Pub Date : 2025-04-17DOI: 10.1186/s13045-025-01692-4
Naimeng Liu, Xiangyu Wang, Zhongzhao Wang, Yonemori Kan, Yi Fang, Jidong Gao, Xiangyi Kong, Jing Wang
In situ vaccination (ISV) has emerged as a promising strategy in cancer immunotherapy, offering a targeted approach that uses the tumor microenvironment (TME) to stimulate an immune response directly at the tumor site. This method minimizes systemic exposure while maintaining therapeutic efficacy and enhancing safety. Recent advances in nanotechnology have enabled new approaches to ISV by utilizing nanomaterials with unique properties, including enhanced permeability, retention, and controlled drug release. ISV employing nanomaterials can induce immunogenic cell death and reverse the immunosuppressive and hypoxic TME, thereby converting a “cold” tumor into a “hot” tumor and facilitating a more robust immune response. This review examines the mechanisms through which nanomaterials-based ISV enhances anti-tumor immunity, summarizes clinical applications of these strategies, and evaluates its capacity to serve as a neoadjuvant therapy for eliminating micrometastases in early-stage cancer patients. Challenges associated with the clinical translation of nanomaterials-based ISV, including nanomaterial metabolism, optimization of treatment protocols, and integration with other therapies such as radiotherapy, chemotherapy, and photothermal therapy, are also discussed. Advances in nanotechnology and immunotherapy continue to expand the possible applications of ISV, potentially leading to improved outcomes across a broad range of cancer types.
{"title":"Nanomaterials-driven in situ vaccination: a novel frontier in tumor immunotherapy","authors":"Naimeng Liu, Xiangyu Wang, Zhongzhao Wang, Yonemori Kan, Yi Fang, Jidong Gao, Xiangyi Kong, Jing Wang","doi":"10.1186/s13045-025-01692-4","DOIUrl":"https://doi.org/10.1186/s13045-025-01692-4","url":null,"abstract":"In situ vaccination (ISV) has emerged as a promising strategy in cancer immunotherapy, offering a targeted approach that uses the tumor microenvironment (TME) to stimulate an immune response directly at the tumor site. This method minimizes systemic exposure while maintaining therapeutic efficacy and enhancing safety. Recent advances in nanotechnology have enabled new approaches to ISV by utilizing nanomaterials with unique properties, including enhanced permeability, retention, and controlled drug release. ISV employing nanomaterials can induce immunogenic cell death and reverse the immunosuppressive and hypoxic TME, thereby converting a “cold” tumor into a “hot” tumor and facilitating a more robust immune response. This review examines the mechanisms through which nanomaterials-based ISV enhances anti-tumor immunity, summarizes clinical applications of these strategies, and evaluates its capacity to serve as a neoadjuvant therapy for eliminating micrometastases in early-stage cancer patients. Challenges associated with the clinical translation of nanomaterials-based ISV, including nanomaterial metabolism, optimization of treatment protocols, and integration with other therapies such as radiotherapy, chemotherapy, and photothermal therapy, are also discussed. Advances in nanotechnology and immunotherapy continue to expand the possible applications of ISV, potentially leading to improved outcomes across a broad range of cancer types.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"4 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143841344","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}
Pub Date : 2025-04-15DOI: 10.1186/s13045-025-01698-y
Yang Chen, Keren Jia, Yi Xie, Jiajia Yuan, Dan Liu, Lei Jiang, Haoxin Peng, Jia Zhong, Jian Li, Xiaotian Zhang, Lin Shen
Gastric cancer is the fifth most common cancer globally and is associated with significant morbidity and mortality. Despite its alarming prevalence, limited comparative evidence exists on its treatment efficacy and prognosis across diverse China populations. To address this, our study used a large-scale dataset from the National Cancer Information Database, including data from 220,304 patients from 53 leading hospitals across 27 provinces in China. From 2017 to 2023, early-stage (Stages I-II) gastric cancer diagnoses increased to 35.63% of all cancer cases. Our study evaluated the neoadjuvant treatment strategies, adjuvant post-operative therapy, first- and second-line management for progressive stages, alongside current gastric cancer treatment guidelines in China. Notably, immunotherapy accounted for 16.17% and 23.28% of first- and second-line treatments for late-stage gastric cancers, and 14.56% and 5.00% for neoadjuvant and adjuvant therapies, respectively. Analysis of survival rates revealed that the 1-, 2-, 3-, 4-, and 5-year survival rates were 74.07%, 54.89%, 44.21%, 37.97%, and 33.53%, respectively. The 5-year survival rates across stages I-IV were 85.07%, 49.34%, 35.56%, and 13.15%, respectively. These findings offer critical insights into the current state of gastric cancer treatment in China and can inform future initiatives to improve therapeutic outcomes for patients with gastric cancer.
