Journal of Hematology & Oncology最新文献

{"title":"Correction: myCAF-derived Exosomal PWAR6 accelerates CRC liver metastasis via altering glutamine availability and NK cell function in the tumor microenvironment","authors":"Hongsheng Fang, Weixing Dai, Ruiqi Gu, Yanbo Zhang, Jin Li, Wenqin Luo, Shanyou Tong, Lingyu Han, Yichao Wang, Chengyao Jiang, Xue Wang, Renjie Wang, Guoxiang Cai","doi":"10.1186/s13045-025-01685-3","DOIUrl":"https://doi.org/10.1186/s13045-025-01685-3","url":null,"abstract":"<p><b>Correction: Journal of Hematology & Oncology (2024) 17:126</b></p><p><b>https://doi.org/10.1186/s13045-024-01643-5</b></p><p>The authors wish to note a correction to an error in Figure 7F (LvPWAR6 group).</p><p>Due to the large number of serial sections of images, one section from the Control group was unintentionally mistakenly placed as the representative figure of the experimental group (LvPWAR6 group) in Fig. 7F. After carefully reviewing the original experimental records and raw data, the authors confirm that this was an unintentional error.</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 1</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01685-3/MediaObjects/13045_2025_1685_Figa_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 1\" aria-describedby=\"Fig1\" height=\"242\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01685-3/MediaObjects/13045_2025_1685_Figa_HTML.png\" width=\"685\"/></picture><p>Experimental records of the NK1.1 immunofluorescence experiment</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><p>The authors conducted three repeat experiments of NK1.1 immunofluorescence for Fig. 7F and all of them reached the similar conclusion.</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 2</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01685-3/MediaObjects/13045_2025_1685_Figb_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 2\" aria-describedby=\"Fig2\" height=\"655\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01685-3/MediaObjects/13045_2025_1685_Figb_HTML.png\" width=\"685\"/></picture><p>Three repetitions of the immunofluorescence experiment</p><span>Full size image</span><svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-chevron-right-small\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></figure><p>The authors would like to emphasize that this error does not impact the scientific conclusions of the article, since the conclusion of Fig. 7F has been validated and supported by the results of the flow cytometry experiments in Fig. 7C-D. The NK1.1 immunofluorescence experiment of Fig.7 F was conducted merely as a further confirmation of the conclusion from Fig. 7C-D.</p><figure><figcaption><b data-test=\"figure-caption-text\">Fig. 3</b></figcaption><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01685-3/MediaObjects/13045_2025_1685_Figc_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 3\" aria-describedby=\"Fig3\" height=\"428\" loading=\"lazy\" src=\"//media.spri","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"90 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653417","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}

{"title":"Circulating tumor DNA in lymphoma: technologies and applications","authors":"Lina Fu, Xuerong Zhou, Xiaoyu Zhang, Xuhua Li, Fan Zhang, Hongcang Gu, Xiaoxue Wang","doi":"10.1186/s13045-025-01673-7","DOIUrl":"https://doi.org/10.1186/s13045-025-01673-7","url":null,"abstract":"Lymphoma, a malignant tumor derived from lymphocytes and lymphoid tissues, presents with complex and heterogeneous clinical manifestations, requiring accurate patient classification for appropriate treatment. While invasive pathological examination of lymph nodes or lymphoid tissue remains the gold standard for lymphoma diagnosis, its utility is limited in cases of deep-seated tumors such as intraperitoneal and central nervous system lymphomas. In addition, biopsy procedures carry an inherent risk of complications. Computed tomography (CT) and positron emission tomography/computed tomography (PET/CT) imaging are essential for treatment assessment and monitoring, but lack the ability to detect early clonal evolution and minimal residual disease (MRD). Liquid biopsy-based analysis of circulating tumor DNA (ctDNA) offers a non-invasive alternative that allows for repeated sampling and overcomes the limitations of spatial heterogeneity and invasive biopsies. ctDNA provides genetic and epigenetic insights into lymphoma and serves as a dynamic, quantifiable biomarker for diagnosis, risk stratification, and treatment response. This review comprehensively summarizes common genetic variations in lymphoma and systematically evaluates ctDNA detection technologies, including PCR-based assays and next-generation sequencing (NGS). Applications of ctDNA detection in noninvasive genotyping, risk stratification, therapeutic response monitoring, and MRD detection are discussed across various lymphoma subtypes, including diffuse large B-cell lymphoma, Hodgkin lymphoma, follicular lymphoma, and T-cell lymphoma. By integrating recent research findings, the review highlights the role of ctDNA profiling in advancing precision medicine, enabling personalized therapeutic strategies, and improving clinical outcomes in lymphoma.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"59 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143589665","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}

