signaling programs and epigenomic remodeling that stabilizes these outputs. We overview genomic alterations across major peripheral T-cell lymphoma entities and analyze epigenomic dysregulation, focusing on DNA methylation, enhancer regulation, and polycomb-mediated gene control. We highlight adult T-cell leukemia/lymphoma as a paradigmatic dual-layer disease, summarize therapeutic approaches based on epigenetic traits, and discuss biomarker-guided strategies and challenges in translating integrated maps into durable disease control.

t细胞淋巴瘤是临床上和生物学上的异质性恶性肿瘤,约占非霍奇金淋巴瘤的10%。一线化疗的结果仍然很差。在过去的十年中,综合基因组学和表观基因组学研究已经定义了复发性异常,这些异常集中在近端t细胞抗原受体/NF -κB/NFAT、JAK/STAT、PI3K/AKT/mTOR和NOTCH通路的共刺激信号,以及染色质修饰剂和DNA甲基化机制的普遍改变。在这篇综述中,我们将外周t细胞淋巴瘤的生物学分为两个相互依赖的层面,包括建立构成信号程序的遗传事件和稳定这些输出的表观基因组重塑。我们概述了主要外周t细胞淋巴瘤实体的基因组改变,并分析了表观基因组失调,重点是DNA甲基化,增强子调控和polycomb介导的基因控制。我们强调成人t细胞白血病/淋巴瘤是一种典型的双层疾病,总结了基于表观遗传特征的治疗方法,并讨论了将整合图谱转化为持久疾病控制的生物标志物引导策略和挑战。
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引用次数: 0
Current status of hematopoietic cell transplantation in patients with peripheral T-cell lymphoma including adult T-cell leukemia-lymphoma. 外周血t细胞淋巴瘤(包括成人t细胞白血病淋巴瘤)患者造血细胞移植的现状
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-24 DOI: 10.1007/s12185-025-04118-6
Shigeo Fuji, Akihiro Ohmoto

Peripheral T-cell lymphomas (PTCLs) are biologically diverse and clinically aggressive, and are difficult to control long-term with conventional immunochemotherapy. Hematopoietic cell transplantation (HCT) is a key treatment option. Autologous HCT (auto-HCT) as first-line consolidation has shown durable progression-free survival in phase 2 studies and in the auto-HCT arm of the randomized AATT trial (intent-to-treat PFS 30-49%), although its routine use after complete metabolic response remains controversial. A phase 3 trial comparing auto-HCT with observation is ongoing. For relapsed/refractory PTCL, expert consensus supports allogeneic HCT (allo-HCT) as the treatment of choice for eligible patients, with early referral and limited salvage therapy. While complete remission is ideal, partial remission is acceptable. Upfront allo-HCT is not recommended for unselected PTCL in light of the results of the AATT trial, but adult T-cell leukemia-lymphoma (ATL) is an exception. Multiple studies have shown graft-versus-ATL effects, supporting allo-HCT in aggressive ATL. Donor sources now include unrelated and haploidentical donors, with outcomes comparable to matched siblings. Despite advances, relapse after HCT remains a major challenge. Novel maintenance strategies and optimized transplant approaches are needed to further improve outcomes in PTCL and ATL.

外周t细胞淋巴瘤(PTCLs)具有生物多样性和临床侵袭性,难以用常规免疫化疗长期控制。造血细胞移植(HCT)是一个关键的治疗选择。自体HCT (auto-HCT)作为一线巩固治疗在2期研究和随机AATT试验的auto-HCT组(意向治疗PFS 30-49%)中显示出持久的无进展生存期,尽管其在完全代谢反应后的常规使用仍存在争议。一项比较auto-HCT与观察的3期试验正在进行中。对于复发/难治性PTCL,专家一致支持同种异体HCT (alloo -HCT)作为符合条件的患者的治疗选择,早期转诊和有限的抢救治疗。完全缓解是理想的,部分缓解也是可以接受的。鉴于AATT试验的结果,不推荐对未选择的PTCL进行前期allot - hct,但成人t细胞白血病淋巴瘤(ATL)是个例外。多项研究显示移植物抗ATL效应,支持同种异体hct治疗侵袭性ATL。现在的供体来源包括无亲缘关系和单倍体相同的供体,其结果与匹配的兄弟姐妹相当。尽管取得了进展,但HCT后的复发仍然是主要挑战。需要新的维持策略和优化的移植方法来进一步改善PTCL和ATL的预后。
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引用次数: 0
Recent advances of cell therapies for AML/MDS: exploring the therapeutic potential of innate immune cells in AML/MDS. AML/MDS细胞治疗的最新进展:探索先天免疫细胞在AML/MDS中的治疗潜力。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-21 DOI: 10.1007/s12185-025-04113-x
Yu-Hsuan Chang, Susumu Goyama

