Leukemia最新文献_第3页

T-cell acute lymphoblastic leukaemia: subtype prevalence, clinical outcome, and emerging targeted treatments t细胞急性淋巴细胞白血病：亚型流行，临床结果，和新兴的靶向治疗

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-17 DOI: 10.1038/s41375-025-02599-2

Maxim Buckley, David T. Yeung, Deborah L. White, Laura N. Eadie

{"title":"T-cell acute lymphoblastic leukaemia: subtype prevalence, clinical outcome, and emerging targeted treatments","authors":"Maxim Buckley, David T. Yeung, Deborah L. White, Laura N. Eadie","doi":"10.1038/s41375-025-02599-2","DOIUrl":"https://doi.org/10.1038/s41375-025-02599-2","url":null,"abstract":"T-cell Acute Lymphoblastic Leukaemia (T-ALL) is a high-risk hematological disease constituting ~20% of acute leukemias. To date, the only subtype recognized by the World Health Organization’s International Consensus Classification is early T-cell precursor ALL. To improve clinical outcomes, several studies have investigated and defined T-ALL genomic subtypes within cohorts of varied ages and geographical locations. These studies have also utilized differing analysis methods including whole transcriptome, exome, or genome sequencing as well as immunophenotyping and cytogenetic testing. As a result, there are significant differences in reported subtypes as well as the frequency at which each occurs. The reported clinical outcomes for specific genomic alterations also depend on patient demographics and treatment protocols. This review synthesizes the data from four T-ALL genomic landscape studies establishing consensus and highlighting differences, details clinical outcomes for the most common genomic alterations observed in T-ALL patients, and proposes novel avenues for future investigation and treatment.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"108 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

An oncolytic adenovirus targeting SLAMF7 demonstrates anti-myeloma efficacy 一种靶向SLAMF7的溶瘤腺病毒显示出抗骨髓瘤的功效

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-17 DOI: 10.1038/s41375-025-02617-3

Georgia Stewart, Simon Tazzyman, Yidan Sun, Rebecca E. Andrews, Jack Harrison, Darren Lath, Jenny Down, Georgia Robinson, Xue Wang, Munitta Muthana, Andrew. D. Chantry, Michelle A. Lawson

{"title":"An oncolytic adenovirus targeting SLAMF7 demonstrates anti-myeloma efficacy","authors":"Georgia Stewart, Simon Tazzyman, Yidan Sun, Rebecca E. Andrews, Jack Harrison, Darren Lath, Jenny Down, Georgia Robinson, Xue Wang, Munitta Muthana, Andrew. D. Chantry, Michelle A. Lawson","doi":"10.1038/s41375-025-02617-3","DOIUrl":"https://doi.org/10.1038/s41375-025-02617-3","url":null,"abstract":"We investigated a novel SLAMF7-promoter driven oncolytic adenovirus (Ad[CE1A]) as a potential therapeutic for multiple myeloma, an incurable hematological malignancy. Ad[CE1A] infection, replication, and oncolysis were assessed in a panel of myeloma cell lines (n = 8) and ex vivo samples from myeloma patients (n = 17) and healthy donors (HDs) (n = 14). Ad[CE1A] efficiently infected, replicated, and induced oncolysis in myeloma cells, but not in control cell lines or HDs, demonstrating selective cytotoxicity. Mechanistic studies revealed Ad[CE1A]-induced cell death is caspase-independent, with a potential involvement of necroptosis. Ad[CE1A] also altered immunogenic cell death markers (calreticulin, CD47, extracellular ATP), enhanced antigen presentation via increased MHC class I and II receptor expression (HLA-ABC and HLA-DR), and stimulated bystander cytokine killing, indicating potential for direct and immune-mediated anti-myeloma responses. In vivo experiments with 5TGM1 syngeneic and U266 xenograft models showed Ad[CE1A] significantly reduced myeloma tumor burden compared to vehicle control. Combination therapy with anti-myeloma drugs, bortezomib, melphalan, panobinostat and pomalidomide, enhanced Ad[CE1A] efficacy, with melphalan upregulating SLAMF7, resulting in increased viral replication. In summary, these findings support Ad[CE1A] as a promising myeloma therapy.<figure></figure>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"9 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847094","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Patient-reported outcomes in Philadelphia chromosome-positive acute lymphoblastic leukemia patients treated with ponatinib or imatinib: results from the PhALLCON trial 患者报告的费城染色体阳性急性淋巴细胞白血病患者接受波纳替尼或伊马替尼治疗的结果：来自PhALLCON试验的结果