{"title":"Novel targeted therapies for immunoglobulin light chain amyloidosis: latest updates from the 2024 ASH annual meeting","authors":"Qiling Bu, Hong-Hu Zhu, Wenming Chen","doi":"10.1186/s13045-025-01681-7","DOIUrl":"https://doi.org/10.1186/s13045-025-01681-7","url":null,"abstract":"Immunoglobulin light chain (AL) amyloidosis is an incurable disease caused by the accumulation and sedimentation of unstable free light chains produced by monoclonal plasma cells. The key to treatment is to achieve a deep hematologic remission in order to improve organ function or reverse organ dysfunction. Conventional treatment has not been able to fully meet the treatment needs of patients with AL, while therapies targeting malignant plasma cells or amyloid have potentially improved treatment outcomes. This study provides an overview of the latest reports on targeted therapies for AL amyloidosis from the 2024 ASH Annual Meeting.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"33 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569433","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}

{"title":"Disruption of the sorcin‒PAX5 protein‒protein interaction induces ferroptosis by promoting the FBXL12-mediated ubiquitination of ALDH1A1 in pancreatic cancer","authors":"Yahui Ding, Yongping Bai, Tianyang Chen, Sisi Chen, Wanjing Feng, Shuoqian Ma, Quan Zhang","doi":"10.1186/s13045-025-01680-8","DOIUrl":"https://doi.org/10.1186/s13045-025-01680-8","url":null,"abstract":"Pancreatic cancer is one of the most malignant cancers, and limited therapeutic options are available. The induction of ferroptosis is considered to be a novel, promising strategy that has potential in cancer treatment, and ferroptosis inducers may be new options for eradicating malignant cancers that are resistant to traditional drugs. The exact mechanism underlying the function of sorcin in the initiation and progression of pancreatic cancer remains unclear. The expression of sorcin in cancer tissues was assessed by analyzing TCGA, GEO and immunohistochemical staining data, and the function of sorcin in the induction of ferroptosis in pancreatic cancer cells was investigated. The mechanism underlying the function of sorcin was revealed through proteomics, co-IP, Ch-IP, and luciferase assays. Natural product screening was subsequently performed to screen for products that interact with sorcin to identify new ferroptosis inducers. We first showed that sorcin expression was positively correlated with the survival and tumor stages of patients with pancreatic cancer, and we revealed that sorcin inhibited ferroptosis through its noncalcium binding function. Furthermore, we discovered that sorcin interacted with PAX5 in the cytoplasm and inhibited PAX5 nuclear translocation, which in turn decreased FBXL12 protein expression and then reduced ALDH1A1 ubiquitination, thus inhibiting ferroptosis. Moreover, an in-house natural product screen revealed that celastrol inhibited the interaction of sorcin and PAX5 by directly binding to the Cys194 residue of the sorcin protein; disruption of the sorcin-PAX5 interaction promoted the nuclear translocation of PAX5, induced the expression of FBXL12, increased the ubiquitylation of ALDH1A1, and eventually induced ferroptosis in pancreatic cancer cells. In this study, we revealed the mechanism of action of sorcin, which is a druggable target for inducing ferroptosis, we identified celastrol as a novel agent that induces ferroptosis, and we showed that disrupting the sorcin-PAX5 interaction is a promising therapeutic strategy for treating pancreatic cancer.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"37 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143569436","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}