Immunotherapy has revolutionized cancer treatments, yet checkpoint inhibitors and CAR-T cells have shown limited efficacy in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS). This limited efficacy is primarily due to the absence of lineage-specific antigens and the presence of suppressive microenvironments. Innate immunity offers a promising alternative, as it acts independently of neoantigens. The key players such as macrophages, dendritic cells, and natural killer (NK) cells not only eliminate malignant cells but also remodel the microenvironment to enhance antileukemic activity. This review highlights recent advances in understanding innate immune mechanisms in AML and MDS and explores therapeutic strategies designed to leverage these pathways, aiming to broaden the scope of immunotherapy.

免疫疗法已经彻底改变了癌症治疗,但检查点抑制剂和CAR-T细胞对急性髓性白血病(AML)和骨髓增生异常综合征(MDS)的疗效有限。这种有限的功效主要是由于缺乏谱系特异性抗原和存在抑制性微环境。先天免疫提供了一个有希望的替代方案,因为它独立于新抗原起作用。巨噬细胞、树突状细胞和自然杀伤(NK)细胞等关键细胞不仅可以消除恶性细胞,还可以重塑微环境以增强抗白血病活性。本文综述了AML和MDS的先天免疫机制的最新进展,并探讨了利用这些途径设计的治疗策略,旨在拓宽免疫治疗的范围。
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引用次数: 0
Clinical impact of glucocorticoid responsiveness-related gene polymorphism on graft-versus-host disease and survival after single-unit cord blood transplantation. 糖皮质激素反应性相关基因多态性对单单位脐带血移植后移植物抗宿主病和存活的临床影响
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-20 DOI: 10.1007/s12185-025-04112-y
Takaaki Konuma, Megumi Hamatani-Asakura, Maki Monna-Oiwa, Seiko Kato, Shohei Andoh, Hirona Ichimura, Kazuaki Yokoyama, Yasuhito Nannya, Satoshi Takahashi

Graft-versus-host disease (GVHD) is a major complication after allogeneic hematopoietic cell transplantation (HCT), and glucocorticoids remain the standard first-line treatment. However, glucocorticoid responses vary widely and are influenced by genetic polymorphisms in glucocorticoid signaling pathways. Their impact after cord blood transplantation (CBT) is unclear. We retrospectively analyzed adult patients who underwent single-unit CBT at our institution between 2005 and 2023 with available donor or recipient DNA. Genotyping of NR3C1 (rs33388) and GLCCI1 (rs37972, rs37973) was performed using TaqMan® assays. In univariate analyses, donor GLCCI1 rs37973 AG/AA genotypes were associated with a higher incidence of grades II to IV acute GVHD but a lower incidence of chronic GVHD compared with GG donors. Multivariate analysis confirmed that GLCCI1 rs37973 AG/AA donors had a significantly reduced risk of chronic GVHD (hazard ratio 0.57, 95% confidence interval 0.35-0.93, P = 0.025). Among 30 patients who developed grades III to IV acute GVHD treated with glucocorticoids, recipient NR3C1 rs33388 TT genotype was associated with significantly lower overall survival compared with AT/AA (24.4% vs. 63.5% at 5 years, P = 0.044). These findings suggest that donor GLCCI1 rs37973 and recipient NR3C1 rs33388 polymorphisms may influence GVHD risk and survival after CBT.

