International Journal of Cancer最新文献

{"title":"Delineation of monocytic and early-stage myeloid-derived suppressor cells in the peripheral blood of patients with hepatocarcinoma.","authors":"Marta Chivite-Lacaba, Iago Justo, Alberto Utrero-Rico, Oscar Caso, Cecilia González-Cuadrado, Manuel J Del Rey, Rocio Laguna-Goya, Javier Arroyo-Ródenas, Ángel Alfocea-Molina, Carlota C Ruigómez-Martín, Manuel Serrano, Lorena Pascual-Palacios, María Esther Mancebo, Estela Paz-Artal","doi":"10.1002/ijc.35390","DOIUrl":"https://doi.org/10.1002/ijc.35390","url":null,"abstract":"<p><p>In patients with hepatocellular carcinoma (HCC), increased myeloid-derived suppressor cells (MDSC) relate to aggressiveness and poor prognosis. Favorable responses with immune checkpoint inhibitors demonstrate that HCC is susceptible to immune activation, suggesting that the elimination of MDSC would provide therapeutic benefits. However, a global analysis of the different MDSC subsets in HCC is still missing. Here we phenotyped circulating myeloid cell subsets (monocytes, M-MDSC, PMN-MDSC and eMDSC) by flow cytometry in HCC and hepatocholangiocarcinoma patients and in healthy donors (HD). Isolated myeloid CD33⁺ cells were analyzed in immunosuppression assays, and cytokines were quantified in the supernatants. Arginase-1 activity (Arg-1) was analyzed in serum samples. All three proportions of MDSC, together with the immunosuppressive Arg-1, were significantly increased in HCC compared with HD. An important proportion of eMDSC expressed CD25, the IL-2 receptor α chain, and CD25⁺ eMDSC were also significantly expanded in HCC patients. HCC-CD33⁺ cells, enriched in M-MDSC and eMDSC, in vitro inhibited both CD4⁺ and CD8⁺ T cell proliferation and IL-2 production, and augmented IL-10, IL-6, and TNF-α. The correlation between the inhibition of T lymphocyte proliferation and M-MDSC was the strongest, while eMDSC or CD25⁺ eMDSC did not show antiproliferative capacity. Despite this functional difference, M-MDSC, CD25⁺ eMDSC, and CD25 expression in eMDSC were more prominent in advanced HCC as defined by a higher number of nodules, TNM stage, and alpha-fetoprotein level. This better delineation of M-MDSC and eMDSC phenotype and function in HCC could help to design therapies more likely to succeed in clinical trials.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to “Chronotherapy in head and neck cancer: A systematic review and meta-analysis”","authors":"","doi":"10.1002/ijc.35396","DOIUrl":"10.1002/ijc.35396","url":null,"abstract":"<p>Abusamak M, Abu-Samak A-A, Cai W, et al. Chronotherapy in head and neck cancer: a systematic review and meta-analysis. <i>Int J Cancer</i>. 2025;156(5):1015–1032. doi:10.1002/ijc.35234</p><p>In the article, there is an error in the acknowledgements.</p><p>The sentence reads:</p><p>The publication of this article was funded by the Qatar National Library.</p><p>This sentence should read:</p><p>Open Access funding provided by the Qatar National Library.</p><p>The online version of the article has been updated.</p><p>We apologize for this error.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"156 11","pages":"E15"},"PeriodicalIF":5.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.35396","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143571739","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Incorporation of Epstein–Barr viral variation implicates significance of Latent Membrane Protein 1 in survival prediction and prognostic subgrouping in Burkitt lymphoma","authors":"Isaac E. Kim Jr.,&nbsp;Cliff Oduor,&nbsp;Julian Stamp,&nbsp;Micah A. Luftig,&nbsp;Ann M. Moormann,&nbsp;Lorin Crawford,&nbsp;Jeffrey A. Bailey","doi":"10.1002/ijc.35384","DOIUrl":"10.1002/ijc.35384","url":null,"abstract":"<p>Although Epstein–Barr virus (EBV) plays a role in Burkitt lymphoma (BL) tumorigenesis, it is unclear if EBV genetic variation impacts clinical outcomes. From 130 publicly available whole-genome tumor sequences of EBV-positive BL patients, we used least absolute shrinkage and selection operator (LASSO) regression and Bayesian variable selection models within a Cox proportional hazards framework to select the top EBV variants, putative driver genes, and clinical features associated with patient survival time. These features were incorporated into survival prediction and prognostic subgrouping models. Our model yielded 22 EBV variants, including seven in latent membrane protein 1 (LMP1), as most associated with patient survival time. Using the top EBV variants, driver genes, and clinical features, we defined three prognostic subgroups that demonstrated differential survival rates, laying the foundation for incorporating EBV variants such as those in LMP1 as predictive biomarker candidates in future studies.