{"title":"Anti-TGF-β/PD-L1 bispecific antibody synergizes with radiotherapy to enhance antitumor immunity and mitigate radiation-induced pulmonary fibrosis","authors":"Yuze Wu, Yuheng Yan, Yarong Guo, Mengke Niu, Binghan Zhou, Jing Zhang, Pengfei Zhou, Qian Chu, Qi Mei, Ming Yi, Kongming Wu","doi":"10.1186/s13045-025-01678-2","DOIUrl":"https://doi.org/10.1186/s13045-025-01678-2","url":null,"abstract":"Despite the success of immune checkpoint inhibitors (ICIs) in multiple malignant tumors, a significant proportion of patients remain unresponsive to treatment. Radiotherapy (RT) elicits immunogenic antitumor responses but concurrently activates several immune evasion mechanisms. Our earlier research demonstrated the efficacy of YM101, an anti-TGF-β/PD-L1 bispecific antibody, in stroma-rich tumors. Nevertheless, YM101 has demonstrated reduced effectiveness in non-inflamed tumors characterized by poor immune cell infiltration. This study investigated the potential synergy between RT and YM101 in overcoming immunotherapy resistance and mitigating RT-induced pulmonary fibrosis. The antitumor activity and survival outcomes of RT plus YM101 treatment in vivo were explored in several non-inflamed murine tumor models. Furthermore, the inhibition of pulmonary metastases was assessed in a pulmonary metastasis model. The impact of RT on dendritic cell (DC) maturation was quantified by flow cytometry, whereas cytokine and chemokine secretions were measured by ELISA. To comprehensively characterize changes in the tumor microenvironment, we utilized a combination of methods, including flow cytometry, IHC staining, multiplex inmunofluorecence and RNA sequencing. Additionally, we evaluated the impact of YM101 on RT-induced pulmonary fibrosis. RT plus YM101 significantly inhibited tumor growth, prolonged survival and inhibited pulmonary metastases compared with monotherapies in non-inflamed tumors with poor immune infiltration. RT promoted DC maturation in a dose-dependent manner and increased the secretions of multiple proinflammatory cytokines. Mechanistically, RT plus YM101 simultaneously increased the infiltration and activation of intratumoral DCs and tumor-infiltrating lymphocytes and reshaped the tumor microenvironment landscape. Notably, YM101 attenuated both RT-induced peritumoral fibrosis and pulmonary fibrosis. Our findings suggest that RT combined with YM101 enhances antitumor immunity and overcomes resistance in non-inflamed tumors in preclinical models, while simultaneously showing potential in mitigating RT-induced fibrosis. This combination therapy demonstrates promise in overcoming ICI resistance, while potentially sparing normal pulmonary tissue, thereby providing a strong rationale for further clinical investigations.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"37 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143546215","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}

{"title":"Breakthroughs in treatment for hematological malignancies: latest updates on molecular glue, PROTACs and RNA degraders from ASH 2024","authors":"Na Li, Jianpeng Sheng, Hong-Hu Zhu","doi":"10.1186/s13045-025-01674-6","DOIUrl":"https://doi.org/10.1186/s13045-025-01674-6","url":null,"abstract":"Degrader therapies have garnered significant attention for their innovative approach to targeting and eliminating malignancy-associated proteins, holding promise for improving outcomes for patients with relapsed or refractory (R/R) hematological malignancies, especially in cases of leukemia, non-Hodgkin lymphoma, and multiple myeloma. Currently, the main categories developed based on degraders include molecular glue (such as Cemsidomide, NX-5948), PROTACs (such as BGB-16673, AC-676, KT-333 ), and RNA degraders (such as SKY-1214). This correspondence summarizes the preclinical and clinical updates on degrader therapies presented at the ASH 2024 annual meeting.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"12 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143546214","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}