移植物抗宿主病(GVHD)是同种异体造血细胞移植(HCT)后的主要并发症,糖皮质激素仍然是标准的一线治疗方法。然而,糖皮质激素的反应差异很大,并受到糖皮质激素信号通路遗传多态性的影响。它们在脐带血移植(CBT)后的影响尚不清楚。我们回顾性分析了2005年至2023年间在我们机构接受单单位CBT的成人患者,并分析了可用的供体或受体DNA。采用TaqMan®方法对NR3C1 (rs33388)和GLCCI1 (rs37972、rs37973)进行基因分型。在单因素分析中,与GG供者相比,供者GLCCI1 rs37973 AG/AA基因型与II至IV级急性GVHD发生率较高相关,但与慢性GVHD发生率较低相关。多因素分析证实,GLCCI1 rs37973 AG/AA供者发生慢性GVHD的风险显著降低(风险比0.57,95%可信区间0.35-0.93,P = 0.025)。在接受糖皮质激素治疗的30例III至IV级急性GVHD患者中,受体NR3C1 rs33388 TT基因型与AT/AA相比,总生存率显著降低(5年生存率为24.4%比63.5%,P = 0.044)。这些发现表明,供体GLCCI1 rs37973和受体NR3C1 rs33388多态性可能影响CBT后GVHD的风险和生存。
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引用次数: 0
Comprehensive assessment of DeVIC therapy for relapsed or refractory diffuse large B-cell lymphoma. DeVIC治疗复发或难治性弥漫性大b细胞淋巴瘤的综合评价。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-19 DOI: 10.1007/s12185-025-04104-y
Yosuke Nakaya, Takuro Yoshimura, Tetsuya Hayashi, Masahiro Yoshida, Yoshiki Hayashi, Takafumi Nakao

Evidence regarding the efficacy and safety of DeVIC (dexamethasone, etoposide, ifosfamide, and carboplatin) therapy for relapsed or refractory diffuse large B-cell lymphoma (r/r DLBCL) is critically lacking. This retrospective study analyzed 78 patients with r/r DLBCL who received DeVIC therapy at a single institution. The overall response rate was 37.2%, comprising 21.8% complete and 15.4% partial responses. A total of 15 (19.2%) patients proceeded to transplantation or cellular therapy. The 3-year overall survival and progression-free survival were 28.2 and 18.0%, respectively. Multivariable analyses identified refractoriness to prior therapy and elevated serum lactate dehydrogenase (LDH) levels as significant predictors of poor response and survival. Decision tree models confirmed these findings, revealing that relapsed cases with low LDH had the most favorable outcomes. Hematological toxicities were frequent, with febrile neutropenia in 52.6% and infection-related mortality in 3.8% of patients. Those with central nervous system involvement had a dismal prognosis, underscoring the need for novel therapeutic approaches. These findings highlight the potential role of DeVIC therapy in selected patients with r/r DLBCL and provide insights into optimizing bridging strategies and subsequent immunocellular therapies.

关于DeVIC(地塞米松、依托泊苷、异环磷酰胺和卡铂)治疗复发或难治性弥漫性大b细胞淋巴瘤(r/r DLBCL)的有效性和安全性的证据严重缺乏。本回顾性研究分析了78例在同一机构接受DeVIC治疗的r/r DLBCL患者。总体应答率为37.2%,其中完全应答21.8%,部分应答15.4%。共有15例(19.2%)患者接受移植或细胞治疗。3年总生存率和无进展生存率分别为28.2%和18.0%。多变量分析发现,既往治疗的难治性和血清乳酸脱氢酶(LDH)水平升高是不良反应和生存的重要预测因素。决策树模型证实了这些发现,显示低LDH的复发病例有最有利的结果。血液学毒性很常见,52.6%的患者出现发热性中性粒细胞减少症,3.8%的患者出现感染相关死亡率。中枢神经系统受累的患者预后不佳,强调需要新的治疗方法。这些发现突出了DeVIC治疗在特定的r/r DLBCL患者中的潜在作用,并为优化桥接策略和随后的免疫细胞治疗提供了见解。
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引用次数: 0
Advances in immune microenvironment profiling during multiple myeloma progression and therapy. 多发性骨髓瘤进展和治疗过程中免疫微环境分析的进展。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-18 DOI: 10.1007/s12185-025-04110-0
Junzhe Bai, Nao Nishimura, Yawara Kawano

Recent therapeutic advances, including immunomodulatory drugs, proteasome inhibitors, monoclonal antibodies, bispecific antibodies, and chimeric antigen receptor-T-cell therapies, have transformed the treatment landscape of multiple myeloma (MM). Beyond direct cytotoxicity, these agents profoundly reshape the bone marrow immune microenvironment, which plays a decisive role in disease initiation, progression, and therapeutic response. MM cells thrive within this specialized niche by recruiting and reprogramming regulatory T cells, myeloid-derived suppressor cells, dendritic cells, and macrophages to suppress antitumor immunity while simultaneously driving functional exhaustion of effector T cells and impairing natural killer cell cytotoxicity. Accumulating evidence demonstrates that these immune alterations emerge even at precursor stages, such as monoclonal gammopathy of undetermined significance and smoldering MM, progressively intensifying disease evolution. In this review, we synthesize recent insights into immune cell dynamics during MM progression, highlighting both regulatory and effector compartments. We further discuss how contemporary therapies modulate these immune interactions, underscoring their dual roles in fostering immune activation while, at times, sustaining immunosuppressive pathways. A comprehensive understanding of the immune landscape in MM will be critical to optimizing existing treatments, overcoming therapeutic resistance, and guiding the development of next-generation immunotherapies.