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-16 DOI: 10.1038/s41375-025-02608-4

Ajibade Ashaye, Ling Shi, Ibrahim Aldoss, Pau Montesinos, Pankit Vachhani, Vanderson Rocha, Cristina Papayannidis, Jessica T. Leonard, Maria R. Baer, Jose-Maria Ribera, James McCloskey, Jianxiang Wang, Sujun Gao, Deepali Rane, Shien Guo

{"title":"Patient-reported outcomes in Philadelphia chromosome-positive acute lymphoblastic leukemia patients treated with ponatinib or imatinib: results from the PhALLCON trial","authors":"Ajibade Ashaye, Ling Shi, Ibrahim Aldoss, Pau Montesinos, Pankit Vachhani, Vanderson Rocha, Cristina Papayannidis, Jessica T. Leonard, Maria R. Baer, Jose-Maria Ribera, James McCloskey, Jianxiang Wang, Sujun Gao, Deepali Rane, Shien Guo","doi":"10.1038/s41375-025-02608-4","DOIUrl":"https://doi.org/10.1038/s41375-025-02608-4","url":null,"abstract":"In the Phase 3 PhALLCON trial (NCT03589326), ponatinib demonstrated superior efficacy and comparable safety profile versus imatinib in adults with newly diagnosed Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL). Here we report patient-reported outcomes (PRO) from PhALLCON assessed as exploratory endpoints using the Functional Assessment of Cancer Therapy-Leukemia (FACT-Leu) and EQ-5D-5L. Primary PRO domains included FACT-G physical well-being, FACT-Leu subscale (FACT-LeuS), Trial Outcome Index (TOI), FACT-Leu total score, FACT-G total score, and EQ-5D visual analogue scale. Differences in least-squares mean score changes from baseline to the end of induction (EOI)/consolidation (EOC) and time to confirmed improvement/deterioration were analyzed. Overall treatment tolerability was assessed using the FACT-GP5. Analyses included 238 patients (ponatinib 159, imatinib 79) with ≥1 PRO assessment. Least-squares mean changes from baseline favored ponatinib, with significant and meaningful differences in FACT-LeuS, TOI, and FACT-Leu total score at EOI and across the primary domains except for FACT-LeuS at EOC. Median time to confirmed improvement was shorter with ponatinib versus imatinib for key measures. Ponatinib-treated patients tended to report being less bothered by treatment side effects as assessed by FACT-GP5. These findings highlight ponatinib’s potentially favorable impact on health-related quality of life, supporting its use as frontline treatment for Ph+ ALL.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"41 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143837020","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Molecular landscape of distinct follicular lymphoma histologic grades: insights from genomic and transcriptome analyses 不同滤泡淋巴瘤组织学分级的分子图谱：基因组和转录组分析的启示

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-15 DOI: 10.1038/s41375-025-02603-9

Cong Sun, Wei Li, Jingwei Yu, Tingting Zhang, Wenchen Gong, Hengqi Liu, Fenghua Gao, Zheng Song, Lanfang Li, Lihua Qiu, Zhengzi Qian, Shiyong Zhou, Bin Meng, Yanan Gao, Junzhi Li, Xia Liu, Weicheng Ren, Qiang Pan-Hammarström, Xianhuo Wang, Huilai Zhang