{"title":"The current landscape of gastric cancer and gastroesophageal junction cancer diagnosis and treatment in China: a comprehensive nationwide cohort analysis","authors":"Yang Chen, Keren Jia, Yi Xie, Jiajia Yuan, Dan Liu, Lei Jiang, Haoxin Peng, Jia Zhong, Jian Li, Xiaotian Zhang, Lin Shen","doi":"10.1186/s13045-025-01698-y","DOIUrl":"https://doi.org/10.1186/s13045-025-01698-y","url":null,"abstract":"Gastric cancer is the fifth most common cancer globally and is associated with significant morbidity and mortality. Despite its alarming prevalence, limited comparative evidence exists on its treatment efficacy and prognosis across diverse China populations. To address this, our study used a large-scale dataset from the National Cancer Information Database, including data from 220,304 patients from 53 leading hospitals across 27 provinces in China. From 2017 to 2023, early-stage (Stages I-II) gastric cancer diagnoses increased to 35.63% of all cancer cases. Our study evaluated the neoadjuvant treatment strategies, adjuvant post-operative therapy, first- and second-line management for progressive stages, alongside current gastric cancer treatment guidelines in China. Notably, immunotherapy accounted for 16.17% and 23.28% of first- and second-line treatments for late-stage gastric cancers, and 14.56% and 5.00% for neoadjuvant and adjuvant therapies, respectively. Analysis of survival rates revealed that the 1-, 2-, 3-, 4-, and 5-year survival rates were 74.07%, 54.89%, 44.21%, 37.97%, and 33.53%, respectively. The 5-year survival rates across stages I-IV were 85.07%, 49.34%, 35.56%, and 13.15%, respectively. These findings offer critical insights into the current state of gastric cancer treatment in China and can inform future initiatives to improve therapeutic outcomes for patients with gastric cancer.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"26 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143831794","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}
Pub Date : 2025-04-12DOI: 10.1186/s13045-025-01693-3
Claudia Cifuentes, Lydia Horndler, Pilar Grosso, Clara L Oeste, Alejandro M. Hortal, Jennifer Castillo, Isabel Fernández-Pisonero, Alberto Paradela, Xosé Bustelo, Balbino Alarcón
Recent research from our group has shown that the overexpression of the wild-type RAS-family GTPase RRAS2 drives the onset of triple-negative breast cancer (TNBC) in mice following one or more pregnancies. This phenomenon mirrors human TNBC, where RRAS2 is overexpressed in approximately 75% of cases, particularly in tumors associated with the postpartum period. These findings underscore the relevance of R-RAS2 in TNBC development and progression. We conducted RNA sequencing on tumors derived from conditional knock-in mice overexpressing human wild-type RRAS2 to identify the somatic mutation landscape associated with TNBC development in these mice. Additionally, we developed a TNBC cell line from RRAS2-overexpressing mice, enabling loss-of-function studies to investigate the role of R-RAS2 in various pathobiological parameters of TNBC cells, including cell migration, invasiveness, metabolic activity, and metastatic spread. Furthermore, proteomic analysis of a freshly isolated tumor identified plasma membrane receptors interacting with R-RAS2. Our findings demonstrate that TNBC driven by RRAS2 overexpression exhibits a pattern of somatic mutations similar to those observed in human breast cancer, particularly in genes involved in stemness, extracellular matrix interactions, and actin cytoskeleton regulation. Proteomic analysis revealed that wild-type R-RAS2 interacts with 245 membrane-associated proteins, including key solute carriers involved in cell metabolism (CD98/LAT1, GLUT1, and basigin), adhesion and matrix interaction proteins (CD44, EpCAM, MCAM, ICAM1, integrin-α6, and integrin-β1), and stem cell markers (β1-catenin, α1-catenin, PTK7, and CD44). We show that R-RAS2 regulates CD98/LAT1 transporter-mediated mTOR pathway activation and mediates CD44-dependent cancer cell migration and invasion, thus providing a mechanism by which R-RAS2 promotes breast cancer cell metastasis. R-RAS2 associates with CD44, CD98/LAT1, and other plasma membrane receptors to regulate metabolic activity, actin cytoskeleton reorganization, cell migration, invasion, and distant metastasis formation in TNBC. These findings establish R-RAS2 as a central driver of TNBC malignancy and highlight its potential as a promising therapeutic target, particularly in aggressive, postpartum-associated breast cancers.
{"title":"The R-RAS2 GTPase is a signaling hub in triple-negative breast cancer cell metabolism and metastatic behavior","authors":"Claudia Cifuentes, Lydia Horndler, Pilar Grosso, Clara L Oeste, Alejandro M. Hortal, Jennifer Castillo, Isabel Fernández-Pisonero, Alberto Paradela, Xosé Bustelo, Balbino Alarcón","doi":"10.1186/s13045-025-01693-3","DOIUrl":"https://doi.org/10.1186/s13045-025-01693-3","url":null,"abstract":"Recent research from our group has shown that the overexpression of the wild-type RAS-family GTPase RRAS2 drives the onset of triple-negative breast cancer (TNBC) in mice following one or more pregnancies. This phenomenon mirrors human TNBC, where RRAS2 is overexpressed in approximately 75% of cases, particularly in tumors associated with the postpartum period. These findings underscore the relevance of R-RAS2 in TNBC development and progression. We conducted RNA sequencing on tumors derived from conditional knock-in mice overexpressing human wild-type RRAS2 to identify the somatic mutation landscape associated with TNBC development in these mice. Additionally, we developed a TNBC cell line from RRAS2-overexpressing mice, enabling loss-of-function studies to investigate the role of R-RAS2 in various pathobiological parameters of TNBC cells, including cell migration, invasiveness, metabolic activity, and metastatic spread. Furthermore, proteomic analysis of a freshly isolated tumor identified plasma membrane receptors interacting with R-RAS2. Our findings demonstrate that TNBC driven by RRAS2 overexpression exhibits a pattern of somatic mutations similar to those observed in human breast cancer, particularly