Experimental Hematology & Oncology最新文献

{"title":"RNA modifications in the tumor microenvironment: insights into the cancer-immunity cycle and beyond.","authors":"You-Peng Ding, Cui-Cui Liu, Ke-Da Yu","doi":"10.1186/s40164-025-00648-1","DOIUrl":"10.1186/s40164-025-00648-1","url":null,"abstract":"<p><p>The chemical modification of biological molecules is a critical regulatory mechanism for controlling molecular functions. Although research has long focused on DNA and proteins, RNA modifications have recently attracted substantial interest with the advancement in detection technologies. In oncology, many studies have identified dysregulated RNA modifications including m6A, m1A, m5C, m7G, pseudouridylation and A to I editing, leading to disrupted downstream pathways. As the concept of the tumor microenvironment has gained prominence, studies have increasingly examined the role of RNA modifications in this context, focusing on interactions among cancer cells, immune cells, stromal cells, and other components. Here we review the RNA modifications in the tumor microenvironment through the perspective of the Cancer-Immunity Cycle. The extracellular RNA modifications including exosomes and influence of microbiome in RNA modifications are potential research questions. Additionally, RNA modifying enzymes including FTO, ALKBH5, METTL3, PUS7 are under investigation as potential biomarkers and targets for combination with immunotherapies. ADCs and mimetics of modified RNA could be potential novel drugs. This review discusses the regulatory roles of RNA modifications within the tumor microenvironment.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"48"},"PeriodicalIF":9.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A one-base therapeutic insertion in the HBG2 distal promoter reactivates γ-globin expression.","authors":"Xiuqin Bao, Yuanyi Gao, Xiaoyi Chen, Zhongju Wang, Xiaoqin Feng, Liren Wang, Jing Du, Yuhua Ye, Feijing Chen, Li Du, Aihua Yin, Xiangmin Xu","doi":"10.1186/s40164-025-00626-7","DOIUrl":"10.1186/s40164-025-00626-7","url":null,"abstract":"<p><strong>Background: </strong>The reactivation of developmental silenced γ-globin genes (HBG1/2) has shown promise as a therapeutic strategy for improving symptoms of β-hemoglobinopathies. Currently, the focus of therapeutic targets is primarily on the major fetal hemoglobin suppressors, such as BCL11A and ZBTB7A and of their binding sites on the proximal HBG promoter. However, the role of the distal HBG promoter in regulating gene expression remains to be explored.</p><p><strong>Methods: </strong>We used CRISPR/Cas9 system to edit the distal HBG promoter. In vitro and in vivo assays, as well as engrafted NCG-Kit-V831M mice, were used for functional validation and mechanistic studies.</p><p><strong>Results: </strong>We discovered an insertion of nucleotide A (insA) between - 1368 and - 1369 bp upstream of the TSS in HBG2 resulting in remarkable increase in γ-globin expression in HUDEP-2 cells. We also observed elevated γ-globin expression in human CD34⁺ erythroid progenitor cells from healthy individuals and those with β-thalassemia when introducing insA mutation. Similarly, engrafted NCG-Kit-V831M mice showed increased γ-globin expression. Importantly, neither did insA have any off-target effects nor did it affect the maturation of erythroid cells. Furthermore, we found that the insA mutation created a binding site for the transcription activator FOXO3, which was activated by AMPK. Additionally, introducing insA specifically demethylated the - 162 CpG site on HBG promoter by reducing the enrichment of DNA methyltransferase 3 A (DNMT3A). At the same time, it activated histone modifications and RNA polymerase II (Pol II) in both distal and proximal HBG promoter and might inhibit the binding of BCL11A and ZBTB7A on -115 and - 200 sites on the HBG promoter respectively. In addition, combination of insA and the - 115 or -200 editing targets resulted in an amplify effect in reactivating γ-globin genes expression.</p><p><strong>Conclusions: </strong>Overall, we presented the preclinical data to support the role of insA on regulating γ-globin expression using CD34⁺ HSPC cells derived from healthy donors or patients with β-thalassemia, and subsequently engrafted mice. Our study suggests that introducing insA mutation leads to significantly boosted fetal globin levels and uncovers new safe therapeutic target or strategy for β-hemoglobinopathies.