{"title":"Molecular landscape of distinct follicular lymphoma histologic grades: insights from genomic and transcriptome analyses","authors":"Cong Sun, Wei Li, Jingwei Yu, Tingting Zhang, Wenchen Gong, Hengqi Liu, Fenghua Gao, Zheng Song, Lanfang Li, Lihua Qiu, Zhengzi Qian, Shiyong Zhou, Bin Meng, Yanan Gao, Junzhi Li, Xia Liu, Weicheng Ren, Qiang Pan-Hammarström, Xianhuo Wang, Huilai Zhang","doi":"10.1038/s41375-025-02603-9","DOIUrl":"https://doi.org/10.1038/s41375-025-02603-9","url":null,"abstract":"The 2022 World Health Organization Classification of Haematolymphoid tumours classifies follicular lymphoma grades 1–2 (FL1-2) and grade 3A (FL3A) as classic follicular lymphoma (cFL) and reclassifies grade 3B (FL3B) as follicular large B-cell lymphoma (FLBL), without addressing cases of patients with concurrent FL and diffuse large B-cell lymphoma (FL/DLBCL). However, genetic information on FL histologic grading remains limited, and the latest classification lacks sufficient evidence to resolve whether these subgroups represent single or multiple distinct biological entities. This study analyzed clinical data from 831 patients, whole-exome sequencing (WES) from 149 patients, and transcriptome sequencing from 63 patients to explore differences among FL1-2, FL3A, FL3B, and FL/DLBCL. Clinical analyses revealed two distinct groups: an indolent group (FL1-2 and FL3A) with favorable prognosis and an aggressive group (FL3B and FL/DLBCL) characterized by poor prognosis. Genomics revealed that FL1-2 and FL3A share a common genetic background, whereas FL3B and FL/DLBCL lack mutations in epigenetic regulators CREBBP and KMT2D but exhibit additional copy number variations (CNVs), such as 1p36.32 losses and 3p21.1 gains, which are linked to poor prognosis. Transcriptomics revealed that with increasing histologic grade, immune-related pathway activity decreases, while the activity of metabolic and cell cycle pathways increases, which may be associated with the upregulation of MYC, IRF4, and BATF expression. Together, these findings define FL3B and FL/DLBCL as biologically and clinically distinct B-cell lymphomas, differing from traditional FL. FL1-2 and FL3A differ in their tumor microenvironments rather than genetic profiles.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"247 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143832128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Dual STAT3/STAT5 inhibition as a novel treatment strategy in T-prolymphocytic leukemia 双重抑制STAT3/STAT5作为t -原淋巴细胞白血病的新治疗策略

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-15 DOI: 10.1038/s41375-025-02577-8

Annika Dechow, Sanna Timonen, Aleksandr Ianevski, Qu Jiang, Linus Wahnschaffe, Yayi Peng, Dennis Jungherz, Kerstin Becker, Heidi A. Neubauer, Susann Schönefeldt, Elvin de Araujo, Patrick Gunning, Roman Fleck, Alexandra Schrader, Michael Hallek, Natali Pflug, Richard Moriggl, Tero Aittokallio, Satu Mustjoki, Till Braun, Marco Herling

