Experimental hematology最新文献_第6页

IF 2.5 4区医学

Experimental hematology Pub Date : 2024-09-18 DOI: 10.1016/S0301-472X(24)00505-8

引用次数: 0

The Pluripotent Path to Immunotherapy 多能免疫疗法之路

IF 2.5 4区医学

Experimental hematology Pub Date : 2024-09-07 DOI: 10.1016/j.exphem.2024.104648

Mame P. Diop, Sjoukje J.C. van der Stegen

{"title":"The Pluripotent Path to Immunotherapy","authors":"Mame P. Diop, Sjoukje J.C. van der Stegen","doi":"10.1016/j.exphem.2024.104648","DOIUrl":"10.1016/j.exphem.2024.104648","url":null,"abstract":"<div><div>Adoptive cell therapy (ACT) enhances the patient's own immune cells’ ability to identify and eliminate cancer cells. Several immune cell types are currently being applied in autologous ACT, including T cells, natural killer (NK) cells, and macrophages. The cells’ inherent antitumor capacity can be used, or they can be targeted toward tumor-associated antigen through expression of a chimeric antigen receptor (CAR). Although CAR-based ACT has achieved great results in hematologic malignancies, the accessibility of ACT is limited by the autologous nature of the therapy. Induced pluripotent stem cells (iPSCs) hold the potential to address this challenge, because they can provide an unlimited source for the in vitro generation of immune cells. Various immune subsets have been generated from iPSC for application in ACT, including several T-cell subsets (αβT cells, mucosal-associated invariant T cells, invariant NKT [iNKT] cells, and γδT cells), as well as NK cells, macrophages, and neutrophils. iPSC-derived αβT, NK, and iNKT cells are currently being tested in phase I clinical trials. The ability to perform (multiplexed) gene editing at the iPSC level and subsequent differentiation into effector populations not only expands the arsenal of ACT but allows for development of ACT utilizing cell types which cannot be efficiently obtained from peripheral blood or engineered and expanded in vitro.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"139 ","pages":"Article 104648"},"PeriodicalIF":2.5,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142282635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Downregulation of autophagy is associated with poor clinical outcome after immunochemotherapy in patients with diffuse large B-cell lymphoma 弥漫大B细胞淋巴瘤患者接受免疫化疗后，自噬功能下调与临床疗效不佳有关。

IF 2.5 4区医学

Experimental hematology Pub Date : 2024-09-05 DOI: 10.1016/j.exphem.2024.104638

Ya-Li Zhang , Meng-Xue Ma , Li-Na Xing , Jing-Nan Zhang , Xiao-Nan Guo , Shu-kai Qiao

{"title":"Downregulation of autophagy is associated with poor clinical outcome after immunochemotherapy in patients with diffuse large B-cell lymphoma","authors":"Ya-Li Zhang , Meng-Xue Ma , Li-Na Xing , Jing-Nan Zhang , Xiao-Nan Guo , Shu-kai Qiao","doi":"10.1016/j.exphem.2024.104638","DOIUrl":"10.1016/j.exphem.2024.104638","url":null,"abstract":"<div><div>This study aimed to determine the expression levels of the autophagy markers Beclin-1 and p62 in patients with diffuse large B-cell lymphoma (DLBCL) and explore the association between autophagy and disease prognosis. The expression of Beclin-1 and p62 was investigated in patients with DLBCL and patients with reactive lymphoproliferative disease (RLD) using immunohistochemistry. The association between the clinical characteristics of patients with DLBCL and autophagy status was further analyzed. Beclin-1 levels were increased in RLD patients compared with those with DLBCL, but the difference was not statistically significant (<em>p</em> > 0.05). p62 levels in DLBCL patients were significantly higher than those in RLD patients (<em>p</em> < 0.05). Beclin-1 expression was associated only with the Ann Arbor stage (<em>p</em> < 0.05), whereas p62 expression was associated with the Ann Arbor stage, IPI score, extranodal involvement, and Ki-67 index (<em>p</em> < 0.05). Beclin-1 and p62 levels were not associated with short-term treatment efficacy in DLBCL patients. Survival analysis showed that Beclin-1 expression had no significant effect on 2-year progression-free survival (PFS) or overall survival (OS) (<em>p</em> > 0.05). However, high p62 expression in DLBCL patients was associated with reduced 2-year PFS compared with that of patients with low p62 expression (<em>p</em> < 0.05); the 2-year OS was not affected (<em>p</em> > 0.05). Our results demonstrate that autophagic activity affects the prognosis of DLBCL patients; the lower the autophagic activity, the shorter the PFS. Targeted p62 knockout may be a novel therapeutic strategy for the treatment of DLBCL patients.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"139 ","pages":"Article 104638"},"PeriodicalIF":2.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Involvement of CREB3L1 in erythropoiesis induced by JAK2 exon 12 mutation CREB3L1参与了JAK2第12外显子突变诱导的红细胞生成。

IF 2.5 4区医学

Experimental hematology Pub Date : 2024-09-04 DOI: 10.1016/j.exphem.2024.104636

Maho Okuda , Marito Araki , Federico De Marchi , Soji Morishita , Misa Imai , Hanaka Fukada , Miki Ando , Norio Komatsu