{"title":"Correction: Immunosenescence: a key player in cancer development","authors":"Jingyao Lian, Ying Yue, Weina Yu, Yi Zhang","doi":"10.1186/s13045-025-01682-6","DOIUrl":"https://doi.org/10.1186/s13045-025-01682-6","url":null,"abstract":"<p><b>Correction: Journal of Hematology & Oncology (2020) 13:151</b></p><p>https://doi.org/10.1186/s13045-020-00986-z</p><p>In the ahead-mentioned sentence in the original article, ‘KLRG1' was incorrectly written as ‘NKG2C’, leading to an inaccurate statement.</p><p>The authors regret this oversight and wish to clarify that the corrected sentence should instead read:</p><p>“It should be noted that, in the process of immunosenescence, the activating receptor expression of natural killer (NK) cell markers NKP30, NKP46, etc., is reduced, while the inhibitory receptor expression of KIR, KLRG1, etc., is increased”.</p><span>Author notes</span><ol><li><p>Jingyao Lian, Ying Yue, and Weina Yu contributed equally to this work</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Biotherapy Center and Cancer Center, The First Affiliated Hospital of Zhengzhou University, 1 Jianshe East Road, Zhengzhou, 450052, Henan, China</p><p>Jingyao Lian, Ying Yue, Weina Yu & Yi Zhang</p></li><li><p>State Key Laboratory of Esophageal Cancer Prevention and Treatment, Zhengzhou, 450052, Henan, China</p><p>Jingyao Lian, Ying Yue, Weina Yu & Yi Zhang</p></li><li><p>Clinical Laboratory, Henan Medical College Hospital Workers, Zhengzhou, 450000, Henan, China</p><p>Ying Yue</p></li></ol><span>Authors</span><ol><li><span>Jingyao Lian</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Ying Yue</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Weina Yu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yi Zhang</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li></ol><h3>Corresponding author</h3><p>Correspondence to Yi Zhang.</p><h3>Publisher’s note</h3><p>Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.</p><p>The online version of the original article can be found at https://doi.org/10.1186/s13045-020-00986-z</p><p><b>Open Access</b> This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyri","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"40 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143546467","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}

{"title":"BCMA-targeted therapies for multiple myeloma: latest updates from 2024 ASH annual meeting","authors":"Huijian Zheng, Huajian Xian, Wenjie Zhang, Chaoqun Lu, Renyao Pan, Han Liu, Zhenshu Xu","doi":"10.1186/s13045-025-01675-5","DOIUrl":"https://doi.org/10.1186/s13045-025-01675-5","url":null,"abstract":"B-cell maturation antigen (BCMA) is currently the most extensively explored target for multiple myeloma (MM). BCMA-targeted therapies such as antibody-drug conjugate (ADC), bispecific antibodies (BsAbs), chimeric antigen receptor T(CAR-T) cell have shown promising therapeutic prospects in MM. We have summarized the latest reports on the three types of drugs for MM at the 2024 ASH Annual Meeting.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"28 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143528212","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}

{"title":"CAR-NK cell therapy: latest updates from the 2024 ASH annual meeting","authors":"Ran Kong, Bingyu Liu, Hua Wang, Tiange Lu, Xiangxiang Zhou","doi":"10.1186/s13045-025-01677-3","DOIUrl":"https://doi.org/10.1186/s13045-025-01677-3","url":null,"abstract":"Natural killer cells, integral to the innate immune response, exhibit the inherent capacity to identify and eliminate cancer cells without prior exposure, positioning them as prime candidates for immunotherapeutic strategies. Chimeric antigen receptor-engineered natural killer (CAR-NK) cells obviate the requirement for human leukocyte antigen compatibility, simplifying personalized schedules and facilitating the manufacture of off-the-shelf products. In addition, CAR-NK cell therapy possesses lower risk of cytokine release syndrome and neurotoxicity, benefitting patients with higher security. Nevertheless, CAR-NK cell therapy is also confronted with challenges, including but not limited to short lifespan and restrictions from tumor microenvironment. Here, we summarized the latest advancements in the preclinical investigations and clinical trials of CAR-NK cell therapy from the 2024 ASH Annual Meeting.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"34 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143528246","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}