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"47"},"PeriodicalIF":9.4,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951516/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The clinical landscape of CAR NK cells.","authors":"Lasse Vedel Jørgensen, Emil Birch Christensen, Mike Bogetofte Barnkob, Torben Barington","doi":"10.1186/s40164-025-00633-8","DOIUrl":"10.1186/s40164-025-00633-8","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR) NK cell therapy has emerged as a promising alternative to CAR T cell therapy, offering significant advantages in terms of safety and versatility. Here we explore the current clinical landscape of CAR NK cells, and their application in hematologic malignancies and solid cancers, as well as their potential for treating autoimmune disorders. Our analysis draws from data collected from 120 clinical trials focused on CAR NK cells, and presents insights into the demographics and characteristics of these studies. We further outline the specific targets and diseases under investigation, along with the major cell sources, genetic modifications, combination strategies, preconditioning- and dosing regimens, and manufacturing strategies being utilized. Initial results from 16 of these clinical trials demonstrate promising efficacy of CAR NK cells, particularly in B cell malignancies, where response rates are comparable to those seen with CAR T cells but with lower rates of severe adverse effects, such as cytokine release syndrome (CRS), immune effector cell-associated neurotoxicity syndrome (ICANS), and graft-versus-host disease (GvHD). However, challenges remain in solid tumor applications, where only modest efficacy has been observed to date. Our analysis reveals that research is increasingly focused on enhancing CAR NK cell persistence, broadening their therapeutic targets, and refining manufacturing processes to improve accessibility and scalability. With recent advancements in NK cell engineering and their increased clinical applications, CAR NK cells are predicted to become an integral component of next-generation immunotherapies, not only for cancer but potentially for immune-mediated diseases as well.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"46"},"PeriodicalIF":9.4,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143729376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatitis B surface antigen: carcinogenesis mechanisms and clinical implications in hepatocellular carcinoma.","authors":"Bingyan Hao, Yachong Liu, Bohan Wang, Haofeng Wu, Yan Chen, Lei Zhang","doi":"10.1186/s40164-025-00642-7","DOIUrl":"10.1186/s40164-025-00642-7","url":null,"abstract":"<p><p>Liver cancer is the third leading cause of death globally, with hepatitis B virus (HBV) infection being identified as the primary risk factor for its development. The occurrence of HBV-related hepatocellular carcinoma (HCC) is attributed to various mechanisms, such as chronic inflammation and liver cell regeneration induced by the cytotoxic immune response triggered by the virus, abnormal activation of oncogenes arising from HBV DNA insertion mutations, and epigenetic alterations mediated by viral oncoproteins. The envelope protein of the HBV virus, known as hepatitis B surface antigen (HBsAg), is a key indicator of increased risk for developing HCC in HBsAg-positive individuals. The HBsAg seroclearance status is found to be associated with recurrence in HCC patients undergoing hepatectomy. Additional evidence indicates that HBsAg is essential to the entire process of tumor development, from initiation to advancement, and acts as an oncoprotein involved in accelerating tumor progression. This review comprehensively analyzes the extensive effects and internal mechanisms of HBsAg during the various stages of the initiation and progression of HCC. Furthermore, it highlights the importance and potential applications of HBsAg in the realms of HCC early diagnosis and personalized therapeutic interventions. An in-depth understanding of the molecular mechanism of HBsAg in the occurrence and development of HCC is provided, which is expected to develop more precise and efficient strategies for the prevention and management of HCC in the future.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"44"},"PeriodicalIF":9.4,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938626/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of resistance to CAR-T cell therapy in multiple myeloma: latest updates from the 2024 ASH annual meeting.","authors":"Yuhan Hu, Jiangxue Hou, Zhongxing Jiang, Quande Lin","doi":"10.1186/s40164-025-00643-6","DOIUrl":"10.1186/s40164-025-00643-6","url":null,"abstract":"<p><p>Chimeric Antigen Receptor T-Cell (CAR-T) therapy demonstrates significant potential in the treatment of multiple myeloma (MM). However, resistance to CAR-T therapy remains a critical challenge. Investigating the mechanisms underlying CAR-T resistance, including antigen escape, immunosuppression, and CAR-T cell exhaustion, is essential for enhancing the long-term efficacy of this therapeutic approach. This study provides an in-depth review of the latest findings presented at the 66th ASH Annual Meeting.