最近的治疗进展,包括免疫调节药物、蛋白酶体抑制剂、单克隆抗体、双特异性抗体和嵌合抗原受体- t细胞疗法,已经改变了多发性骨髓瘤(MM)的治疗前景。除了直接的细胞毒性外,这些药物还深刻地重塑骨髓免疫微环境,这在疾病的发生、进展和治疗反应中起着决定性作用。MM细胞通过招募和重编程调节性T细胞、髓源性抑制细胞、树突状细胞和巨噬细胞来抑制抗肿瘤免疫,同时驱动效应T细胞的功能衰竭和损害自然杀伤细胞的细胞毒性。越来越多的证据表明,这些免疫改变甚至出现在前体阶段,如意义不明的单克隆γ病和阴烧性MM,逐渐加剧疾病演变。在这篇综述中,我们综合了最近对MM进展过程中免疫细胞动力学的见解,强调了调节和效应区室。我们进一步讨论了当代疗法如何调节这些免疫相互作用,强调了它们在促进免疫激活的同时,有时维持免疫抑制途径的双重作用。全面了解MM的免疫景观对于优化现有治疗、克服治疗耐药性和指导下一代免疫疗法的发展至关重要。
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引用次数: 0
Advances in treatment of chronic graft-versus-host disease. 慢性移植物抗宿主病的治疗进展。
IF 1.8 4区 医学 Q3 HEMATOLOGY Pub Date : 2025-11-17 DOI: 10.1007/s12185-025-04102-0
Takanobu Morishita, Yoshihiro Inamoto

Chronic graft-versus-host disease (cGVHD) is a leading cause of late morbidity and mortality after allogeneic hematopoietic cell transplantation. Corticosteroids remain the standard first-line therapy; however, many patients develop steroid-refractory or steroid-dependent disease, underscoring the need for more effective and better-tolerated treatments. Ruxolitinib has emerged as the most evidence-supported option for steroid-refractory cGVHD, with the phase 3 REACH3 trial demonstrating higher response rates, durable disease control, and clinically meaningful improvements in symptom burden compared with best available therapy. Belumosudil and axatilimab have also shown encouraging efficacy and safety in heavily pretreated populations. The addition of novel agents to standard corticosteroid-based therapy has been explored in clinical trials. Interest in combination strategies, such as ruxolitinib with extracorporeal photopheresis or belumosudil, is increasing, though prospective studies are required to define their role. Key challenges include optimizing long-term safety, mitigating infectious complications, and preserving the graft-versus-leukemia effect. This review summarizes current therapeutic strategies and discusses evolving treatment algorithms, emphasizing practical considerations in therapy selection. Approaches targeting specific pathogenic mechanisms, combining agents with distinct mechanisms of action, and incorporating biomarker-driven strategies are expected to further improve outcomes and quality of life for patients with cGVHD.

慢性移植物抗宿主病(cGVHD)是异基因造血细胞移植后晚期发病和死亡的主要原因。皮质类固醇仍然是标准的一线治疗;然而,许多患者发展为类固醇难治性或类固醇依赖性疾病,强调需要更有效和耐受性更好的治疗。Ruxolitinib已成为类固醇难治性cGVHD的最具证据支持的选择,与最佳可用治疗相比,3期REACH3试验显示更高的缓解率,持久的疾病控制和临床有意义的症状负担改善。白莫硫地尔和阿替利单抗在大量预处理人群中也显示出令人鼓舞的疗效和安全性。在临床试验中探索了在标准皮质类固醇基础治疗中添加新药物的方法。尽管需要前瞻性研究来确定其作用,但对联合策略的兴趣正在增加,例如ruxolitinib与体外光化学或belumosudil。关键的挑战包括优化长期安全性,减轻感染并发症,并保持移植物抗白血病的效果。这篇综述总结了目前的治疗策略,并讨论了不断发展的治疗算法,强调了治疗选择的实际考虑。针对特定致病机制的方法,结合具有不同作用机制的药物,以及结合生物标志物驱动的策略,有望进一步改善cGVHD患者的预后和生活质量。
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引用次数: 0
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International Journal of Hematology
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