in genes involved in stemness, extracellular matrix interactions, and actin cytoskeleton regulation. Proteomic analysis revealed that wild-type R-RAS2 interacts with 245 membrane-associated proteins, including key solute carriers involved in cell metabolism (CD98/LAT1, GLUT1, and basigin), adhesion and matrix interaction proteins (CD44, EpCAM, MCAM, ICAM1, integrin-α6, and integrin-β1), and stem cell markers (β1-catenin, α1-catenin, PTK7, and CD44). We show that R-RAS2 regulates CD98/LAT1 transporter-mediated mTOR pathway activation and mediates CD44-dependent cancer cell migration and invasion, thus providing a mechanism by which R-RAS2 promotes breast cancer cell metastasis. R-RAS2 associates with CD44, CD98/LAT1, and other plasma membrane receptors to regulate metabolic activity, actin cytoskeleton reorganization, cell migration, invasion, and distant metastasis formation in TNBC. These findings establish R-RAS2 as a central driver of TNBC malignancy and highlight its potential as a promising therapeutic target, particularly in aggressive, postpartum-associated breast cancers.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"250 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143824880","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}
Innate immunity represents the body’s first line of defense, effectively countering the invasion of external pathogens. Recent studies have highlighted the crucial role of innate immunity in antitumor defense, beyond its established function in protecting against external pathogen invasion. Enhancing innate immune signaling has emerged as a pivotal strategy in cancer therapy. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway is a key innate immune signal that activates the immune response and exerts antitumor effects; this is primarily attributed to the DNA receptor function of cGAS, which recognizes exogenous DNA to activate downstream STING signaling. This, in turn, promotes the activation of downstream targets such as IRF-3(Interferon Regulatory Factor 3) and NF-κB, leading to the secretion of type I interferons and proinflammatory cytokines, thereby increasing cellular immune activity. The activation of the cGAS-STING pathway may thus play a crucial role in enhancing anticancer immunity. In this paper, we reviewed the role of cGAS-STING signaling in anticancer immunity and its molecular mechanisms. Additionally, we briefly discuss the current applications of the cGAS-STING pathway in cancer immunity, summarize recent developments in STING agonists, and address the challenges facing the use of the cGAS-STING pathway in cancer therapy. Finally, we provide insights into the role of the cGAS‒STING pathway in cancer and propose new directions for cancer immunotherapy.
{"title":"The cGAS‒STING pathway in cancer immunity: mechanisms, challenges, and therapeutic implications","authors":"Mengzhou Shen, Xianjie Jiang, Qiu Peng, Linda Oyang, Zongyao Ren, Jiewen Wang, Mingjing Peng, Yujuan Zhou, Xiyun Deng, Qianjin Liao","doi":"10.1186/s13045-025-01691-5","DOIUrl":"https://doi.org/10.1186/s13045-025-01691-5","url":null,"abstract":"Innate immunity represents the body’s first line of defense, effectively countering the invasion of external pathogens. Recent studies have highlighted the crucial role of innate immunity in antitumor defense, beyond its established function in protecting against external pathogen invasion. Enhancing innate immune signaling has emerged as a pivotal strategy in cancer therapy. The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway is a key innate immune signal that activates the immune response and exerts antitumor effects; this is primarily attributed to the DNA receptor function of cGAS, which recognizes exogenous DNA to activate downstream STING signaling. This, in turn, promotes the activation of downstream targets such as IRF-3(Interferon Regulatory Factor 3) and NF-κB, leading to the secretion of type I interferons and proinflammatory cytokines, thereby increasing cellular immune activity. The activation of the cGAS-STING pathway may thus play a crucial role in enhancing anticancer immunity. In this paper, we reviewed the role of cGAS-STING signaling in anticancer immunity and its molecular mechanisms. Additionally, we briefly discuss the current applications of the cGAS-STING pathway in cancer immunity, summarize recent developments in STING agonists, and address the challenges facing the use of the cGAS-STING pathway in cancer therapy. Finally, we provide insights into the role of the cGAS‒STING pathway in cancer and propose new directions for cancer immunotherapy.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"59 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143784787","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}
Pub Date : 2025-04-02DOI: 10.1186/s13045-025-01689-z
Ping Yang, Zhibo Li, Xi Chen, Chiyuan Ma, Yiyuan Han, Xiaoshan Zhang, Xiaodong Wei, Yueyue Lei, Tonghui Ma, Fangfang Jin
Identifying robust diagnostic biomarkers for gastric cancer (GC) remains a significant challenge. Emerging studies highlight extracellular vesicle (EV)-derived RNAs in cancer biology, but the diagnostic potential of circulating EV-derived small non-coding RNAs (sncRNAs) in GC is poorly understood. Using panoramic RNA display by overcoming RNA modification aborted sequencing (PANDORA-seq), we mapped non-canonical sncRNAs—specifically ribosomal RNA-derived small RNAs (rsRNAs) and transfer RNA-derived small RNAs (tsRNAs)—in plasma EVs. We identified a three-rs/tsRNA signature that discriminates GC patients from healthy individuals with high sensitivity (80.42%) and specificity (87.43%) (143 GC vs 167 controls). For early-stage GC (stage I), sensitivity and specificity were 81.97% and 81.44%, respectively. Furthermore, the three-rs/tsRNA signature was evaluated in two independent cohorts, resulting in AUC values of 0.97 and 0.91 for distinguishing GC from healthy controls. Functional analyses revealed that these rs/tsRNAs regulate the ErbB/Hippo pathways, suggesting them in the underlying pathogenesis and therapeutic potential. This study establishes a novel EV-derived sncRNA signature for early GC detection.