{"title":"Dual STAT3/STAT5 inhibition as a novel treatment strategy in T-prolymphocytic leukemia","authors":"Annika Dechow, Sanna Timonen, Aleksandr Ianevski, Qu Jiang, Linus Wahnschaffe, Yayi Peng, Dennis Jungherz, Kerstin Becker, Heidi A. Neubauer, Susann Schönefeldt, Elvin de Araujo, Patrick Gunning, Roman Fleck, Alexandra Schrader, Michael Hallek, Natali Pflug, Richard Moriggl, Tero Aittokallio, Satu Mustjoki, Till Braun, Marco Herling","doi":"10.1038/s41375-025-02577-8","DOIUrl":"https://doi.org/10.1038/s41375-025-02577-8","url":null,"abstract":"T-prolymphocytic leukemia (T-PLL) is a rare, aggressive T-cell malignancy with poor outcomes and an urgent need for new therapeutic approaches. Integrating genomic data and new transcriptomic profiling, we identified recurrent JAK/STAT mutations (predominantly in JAK3 and STAT5B) as hallmarks in a cohort of 335 T-PLL cases. In line, transcriptomic and protein analyses revealed constitutive JAK/STAT activation in virtually all samples. Consequently, we explored the anti-leukemic potential of dual STAT3/STAT5 non-PROTAC degraders in T-PLL, with JPX-1244 as our lead substance. JPX-1244 efficiently and selectively induced cell death in primary T-PLL samples, including those resistant to conventional therapies, by blocking STAT3 and STAT5 phosphorylation and by inducing their degradation. The extent of STAT3/STAT5 degradation directly correlated with cytotoxicity. RNA-sequencing confirmed the treatment-related downregulation of STAT5 target genes. While JAK/STAT mutations did not predict responses to pharmacologic STAT3/STAT5 degradation, elevated expression of TOX, PAK6, and SPINT1 were associated with drug sensitivity. In subsequent combination screenings, cladribine, venetoclax, and azacytidine emerged as most effective combination partners of STAT3/STAT5 degraders, even in low-responding T-PLL samples, all synergistically reducing STAT5 phosphorylation. These findings highlight dual STAT3/STAT5 inhibition, particularly in combination with hypomethylating and BCL2-targeting agents, as a promising interventional approach in T-PLL, warranting further investigation.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"15 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143832129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Remission induction in refractory, drug resistant pediatric PICALM::MLLT10+ B-cell acute lymphoblastic leukemia by venetoclax venetoclax对难治性耐药儿童PICALM::MLLT10+ b细胞急性淋巴细胞白血病的缓解诱导

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-15 DOI: 10.1038/s41375-025-02591-w

Alexandra Niedermayer, Jana Stursberg, Anke Katharina Bergmann, Martin Zimmermann, Gunnar Cario, Monika Brüggemann, Rolf Köhler, Daniel Steinbach, Christian Reimann, Felix Seyfried, Lüder Hinrich Meyer, Klaus-Michael Debatin

引用次数: 0

Prognostic scoring systems in chronic myeloid leukaemia 慢性髓性白血病的预后评分系统

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-15 DOI: 10.1038/s41375-025-02606-6

Michael Lauseker, Verena S. Hoffmann, Markus Pfirrmann

引用次数: 0

All genetic subtypes of B-cell acute lymphoblastic leukemia exhibit increased incidence rates in children with Down syndrome 所有遗传亚型的b细胞急性淋巴细胞白血病在唐氏综合症儿童中发病率增加

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-11 DOI: 10.1038/s41375-025-02602-w

Ching-Ju Hsu, Jeremy M. Schraw, Tania A. Desrosiers, Amanda E. Janitz, Russell S. Kirby, Eirini Nestoridi, Wendy N. Nembhard, Jason L. Salemi, Charles Shumate, Jean Paul Tanner, Mahsa M. Yazdy, Michael E. Scheurer, Karen R. Rabin, Philip J. Lupo

{"title":"All genetic subtypes of B-cell acute lymphoblastic leukemia exhibit increased incidence rates in children with Down syndrome","authors":"Ching-Ju Hsu, Jeremy M. Schraw, Tania A. Desrosiers, Amanda E. Janitz, Russell S. Kirby, Eirini Nestoridi, Wendy N. Nembhard, Jason L. Salemi, Charles Shumate, Jean Paul Tanner, Mahsa M. Yazdy, Michael E. Scheurer, Karen R. Rabin, Philip J. Lupo","doi":"10.1038/s41375-025-02602-w","DOIUrl":"https://doi.org/10.1038/s41375-025-02602-w","url":null,"abstract":"Children with Down syndrome (DS) have a 20-fold increased risk and 2% lifetime risk of developing B-cell acute lymphoblastic leukemia (B-ALL) [1,2,3]. Despite improvements over time, survival in DS-ALL remains consistently 10 to 20% lower compared to non-DS-ALL, due to both increased relapse and more frequent and severe treatment-related toxicities [4,5,6].Notably, the somatic genomic landscape of DS-ALL differs from that of non-DS-ALL. CRLF2 rearrangements (CRLF2-r) and JAK2 mutations are more frequent in DS-ALL, whereas most other subtypes are less frequent [4, 7,8,9,10,11]. A recent study of 295 DS-ALL cases in comparison to 2 257 non-DS-ALL cases showed that CRLF2-r was 9 times more frequent in DS-ALL (54.2% vs 6.0%), along with an increased prevalence of JAK2 mutations (26.2% vs 3.5%) [12]. This study also identified eight additional subtypes with significantly different frequencies between DS-ALL and non-DS-ALL: C/EBPalt and IGH::IGF2BP1 subtypes were highly enriched in the DS-ALL cohort, whereas high hyperdiploid, BCR::ABL1-like, BCR::ABL1, KMT2A-rearranged (KMT2A-r), DUX4-rearranged (DUX4-r), and intrachromosomal amplification of chromosome 21 (iAMP21) subtypes were underrepresented in DS-ALL compared with non-DS-ALL.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"3 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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