{"title":"Involvement of CREB3L1 in erythropoiesis induced by JAK2 exon 12 mutation","authors":"Maho Okuda , Marito Araki , Federico De Marchi , Soji Morishita , Misa Imai , Hanaka Fukada , Miki Ando , Norio Komatsu","doi":"10.1016/j.exphem.2024.104636","DOIUrl":"10.1016/j.exphem.2024.104636","url":null,"abstract":"<div><div><em>CREB3L1</em>, a gene encoding the endoplasmic reticulum stress transducer, is specifically overexpressed in platelet RNA from patients with myeloproliferative neoplasms (MPNs). However, the pathophysiological roles of <em>CREB3L1</em> overexpression remain unclear. In the present study, we aimed to study <em>CREB3L1</em> messenger RNA (mRNA) expression in the red blood cells (RBCs) of patients with MPN and its role in erythrocytosis. Elevated expression of <em>CREB3L1</em> was exclusively observed in the RBCs of patients with polycythemia vera (PV) harboring <em>JAK2</em> exon 12 mutations, but not in those harboring <em>JAK2</em> V617F mutation or control subjects. In erythropoiesis, <em>CREB3L1</em> expression was sharply induced in erythroblasts of bone marrow cells collected from patients with <em>JAK2</em> exon 12 mutation. This was also evident when erythropoiesis was induced in vitro using hematopoietic stem and progenitor cells (HSPCs) with <em>JAK2</em> exon 12 mutation. Interestingly, overexpression of <em>CREB3L1</em> in RBCs was observed in patients with reactive erythrocytosis whose serum erythropoietin (EPO) levels exceeded 100 mIU/mL. Elevated <em>CREB3L1</em> expression was also observed in the erythroblasts of a patient with acute erythroid leukemia. EPO-dependent induction of <em>CREB3L1</em> was evident in erythroblasts differentiated from HSPCs in vitro, regardless of driver mutation status or MPN pathogenesis. These data strongly suggest that <em>CREB3L1</em> overexpression in RBCs is associated with hyperactivation of the EPO receptor and its downstream molecule, JAK2. Short hairpin RNA (shRNA) knockdown of <em>CREB3L1</em> expression in HSPCs blocked erythroblast formation in vitro. These results suggest that <em>CREB3L1</em> is required for erythropoiesis in the presence of <em>JAK2</em> exon 12 mutation or high level of EPO, possibly by antagonizing cellular stress.</div></div>","PeriodicalId":12202,"journal":{"name":"Experimental hematology","volume":"139 ","pages":"Article 104636"},"PeriodicalIF":2.5,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

IFC Editorial Board 国际金融公司编辑委员会

IF 2.5 4区医学

Experimental hematology Pub Date : 2024-09-01 DOI: 10.1016/S0301-472X(24)00493-4

引用次数: 0

3216 – FORMATION OF PRE-LEUKEMIC STEM CELLS IN A KMT2A::AFF1 MURINE MODEL REQUIRES AN EMBRYONIC TARGET CELL 3216 - 在 kmt2a::aff1 小鼠模型中形成前白血病干细胞需要胚胎靶细胞

IF 2.6 4区医学

Experimental hematology Pub Date : 2024-08-29 DOI: 10.1016/j.exphem.2024.104536

Charlotta Böiers, Ariana Calderón, Roshanak Ghazanfari, Shabnam Khazari, Stefan Lang, Mohamed Eldeeb, Sara Palo, Shamit Soneji, David Bryder, Charlotta Böiers

引用次数: 0

3203 – PROTEIN TYROSINE PHOSPHATASE PRL2 PROMOTES MLL-AF9 DRIVEN LEUKEMOGENESIS VIA INHIBITING THE P53 PATHWAY 3203 - 蛋白酪氨酸磷酸酶 prl2 通过抑制 p53 通路促进 mll-af9 驱动的白血病发生

IF 2.6 4区医学

Experimental hematology Pub Date : 2024-08-29 DOI: 10.1016/j.exphem.2024.104523

Shiyu Xiao, Hongxia Chen, Michihiro Kobayashi, Sergio Barajas, Wenjie Cai, Yunpeng Bai, Zhong-Yin Zhang, Yan Liu

引用次数: 0

3194 – CLONAL HEMATOPOIESIS-ASSOCIATED DNMT3A MUTATIONS CAUSE INCREASED T CELL ACTIVATION AND DECREASED LEUKEMIC TUMOR BURDEN 3194 - 克隆造血相关的 dnmt3a 突变导致 t 细胞活化增加和白血病肿瘤负荷减少

IF 2.6 4区医学

Experimental hematology Pub Date : 2024-08-29 DOI: 10.1016/j.exphem.2024.104514

LaShanale Wallace, Mark Engelken, Amina Metidji, Jacquelyn Myers, Heather Sheppard, Jeremy Crawford, John Harper, David Cullins, Paul Thomas, Esther Obeng

引用次数: 0

3207 – PLCL1 REGULATES HSC QUIESCENCE VIA INTRACELLULAR CA2+ ALTERATIONS 3207 - plcl1 通过细胞内 ca2+ 的变化调节 HSC 的静止状态

IF 2.6 4区医学

Experimental hematology Pub Date : 2024-08-29 DOI: 10.1016/j.exphem.2024.104527

Tomohiro Yabushita, Yosuke Tanaka, Toshio Suda

引用次数: 0

3202 – 6-O HEPARAN SULFATION REGULATES ACUTE MYELOID LEUKEMIA CHEMOTHERAPY RESISTANCE 3202 - 6-o 天冬酰胺硫酸化调节急性髓性白血病的化疗耐药性

IF 2.6 4区医学

Experimental hematology Pub Date : 2024-08-29 DOI: 10.1016/j.exphem.2024.104522

Kelsey Woodruff, Nicollette Setiawan, Cyd McKay, Christina Root, Soheil Meshinchi, Christina Termini

引用次数: 0