确定胃癌（GC）的可靠诊断生物标志物仍然是一个重大挑战。新兴研究强调细胞外囊泡（EV）衍生的rna在癌症生物学中的作用，但循环EV衍生的小非编码rna （sncRNAs）在GC中的诊断潜力尚不清楚。通过克服RNA修饰流产测序（PANDORA-seq），利用全景RNA显示技术，我们在血浆ev中绘制了非规范sncrnas，特别是核糖体RNA衍生的小RNA （rsRNAs）和转移RNA衍生的小RNA （tsRNAs）。我们发现了一个3 rs/tsRNA标记，该标记以高灵敏度（80.42%）和特异性（87.43%）将GC患者与健康个体区分开来（143例GC vs 167例对照）。早期GC （I期）的敏感性为81.97%，特异性为81.44%。此外，在两个独立的队列中评估了3 rs/tsRNA特征，得出区分GC与健康对照的AUC值分别为0.97和0.91。功能分析显示，这些rs/tsRNAs调控ErbB/Hippo通路，提示它们具有潜在的发病机制和治疗潜力。本研究建立了一种新的ev衍生sncRNA特征，用于早期GC检测。
{"title":"Non-canonical small noncoding RNAs in the plasma extracellular vesicles as novel biomarkers in gastric cancer","authors":"Ping Yang, Zhibo Li, Xi Chen, Chiyuan Ma, Yiyuan Han, Xiaoshan Zhang, Xiaodong Wei, Yueyue Lei, Tonghui Ma, Fangfang Jin","doi":"10.1186/s13045-025-01689-z","DOIUrl":"https://doi.org/10.1186/s13045-025-01689-z","url":null,"abstract":"Identifying robust diagnostic biomarkers for gastric cancer (GC) remains a significant challenge. Emerging studies highlight extracellular vesicle (EV)-derived RNAs in cancer biology, but the diagnostic potential of circulating EV-derived small non-coding RNAs (sncRNAs) in GC is poorly understood. Using panoramic RNA display by overcoming RNA modification aborted sequencing (PANDORA-seq), we mapped non-canonical sncRNAs—specifically ribosomal RNA-derived small RNAs (rsRNAs) and transfer RNA-derived small RNAs (tsRNAs)—in plasma EVs. We identified a three-rs/tsRNA signature that discriminates GC patients from healthy individuals with high sensitivity (80.42%) and specificity (87.43%) (143 GC vs 167 controls). For early-stage GC (stage I), sensitivity and specificity were 81.97% and 81.44%, respectively. Furthermore, the three-rs/tsRNA signature was evaluated in two independent cohorts, resulting in AUC values of 0.97 and 0.91 for distinguishing GC from healthy controls. Functional analyses revealed that these rs/tsRNAs regulate the ErbB/Hippo pathways, suggesting them in the underlying pathogenesis and therapeutic potential. This study establishes a novel EV-derived sncRNA signature for early GC detection.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"38 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766567","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}
Small cell lung cancer (SCLC) is an aggressive malignancy characterized by rapid proliferation and high metastatic potential. It is characterized by universal inactivation of and RB1, overexpression of the MYC family and dysregulation of multiple oncogenic signaling pathways. Among different patients, SCLCs are similar at the genetic level but exhibit significant heterogeneity at the molecular level. The classification of SCLC has evolved from a simple neuroendocrine (NE)/non-neuroendocrine (non-NE) classification system to a transcription factor-based molecular subtype system; lineage plasticity adds further complexity and poses challenges for therapeutic development. While SCLC is initially sensitive to platinum-based chemotherapy, resistance develops rapidly, leading to a dismal prognosis. Various antibodies, including PD-1/PD-L1 inhibitors and antibody‒drug conjugates, have been introduced into clinical practice or are being evaluated in clinical trials. However, their therapeutic benefits for SCLC patients remain limited. This review summarizes SCLC carcinogenic mechanisms, tumor heterogeneity, and the immune microenvironment of SCLC, with a focus on recent advances in metastasis and resistance mechanisms. Additionally, the corresponding clinical progress in tackling these challenges is discussed.
{"title":"Current and future therapies for small cell lung carcinoma","authors":"Xiaoqian Zhai, Zhengkun Zhang, Yuxin Chen, Yanmou Wu, Cheng Zhen, Yu Liu, Yiyun Lin, Chong Chen","doi":"10.1186/s13045-025-01690-6","DOIUrl":"https://doi.org/10.1186/s13045-025-01690-6","url":null,"abstract":"Small cell lung cancer (SCLC) is an aggressive malignancy characterized by rapid proliferation and high metastatic potential. It is characterized by universal inactivation of and RB1, overexpression of the MYC family and dysregulation of multiple oncogenic signaling pathways. Among different patients, SCLCs are similar at the genetic level but exhibit significant heterogeneity at the molecular level. The classification of SCLC has evolved from a simple neuroendocrine (NE)/non-neuroendocrine (non-NE) classification system to a transcription factor-based molecular subtype system; lineage plasticity adds further complexity and poses challenges for therapeutic development. While SCLC is initially sensitive to platinum-based chemotherapy, resistance develops rapidly, leading to a dismal prognosis. Various antibodies, including PD-1/PD-L1 inhibitors and antibody‒drug conjugates, have been introduced into clinical practice or are being evaluated in clinical trials. However, their therapeutic benefits for SCLC patients remain limited. This review summarizes SCLC carcinogenic mechanisms, tumor heterogeneity, and the immune microenvironment of SCLC, with a focus on recent advances in metastasis and resistance mechanisms. Additionally, the corresponding clinical progress in tackling these challenges is discussed.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"36 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744878","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}
Pub Date : 2025-04-01DOI: 10.1186/s13045-025-01687-1
Óscar Herranz, Pablo Berrocal, Carmen Sicilia-Navarro, Cristina Fernández-Infante, Luis Hernández-Cano, Almudena Porras, Carmen Guerrero
C3G, a Rap1 GEF, promotes megakaryopoiesis and platelet function. Using transgenic and knock-out mouse models targeting C3G in megakaryocytes, we investigated whether C3G also affects the niche function of megakaryocytes during bone marrow (BM) recovery after myeloablation induced by 5-fluorouracil (5-FU), or total body irradiation (TBI) followed by bone marrow transplantation. C3G promoted megakaryocyte maturation and platelet production during recovery, along with increased white and red blood cell counts and enhanced survival of female mice after repeated doses of 5-FU. Additionally, megakaryocytes favored adipocyte differentiation through a C3G-mediated mechanism, likely involving Fgf1. Changes in the number or behavior of BM megakaryocytes and adipocytes influenced the hematopoietic stem cell pool, with C3G promoting its bias towards the myeloid-megakaryocytic lineage in both 5-FU- and TBI-ablated models. Therefore, C3G could be a potential target in therapies aimed at enhancing hematopoiesis in patients undergoing chemotherapy and/or BM transplantation.