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"45"},"PeriodicalIF":9.4,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11938694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143718342","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MMP14 from BM-MSCs facilitates progression and Ara-C resistance in acute myeloid leukemia via the JAK/STAT pathway.","authors":"Jinxian Wu, Xinqi Li, Yin Liu, Guopeng Chen, Ruihang Li, Hongqiang Jiang, Wanyue Yin, Xiqin Tong, Rui Cao, Xianwang Wang, Xiaoyan Liu, Fuling Zhou","doi":"10.1186/s40164-025-00635-6","DOIUrl":"10.1186/s40164-025-00635-6","url":null,"abstract":"<p><p>Growing evidence underscores the pivotal impact of crosstalk between leukemic stem cells (LSCs) and mesenchymal stromal cells (MSCs) within their niche on leukemia initiation, progression, and therapy response. Although MMP14 plays an important role in inflammation and cancer, the regulation and role of MSC-derived MMP14 in acute myeloid leukemia (AML) are largely unknown. Here, we found that AML patient-derived MSCs (AML-MSCs) were more supportive of AML cell growth compared to healthy donor-derived MSCs (HD-MSCs). Moreover, AML-MSCs and HD-MSCs showed significant differences in gene expression and protein expression profiles. Knockdown of MMP14 in MSCs inhibited the CFU-F ability of MSC cells and increased the proportion of cells in the G0 phase, thereby inhibiting proliferation. Co-culture with MSCs inhibited the proliferation and cell cycle progression of leukemia cells, while increasing the apoptosis rate, thus impairing the leukemogenic potential of AML cells both in vitro and in vivo. Mechanistic studies revealed that MMP14-mediated alterations in the AML stromal microenvironment are driven by PGE2 secretion and activation of the JAK-STAT pathway, promoting leukemia progression. Notably, inhibition of MMP14 can attenuate the chemotherapy resistance of AML cells induced by MSCs to cytarabine (Ara-C). Together, our study, for the first time, demonstrates the critical role of MSC-derived MMP14 in promoting AML progression and chemoresistance. Targeting MMP14 signaling pathways may offer novel therapeutic options for AML.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"43"},"PeriodicalIF":9.4,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11929205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamin2 mutations in newly diagnosed acute myeloid leukemia: clinical characteristics, and prognostic significance.","authors":"Kunpeng Luo, Jiayuan Chen, Wenting Wang, Yan Hui, Shaowei Qiu, Bingcheng Liu, Yingchang Mi, Jianxiang Wang, Hui Wei","doi":"10.1186/s40164-025-00628-5","DOIUrl":"10.1186/s40164-025-00628-5","url":null,"abstract":"<p><p>Acute myeloid leukemia (AML) is a highly heterogeneous myeloid malignancy which can be classified by genetic aberrations. To evaluate the impact of the dynamin 2 mutation in AML, we systematically assessed the characteristics and prognostic of DNM2 mutated patients in AML. In 912 AML patients, 20 somatic mutations in the DNM2 gene were identified among the 18 DNM2 mutated AML patients (2%). Of the mutation events, 60% (12/20) were in the dynamin central region of DNM2. DNM2mutations were preferentially occurred in AML with CEBPA mutation (11/18, 61.1%), or RUNX1::RUNX1T1 fusion gene (6/18, 33.3%). DNM2 mutations were associated with better overall survival (P = 0.028), event-free survival (P = 0.0093) and trends towards better relapse-free survival (P = 0.08), which seems potentially attribute to its coexisting with CEBPA mutation and RUNX1::RUNX1T1 fusion gene. Our study demonstrated the clinical characteristics and the role of DNM2 mutations in AML, which might facilitate understanding the pathogenesis of AML.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"42"},"PeriodicalIF":9.4,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11927327/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143676769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibody-drug conjugates in breast cancer: current evidence and future directions.","authors":"Ning Li, Lu Yang, Zixuan Zhao, Tian Du, Gehao Liang, Na Li, Jun Tang","doi":"10.1186/s40164-025-00632-9","DOIUrl":"10.1186/s40164-025-00632-9","url":null,"abstract":"<p><p>Antibody-drug conjugates (ADCs) are a rapidly evolving class of antitumor drugs and have already revolutionized the treatment strategy of many hematologic and solid cancers. So far, trastuzumab emtansine (T-DM1), trastuzumab deruxtecan (T-DXd), sacituzumab govitecan (SG) and datopotamab deruxtecan (Dato-DXd) are the four ADCs that have been approved by US food and drug administration (FDA) in treatment of breast cancer, and SKB264 has been approved by Chinese national medical products administration (NMPA). Many ADCs for treatment of breast cancer are currently being tested in late-phase clinical trials, with several encouraging results achieved recently. However, major issues arise during the use of ADCs, including emergence of acquired resistance, occurrence of treated-related toxicities, and identification of biomarkers of response and resistance. ADCs are being increasingly tested in combination with other agents, and novel next-generation ADC development is progressing rapidly. A better understanding of the design and development of ADCs will promote ADC development for cancer treatment. In this review, we aim to provide a broad overview of the design and the recent advances of ADCs in breast cancer. We also propose several notable future directions of ADCs in treatment of breast cancer.