{"title":"Correction: Incorporation of a hinge domain improves the expansion of chimeric antigen receptor T cells","authors":"Le Qin, Yunxin Lai, Ruocong Zhao, Xinru Wei, Jianyu Weng, Peilong Lai, Baiheng Li, Simiao Lin, Suna Wang, Qiting Wu, Qiubin Liang, Yangqiu Li, Xuchao Zhang, Yilong Wu, Pentao Liu, Yao Yao, Duanqing Pei, Xin Du, Peng Li","doi":"10.1186/s13045-025-01672-8","DOIUrl":"https://doi.org/10.1186/s13045-025-01672-8","url":null,"abstract":"<p><b>Correction: Journal of Hematology & Oncology (2017) 10:68 </b><b>https://doi.org/10.1186/s13045-017-0437-8</b></p><p>The authors wish to note the following:</p><p>In Supplemental Figure 1, the flow cytometry data that represent the transfection efficiencies of Meso.28z T cells on Day 12 and Day 15 were mistakenly duplicated. Both panels display a percentage of 34.9%, but upon reviewing our raw data, we found that the correct transfection efficiency for Day 15 should be 34.4%, not 34.9%. This discrepancy was caused by an error in copying and pasting during data preparation.</p><p>We confirm that this correction does not impact the overall conclusions or interpretation of the results presented in the article. To address this mistake, we kindly request the opportunity to replace the original Supplemental Figure 1 with a revised figure that accurately reflects the values. The original and revised Supplementary Figure 1 can be viewed via this Correction article.</p><span>Author notes</span><ol><li><p>Le Qin and Yunxin Lai are equal contributors.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Key Laboratory of Regenerative Biology, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China</p><p>Le Qin, Yunxin Lai, Ruocong Zhao, Xinru Wei, Baiheng Li, Simiao Lin, Suna Wang, Qiting Wu, Yao Yao, Duanqing Pei & Peng Li</p></li><li><p>Guangdong Provincial Key Laboratory of Stem Cell and Regenerative Medicine, South China Institute for Stem Cell Biology and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China</p><p>Le Qin, Yunxin Lai, Ruocong Zhao, Xinru Wei, Baiheng Li, Simiao Lin, Suna Wang, Qiting Wu, Yao Yao, Duanqing Pei & Peng Li</p></li><li><p>State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, 510530, China</p><p>Le Qin, Yunxin Lai, Ruocong Zhao, Xinru Wei, Baiheng Li, Simiao Lin, Suna Wang, Qiting Wu, Yao Yao & Peng Li</p></li><li><p>Department of Hematology, Guangdong General Hospital/Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China</p><p>Jianyu Weng, Peilong Lai & Xin Du</p></li><li><p>InVivo Biomedicine Co. Ltd, Guangzhou, 510000, China</p><p>Qiubin Liang</p></li><li><p>Institute of Hematology, Medical College, Jinan University, Guangzhou, 510632, China</p><p>Yangqiu Li</p></li><li><p>Guangdong Lung Cancer Institute, Medical Research Center, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China</p><p>Xuchao Zhang & Yilong Wu</p></li><li><p>Wellcome Trust Sanger Institute, Hinxton, Cambridge, England, CB10 1HH, UK</p><p>Pentao Liu</p></li></ol><span>Authors</span><ol><li><span>Le Qin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Sch","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"49 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143485821","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}