{"title":"C3G promotes bone marrow adipocyte expansion and hematopoietic regeneration after myeloablation by enhancing megakaryocyte niche function","authors":"Óscar Herranz, Pablo Berrocal, Carmen Sicilia-Navarro, Cristina Fernández-Infante, Luis Hernández-Cano, Almudena Porras, Carmen Guerrero","doi":"10.1186/s13045-025-01687-1","DOIUrl":"https://doi.org/10.1186/s13045-025-01687-1","url":null,"abstract":"C3G, a Rap1 GEF, promotes megakaryopoiesis and platelet function. Using transgenic and knock-out mouse models targeting C3G in megakaryocytes, we investigated whether C3G also affects the niche function of megakaryocytes during bone marrow (BM) recovery after myeloablation induced by 5-fluorouracil (5-FU), or total body irradiation (TBI) followed by bone marrow transplantation. C3G promoted megakaryocyte maturation and platelet production during recovery, along with increased white and red blood cell counts and enhanced survival of female mice after repeated doses of 5-FU. Additionally, megakaryocytes favored adipocyte differentiation through a C3G-mediated mechanism, likely involving Fgf1. Changes in the number or behavior of BM megakaryocytes and adipocytes influenced the hematopoietic stem cell pool, with C3G promoting its bias towards the myeloid-megakaryocytic lineage in both 5-FU- and TBI-ablated models. Therefore, C3G could be a potential target in therapies aimed at enhancing hematopoiesis in patients undergoing chemotherapy and/or BM transplantation.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"25 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744874","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}
Cancer-associated fibroblasts (CAFs) are key players in cancer development and therapy, and they exhibit multifaceted roles in the tumor microenvironment (TME). From their diverse cellular origins, CAFs undergo phenotypic and functional transformation upon interacting with tumor cells and their presence can adversely influence treatment outcomes and the severity of the cancer. Emerging evidence from single-cell RNA sequencing (scRNA-seq) studies have highlighted the heterogeneity and plasticity of CAFs, with subtypes identifiable through distinct gene expression profiles and functional properties. CAFs influence cancer development through multiple mechanisms, including regulation of extracellular matrix (ECM) remodeling, direct promotion of tumor growth through provision of metabolic support, promoting epithelial-mesenchymal transition (EMT) to enhance cancer invasiveness and growth, as well as stimulating cancer stem cell properties within the tumor. Moreover, CAFs can induce an immunosuppressive TME and contribute to therapeutic resistance. In this review, we summarize the fundamental knowledge and recent advances regarding CAFs, focusing on their sophisticated roles in cancer development and potential as therapeutic targets. We discuss various strategies to target CAFs, including ECM modulation, direct elimination, interruption of CAF-TME crosstalk, and CAF normalization, as approaches to developing more effective treatments. An improved understanding of the complex interplay between CAFs and TME is crucial for developing new and effective targeted therapies for cancer.