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"41"},"PeriodicalIF":9.4,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"All-in-one CRISPR/Cas-engineered glucocorticoid-receptor knock-out EBV-gp350-CAR knock-in T cells are potent and resistant to dexamethasone.","authors":"Theresa Kaeuferle, Maximilian Zwermann, Nadine Stoll, Paulina Ferrada-Ernst, Lena Jablonowski, Reinhard Zeidler, Semjon Willier, Dana Stenger, Abdallah Yassin, Renata Stripecke, Tobias Feuchtinger","doi":"10.1186/s40164-025-00631-w","DOIUrl":"10.1186/s40164-025-00631-w","url":null,"abstract":"<p><strong>Background: </strong>Epstein-Barr virus (EBV) reactivation in immunocompromised patients and post-transplantation is associated with morbidity, mortality and with the onset of a variety of malignant diseases. Adoptive T-cell therapies have emerged as promising therapeutic options, but post-transplant immunosuppression jeopardizes the protective anti-EBV immune surveillance by adoptively transferred T cells.</p><p><strong>Methods: </strong>Using an all-in-one CRISPR/Cas-mediated approach, we inserted an anti-EBV (gp350) CAR into the T-cell receptor (TRAC) locus and simultaneously knocked-out the glucocorticoid receptor (GR) on a good manufacturing practice (GMP)-compatible platform.</p><p><strong>Results: </strong>CAR knock-in (CAR^KI) was confirmed in primary human T cells on genetic and on protein level with a mean efficiency of 41%. With 83%, additional GR knock-out was highly efficient in CAR^KI cells. On a functional level CAR^KIGR^KO T cells showed target-specific potency in terms of cytokine secretion patterns, proliferative capacity and cytotoxic activity against gp350-expressing target cells. Further, CAR^KIGR^KO T cells were insensitive to dexamethasone treatment and maintained T-cell functionality. In contrast, CAR^KIGR^KO T cells were sensitive to the GR-independent immunosuppressant cyclosporine A (CsA), thereby providing a rescue treatment for patients in case of safety issues.</p><p><strong>Conclusions: </strong>The study lays the proof-of-concept for virus-free all-in-one GMP-manufacturing of glucocorticoid-resistant CAR T-cell products. Further, the glucocorticoid-resistant gp350-CAR T cells can provide a future therapeutic option for high-risk post-transplant patients with EBV-reactivations or patients with EBV-associated pathologies requiring steroid treatment.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"40"},"PeriodicalIF":9.4,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11921674/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disparities in the incidence, mortality and disability-adjusted life years of 33 early-onset cancer groups globally, 2012-2021: a systematic analysis.","authors":"Wenxin Yan, Min Liu, Wenzhan Jing, Liangyu Kang, Ning Zhang, Haoran Sun, Jinyu He, Zhongdan Chen, Jue Liu, Wannian Liang, Jiahong Dong","doi":"10.1186/s40164-025-00634-7","DOIUrl":"10.1186/s40164-025-00634-7","url":null,"abstract":"<p><strong>Background: </strong>The global cancer burden is rising, with early-onset cancers becoming more prevalent. We aimed to investigate the burden, trend and population disparity in 33 early-onset cancers from 2012 to 2021.</p><p><strong>Methods: </strong>Annual incidence, death, and disability-adjusted life years (DALY) numbers and rates for early-onset (15-49 years) cancer groups were calculated from Global Burden of Diseases (GBD) 2021 dataset, covering 2012-2021 across global, five SDI groupings, and 204 countries and territories. Estimated annual percentage change (EAPC) in the incidence, mortality and DALY rates was calculated to quantify temporal trends, while spearman correlation analysis was used to examine the correlation between rates, EAPC and SDI.</p><p><strong>Results: </strong>In 2021, there were 2.65 million new early-onset cancer cases excluding non-melanoma skin cancer (NMSC), resulting in 0.99 million deaths and 50.7 million DALYs. Breast, tracheal, bronchus and lung (TBL), cervical, colon and stomach cancers were the leading causes of DALYs. The DALY rate for early-onset cancer excluding NMSC changed from 65.7 million in 2012 to 67.0 million in 2021, with an estimated annual percentage change (EAPC) of -0.49%. While the DALY rate plateaued for females, it decreased by -0.95% for males. Ten of 33 cancer groups exhibited an EAPC > 0. The high SDI quintile had 1,100 DALYs per 100,000 caused by early-onset cancers excluding NMSC, with the highest declining trend in DALY and mortality rates, while the high-middle SDI quintile had the highest early-onset mortality rates. Rising trends in cancer incidence and mortality were especially notable among females in the middle, low-middle, and low SDI quintiles.</p><p><strong>Conclusion: </strong>The global burden of early-onset cancer differs significantly by SDI quintile and gender. The increasing burden across multiple cancer groups poses a significant public health challenge. The rising burden of multiple cancer types is alarming, highlighting the need for increased policy support and targeted medical assistance to address the disparities in their impact.</p>","PeriodicalId":12180,"journal":{"name":"Experimental Hematology & Oncology","volume":"14 1","pages":"38"},"PeriodicalIF":9.4,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11912769/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}