Multiplex imaging of murine bone marrow using Phenocycler 2.0™ 使用Phenocycler 2.0™对小鼠骨髓进行多重成像

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-11 DOI: 10.1038/s41375-025-02596-5

Sonali J. Karnik, Connor Gulbronson, Paige C. Jordan, Rahul Kanumuri, Baskar Ramdas, Ramesh Kumar, Melissa L. Hartman, Izza Khurram, Drew M. Brown, Karen E. Pollok, Pratibha Singh, Reuben Kapur, Melissa A. Kacena

引用次数: 0

Interferon-γ-mediated selective inhibition of hematopoiesis and the clonal advantage of HLA-lacking hematopoietic stem progenitor cells in aplastic anemia 干扰素γ介导的再生障碍性贫血中造血的选择性抑制和缺乏hla的造血干细胞祖细胞的克隆优势

IF 11.4 1区医学

Leukemia Pub Date : 2025-04-11 DOI: 10.1038/s41375-025-02595-6

Rio Takahashi, Honoka Takahashi, Luna Seoka, Hiroka Iwasaki, Hiroyuki Takamatsu, Tatsuya Imi, Yoshitaka Zaimoku, Kohei Hosokawa, Takamasa Katagiri

{"title":"Interferon-γ-mediated selective inhibition of hematopoiesis and the clonal advantage of HLA-lacking hematopoietic stem progenitor cells in aplastic anemia","authors":"Rio Takahashi, Honoka Takahashi, Luna Seoka, Hiroka Iwasaki, Hiroyuki Takamatsu, Tatsuya Imi, Yoshitaka Zaimoku, Kohei Hosokawa, Takamasa Katagiri","doi":"10.1038/s41375-025-02595-6","DOIUrl":"https://doi.org/10.1038/s41375-025-02595-6","url":null,"abstract":"Acquired aplastic anemia (AA) is an immune-mediated bone marrow failure caused by autoreactive cytotoxic T lymphocytes targeting hematopoietic stem progenitor cells (HSPCs). Approximately 30% of AA patients exhibit leukocytes lacking HLA class I alleles (HLA[-]). In addition to this direct immune assault, the pathogenesis of AA is thought to involve indirect suppression mediated by the proinflammatory cytokine interferon-gamma (IFN-γ). Using HSPCs derived from induced pluripotent stem cells (iPSCs) with different HLA genotypes, HLA(-) HSPCs were found to be resistant to the suppressive effects of IFN-γ, whereas IFN-γ effectively suppressed the growth and development of HSPCs expressing HLA class I molecules. Further analysis showed that, in contrast to HLA(-) HSPCs, WT HSPCs showed enhanced CD119 expression in response to IFN-γ, activating downstream signaling pathways that promote apoptosis, suggesting that transcription factors involved in the apoptotic pathway following IFN-γ stimulation are differentially expressed between WT and HLA(-) HSPCs. Notably, IFN-γ stimulation reduced the expression of pSTAT3, a key regulator of apoptosis, in WT HSPCs, whereas its expression was elevated in HLA(-) HSPCs. In conclusion, this study showed that the selective hematopoietic inhibition of HSPCs by IFN-γ likely facilitates clonal hematopoiesis and contributes to the persistence of HLA(-) HSPCs in patients with AA.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"108 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143819322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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