{"title":"Cancer associated fibroblasts in cancer development and therapy","authors":"Hongyuan Jia, Xingmin Chen, Linling Zhang, Meihua Chen","doi":"10.1186/s13045-025-01688-0","DOIUrl":"https://doi.org/10.1186/s13045-025-01688-0","url":null,"abstract":"Cancer-associated fibroblasts (CAFs) are key players in cancer development and therapy, and they exhibit multifaceted roles in the tumor microenvironment (TME). From their diverse cellular origins, CAFs undergo phenotypic and functional transformation upon interacting with tumor cells and their presence can adversely influence treatment outcomes and the severity of the cancer. Emerging evidence from single-cell RNA sequencing (scRNA-seq) studies have highlighted the heterogeneity and plasticity of CAFs, with subtypes identifiable through distinct gene expression profiles and functional properties. CAFs influence cancer development through multiple mechanisms, including regulation of extracellular matrix (ECM) remodeling, direct promotion of tumor growth through provision of metabolic support, promoting epithelial-mesenchymal transition (EMT) to enhance cancer invasiveness and growth, as well as stimulating cancer stem cell properties within the tumor. Moreover, CAFs can induce an immunosuppressive TME and contribute to therapeutic resistance. In this review, we summarize the fundamental knowledge and recent advances regarding CAFs, focusing on their sophisticated roles in cancer development and potential as therapeutic targets. We discuss various strategies to target CAFs, including ECM modulation, direct elimination, interruption of CAF-TME crosstalk, and CAF normalization, as approaches to developing more effective treatments. An improved understanding of the complex interplay between CAFs and TME is crucial for developing new and effective targeted therapies for cancer. ","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"101 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733941","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}
Pub Date : 2025-03-27DOI: 10.1186/s13045-025-01679-1
Po-Lan Su, Naoki Furuya, Alahmadi Asrar, Christian Rolfo, Zihai Li, David P. Carbone, Kai He
The development of targeted therapy with small-molecule tyrosine kinase inhibitors and immunotherapy with immune checkpoints inhibitors has ushered in the era of precision medicine in treating lung cancer, which remains the leading cause of cancer-related deaths worldwide. Both targeted therapy and immunotherapy have significantly improved the survival of patients with metastatic non-small-cell lung cancer (NSCLC). Additionally, recent groundbreaking studies have demonstrated their efficacy in both the perioperative setting and following concurrent chemoradiotherapy in early-stage NSCLC. Despite significant advancements in first-line treatment options, disease progression remains inevitable for most patients with advanced NSCLC, necessitating the exploration and optimization of subsequent therapeutic strategies. Emerging novel agents are expanding treatment options in the first-line setting and beyond. Recently, emerging bispecific antibodies have shown enhanced efficacy. For instance, amivantamab has been approved as a treatment for epidermal growth factor receptor (EGFR)-mutant NSCLC, including those with EGFR exon 20 insertion mutations. Additionally, antibody–drug conjugates (ADCs), including HER2-targeting trastuzumab deruxtecan, TROP2-targeting ADCs, HER3-targeting patritumab deruxtecan, and MET-targeting telisotuzumab vedotin, have demonstrated promising outcomes in several clinical trials. This review summarizes the recent advancements and challenges associated with the evolving NSCLC therapeutic landscape.
{"title":"Recent advances in therapeutic strategies for non-small cell lung cancer","authors":"Po-Lan Su, Naoki Furuya, Alahmadi Asrar, Christian Rolfo, Zihai Li, David P. Carbone, Kai He","doi":"10.1186/s13045-025-01679-1","DOIUrl":"https://doi.org/10.1186/s13045-025-01679-1","url":null,"abstract":"The development of targeted therapy with small-molecule tyrosine kinase inhibitors and immunotherapy with immune checkpoints inhibitors has ushered in the era of precision medicine in treating lung cancer, which remains the leading cause of cancer-related deaths worldwide. Both targeted therapy and immunotherapy have significantly improved the survival of patients with metastatic non-small-cell lung cancer (NSCLC). Additionally, recent groundbreaking studies have demonstrated their efficacy in both the perioperative setting and following concurrent chemoradiotherapy in early-stage NSCLC. Despite significant advancements in first-line treatment options, disease progression remains inevitable for most patients with advanced NSCLC, necessitating the exploration and optimization of subsequent therapeutic strategies. Emerging novel agents are expanding treatment options in the first-line setting and beyond. Recently, emerging bispecific antibodies have shown enhanced efficacy. For instance, amivantamab has been approved as a treatment for epidermal growth factor receptor (EGFR)-mutant NSCLC, including those with EGFR exon 20 insertion mutations. Additionally, antibody–drug conjugates (ADCs), including HER2-targeting trastuzumab deruxtecan, TROP2-targeting ADCs, HER3-targeting patritumab deruxtecan, and MET-targeting telisotuzumab vedotin, have demonstrated promising outcomes in several clinical trials. This review summarizes the recent advancements and challenges associated with the evolving NSCLC therapeutic landscape.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"88 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143713047","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}
Pub Date : 2025-03-19DOI: 10.1186/s13045-025-01683-5
Zwi N. Berneman, Maxime De Laere, Paul Germonpré, Manon T. Huizing, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Van den Bossche, Jan Van den Brande, Pol Specenier, Sevilay Altintas, Peter A. van Dam, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Annemiek Snoeckx, Bart Op de Beeck, Kirsten Saevels, Lynn Rutsaert, Irma Vandenbosch, Gizem Oner, Martin Lammens, Pierre Van Damme, Sian Llewellyn-Lacey, David A. Price, Yoshihiro Oka, Yusuke Oji, Haruo Sugiyama, Marie M. Couttenye, Ann L. Van de Velde, Viggo F. Van Tendeloo, Marc Peeters, Sébastien Anguille, Evelien L. J. M. Smits
Correction: Journal of Hematology & Oncology (2025) 18:9https://doi.org/10.1186/s13045-025-01661-x
The authors wish to note the following corrections to the information for references #2 and #9 in the original article:
- Reference #2 should instead begin as ‘Anguille S, Van de Velde AL, Smits EL, Van Tendeloo VF, Juliusson G, Cools N, et al. […]’.
- Reference #9 should imstead begin as ‘van der Burg SH […]’.
Authors and Affiliations
Center for Cell Therapy & Regenerative Medicine (CCRG), Antwerp University Hospital (UZA), Edegem, Belgium
Zwi N. Berneman, Maxime De Laere, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Van den Bossche, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Irma Vandenbosch, Ann L. Van de Velde, Viggo F. Van Tendeloo, Sébastien Anguille & Evelien L. J. M. Smits
Division of Hematology & Multidisciplinary Oncological Center Antwerp (MOCA), Antwerp University Hospital, Edegem, Belgium
Zwi N. Berneman, Maxime De Laere, Kim Caluwaerts, Kirsten Saevels, Lynn Rutsaert, Irma Vandenbosch, Ann L. Van de Velde & Sébastien Anguille
Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium
Zwi N. Berneman, Maxime De Laere, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Van den Bossche, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Ann L. Van de Velde, Viggo F. Van Tendeloo & Sébastien Anguille
Department of Pneumology, Maria Middelares General Hospital, Ghent, Belgium
Paul Germonpré
Division of Oncology & Multidisciplinary Oncological Center Antwerp, Antwerp University Hospital, Edegem, Belgium
Manon T. Huizing, Yannick Willemen, Jan Van den Brande, Pol Specenier, Sevilay Altintas & Marc Peeters
Bio and Tissue Bank, Antwerp University Hospital, Edegem, Belgium
Manon T. Huizing, Griet Nijs, Barbara Stein & Kim Caluwaerts
Department of Antwerp Surgical Training, Anatomy and Research Centre (ASTARC), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium
Manon T. Huizing
Center for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), Department of Molecular Imaging, Pathology, Radiotherapy and Oncology (MIPRO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium
Yannick Willemen, Jan Van den Brande, Pol Specenier, Sevilay Altintas, Peter A. van Dam, Gizem Oner, Martin Lammens, Marc Peeters & Evelien L. J. M. Smits
Division of Gynecological Oncology & Multidisciplinary Oncological Center Antwerp, Antwerp University Hospital, Edegem, Belgium
Peter A. van Dam & Gizem Oner
Clinical Research Center (CRC)
更正：Journal of Hematology &；肿瘤学（2025）18:9 https://doi.org/10.1186/s13045-025-01661-xThe作者希望对原文中参考文献#2和#9的信息进行以下更正：-参考文献#2应该改为“Anguille S, Van de Velde AL, Smits EL, Van Tendeloo VF, Juliusson G, cooks N, et AL .[…]”。-参考文献#9应该以“van der Burg SH[…]”开头。细胞治疗中心；再生医学（CCRG），安特卫普大学医院（UZA），比利时Edegem zwi N. Berneman, Maxime De Laere, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Vanden Bossche, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Irma Vandenbosch, Ann L. Van De Velde, Viggo F. Van Tendeloo, ssambastien Anguille &；evelen L. J. M. SmitsDivision of Hematology &；安特卫普多学科肿瘤中心（MOCA），安特卫普大学医院，比利时Edegem zwi N. Berneman, Maxime De Laere, Kim Caluwaerts, Kirsten Saevels, Lynn Rutsaert, Irma Vandenbosch, Ann L. Van De Velde等；比利时安特卫普大学医学与健康科学学院疫苗与传染病研究所实验血液学实验室zwi N. Berneman、Maxime De Laere、Yannick Willemen、Eva Lion、Hans De Reu、Jolien Van den Bossche、Nathalie Cools、Griet Nijs、Barbara Stein、Kim Caluwaerts、Ann L. Van De Velde、Viggo F. Van Tendeloo；比利时根特Maria Middelares总医院肺内科；比利时安特卫普大学医院安特卫普多学科肿瘤中心manon T. huzing, Yannick Willemen, Jan Van den Brande, Pol Specenier， Sevilay Altintas等；Marc peeters比利时安特卫普大学医院生物和组织库manon T. Huizing, Griet Nijs, Barbara Stein &；安特卫普大学医学和健康科学学院安特卫普外科培训、解剖和研究中心（ASTARC） manon T. huizing肿瘤研究中心（CORE）、综合个性化和精确肿瘤网络（IPPON）、安特卫普大学医学和健康科学学院分子成像、病理学、放疗和肿瘤学（MIPRO）、比利时yannick Willemen， Jan Van den Brande, Pol Specenier, Sevilay Altintas, Peter A. Van Dam, Gizem Oner, Martin Lammens, Marc Peeters &；evelen L. J. M. smits妇科肿瘤科；安特卫普多学科肿瘤中心，安特卫普大学医院，比利时EdegemGizem onr临床研究中心（CRC）安特卫普，安特卫普大学医院，比利时，Edegem； griet nijs放射科，安特卫普大学医院，比利时，Edegem比利时安特卫普大学医学和医学科学学院分子形态学和显微镜学系（mVISION）；比利时安特卫普大学医院解剖病理学部（Edegem）；比利时安特卫普大学医学和医学科学学院疫苗和传染病研究所（CEV）；卡迪夫大学医学院，卡迪夫，英国David A. PriceSystems免疫研究所，卡迪夫大学医学院，卡迪夫，英国；David A. pricessystem免疫研究所，大阪大学医学院，大阪，日本；大阪大学医学院，大阪，大阪；安特卫普大学附属医院肾内科（比利时）marie M. couttenye比利时安特卫普大学医学与健康科学学院免疫学与炎症转化研究部（TWI2N）；比利时marie M. coutenyeauthorszwi N. BernemanView作者出版物您也可以在pubmed谷歌ScholarMaxime De LaereView作者出版物您也可以在pubmed谷歌ScholarPaul germonpr<s:1>查看作者出版物您也可以在pubmed谷歌ScholarManon T中搜索该作者。 HuizingView作者出版物您也可以在pubmed谷歌ScholarYannick WillemenView作者出版物中搜索此作者您也可以在pubmed谷歌ScholarEva LionView作者出版物中搜索此作者您也可以在pubmed谷歌ScholarHans De ReuView作者出版物中搜索此作者您也可以在pubmed谷歌ScholarJolien Van den BosscheView作者出版物中搜索此作者您也可以在pubmed谷歌ScholarJan Van den中搜索此作者BrandeView作者出版物您也可以搜索这个作者在pubmed谷歌ScholarPol SpecenierView作者出版物您也可以搜索这个作者在pubmed谷歌ScholarSevilay AltintasView作者出版物您也可以搜索这个作者在pubmed谷歌ScholarPeter A. van DamView作者出版物您也可以搜索这个作者在pubmed谷歌ScholarNathalie CoolsView作者出版物您也可以搜索这个作者在pubmed谷歌ScholarGriet NijsView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarBarbara SteinView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarKim CaluwaertsView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarAnnemiek SnoeckxView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarBart Op de BeeckView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarKirsten SaevelsView作者你也可以搜索这个作者在pubmed谷歌ScholarLynn RutsaertView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarIrma VandenboschView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarGizem OnerView作者出版物你也可以搜索这个作者在pubmed谷歌ScholarMartin Lamme
{"title":"Correction: WT1-mRNA dendritic cell vaccination of patients with glioblastoma multiforme, malignant pleural mesothelioma, metastatic breast cancer, and other solid tumors: type 1 T-lymphocyte responses are associated with clinical outcome","authors":"Zwi N. Berneman, Maxime De Laere, Paul Germonpré, Manon T. Huizing, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Van den Bossche, Jan Van den Brande, Pol Specenier, Sevilay Altintas, Peter A. van Dam, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Annemiek Snoeckx, Bart Op de Beeck, Kirsten Saevels, Lynn Rutsaert, Irma Vandenbosch, Gizem Oner, Martin Lammens, Pierre Van Damme, Sian Llewellyn-Lacey, David A. Price, Yoshihiro Oka, Yusuke Oji, Haruo Sugiyama, Marie M. Couttenye, Ann L. Van de Velde, Viggo F. Van Tendeloo, Marc Peeters, Sébastien Anguille, Evelien L. J. M. Smits","doi":"10.1186/s13045-025-01683-5","DOIUrl":"https://doi.org/10.1186/s13045-025-01683-5","url":null,"abstract":"<p><b>Correction: Journal of Hematology & Oncology (2025) 18:9</b> <b>https://doi.org/10.1186/s13045-025-01661-x</b></p><br/><p>The authors wish to note the following corrections to the information for references #2 and #9 in the original article:</p><br/><p>- Reference #2 should instead begin as ‘Anguille S, Van de Velde AL, Smits EL, Van Tendeloo VF, Juliusson G, Cools N, et al. […]’.</p><br/><p>- Reference #9 should imstead begin as ‘van der Burg SH […]’.</p><h3>Authors and Affiliations</h3><ol><li><p>Center for Cell Therapy & Regenerative Medicine (CCRG), Antwerp University Hospital (UZA), Edegem, Belgium</p><p>Zwi N. Berneman, Maxime De Laere, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Van den Bossche, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Irma Vandenbosch, Ann L. Van de Velde, Viggo F. Van Tendeloo, Sébastien Anguille & Evelien L. J. M. Smits</p></li><li><p>Division of Hematology & Multidisciplinary Oncological Center Antwerp (MOCA), Antwerp University Hospital, Edegem, Belgium</p><p>Zwi N. Berneman, Maxime De Laere, Kim Caluwaerts, Kirsten Saevels, Lynn Rutsaert, Irma Vandenbosch, Ann L. Van de Velde & Sébastien Anguille</p></li><li><p>Laboratory of Experimental Hematology, Vaccine and Infectious Disease Institute (VAXINFECTIO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium</p><p>Zwi N. Berneman, Maxime De Laere, Yannick Willemen, Eva Lion, Hans De Reu, Jolien Van den Bossche, Nathalie Cools, Griet Nijs, Barbara Stein, Kim Caluwaerts, Ann L. Van de Velde, Viggo F. Van Tendeloo & Sébastien Anguille</p></li><li><p>Department of Pneumology, Maria Middelares General Hospital, Ghent, Belgium</p><p>Paul Germonpré</p></li><li><p>Division of Oncology & Multidisciplinary Oncological Center Antwerp, Antwerp University Hospital, Edegem, Belgium</p><p>Manon T. Huizing, Yannick Willemen, Jan Van den Brande, Pol Specenier, Sevilay Altintas & Marc Peeters</p></li><li><p>Bio and Tissue Bank, Antwerp University Hospital, Edegem, Belgium</p><p>Manon T. Huizing, Griet Nijs, Barbara Stein & Kim Caluwaerts</p></li><li><p>Department of Antwerp Surgical Training, Anatomy and Research Centre (ASTARC), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium</p><p>Manon T. Huizing</p></li><li><p>Center for Oncological Research (CORE), Integrated Personalized and Precision Oncology Network (IPPON), Department of Molecular Imaging, Pathology, Radiotherapy and Oncology (MIPRO), Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium</p><p>Yannick Willemen, Jan Van den Brande, Pol Specenier, Sevilay Altintas, Peter A. van Dam, Gizem Oner, Martin Lammens, Marc Peeters & Evelien L. J. M. Smits</p></li><li><p>Division of Gynecological Oncology & Multidisciplinary Oncological Center Antwerp, Antwerp University Hospital, Edegem, Belgium</p><p>Peter A. van Dam & Gizem Oner</p></li><li><p>Clinical Research Center (CRC) ","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"57 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661357","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}
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