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"156 11","pages":"2188-2199"},"PeriodicalIF":5.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting fatty acid oxidation: A potential strategy for treating gastrointestinal tumors.","authors":"Yingsong Zheng, Zhengchen Jiang, Li Yuan, Xiangdong Cheng, Weiyang He, Xiaodong Chen","doi":"10.1002/ijc.35380","DOIUrl":"https://doi.org/10.1002/ijc.35380","url":null,"abstract":"<p><p>Gastrointestinal cancers including esophageal squamous cell carcinoma (ESCC), gastric cancer (GC), and colorectal cancer (CRC) are common and highly lethal types of cancer worldwide. Metabolic reprogramming plays a critical role in cancer progression and involves metabolic processes such as glucose and lipid metabolism. Fatty acid oxidation (FAO) has a profound impact on cancer, with many genes and cytokines influencing cancer cell initiation, development, metastasis, and resistance by regulating FAO. Additionally, FAO further promotes cancer progression by affecting the tumor microenvironment (TME). The role of FAO in gastrointestinal cancers has garnered increasing attention, and related anticancer drugs are currently being developed.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-mediated high expression of TRIM15 promotes malignant progression of high-grade serous ovarian cancer through activation of AKT signaling pathway by K63 ubiquitination.","authors":"Wei Wei, Yang Zhang, Yibing Li, Jiazhen Huang, Fuli Kang, Shuang Tan, Lin Lin, Xiaohang Lu, Heng Wei, Ning Wang","doi":"10.1002/ijc.35387","DOIUrl":"https://doi.org/10.1002/ijc.35387","url":null,"abstract":"<p><p>The tripartite motif (TRIM) family member TRIM15 is an E3 ubiquitin ligase that is abnormally expressed in a variety of tumors, but its role and mechanism in high-grade serous ovarian cancer (HGSOC) are unclear. Here, we found for the first time that TRIM15 was upregulated in HGSOC and was associated with poor overall survival. Functional experiments showed that TRIM15 drove the proliferation of HGSOC cells and inhibited the apoptosis of tumor cells in vivo and in vitro. In terms of mechanism, we found that TRIM15 contributed to the malignant proliferation of HGSOC cells by promoting the activation of AKT and that there was a direct binding between them. TRIM15 induced lysine-63 (K63) ubiquitination of AKT through its Ring domain, which in turn activated the AKT signaling pathway. In addition, TRIM15-mediated K63 ubiquitination occurs mainly in the pleckstrin homology (PH) domain of AKT. We further identified other proteins and their functions regulated by TRIM15 in HGSOC cells by ubiquitin proteomic analysis. Furthermore, hypoxia-inducible factor-1α promoted TRIM15 transcriptional activation by binding to the hypoxia response elements of the TRIM15 promoter. Our study suggests that TRIM15 induces K63 ubiquitination of the AKT PH domain through its Ring domain and activates the AKT signaling pathway, thereby promoting HGSOC progression. In addition, the abnormally high expression of TRIM15 was associated with the hypoxic microenvironment of HGSOC tissues.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536288","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Global landscape of cervical cancer incidence and mortality in 2022 and predictions to 2030: The urgent need to address inequalities in cervical cancer.","authors":"Zhuang Li, Penglin Liu, Aijun Yin, Bingxin Zhang, Jiaqi Xu, Zhongshao Chen, Zhaoyang Zhang, Yawen Zhang, Shuaixin Wang, Lingliya Tang, Beihua Kong, Kun Song","doi":"10.1002/ijc.35369","DOIUrl":"https://doi.org/10.1002/ijc.35369","url":null,"abstract":"<p><p>Cervical cancer remains a major public health challenge worldwide, despite being largely preventable through effective interventions. Timely evidence regarding the global landscape of cervical cancer is crucial for measuring the magnitude of inequalities and monitoring progress towards cervical cancer elimination. We aimed to provide an updated overview of the global burden of cervical cancer using the GLOBOCAN 2022 database. Age-standardized rates of incidence and mortality were presented according to countries, 20 United Nations-defined world regions, and four-tier Human Development Index (HDI) levels. The predicted burden of cervical cancer for 2030 was calculated based on global demographic projections. Globally, an estimated 662,301 new cervical cancer cases and 348,874 deaths occurred in 2022. Substantial geographic disparities in cervical cancer burden existed across countries and world regions. Low HDI countries exhibited two times higher incidence rates and five times higher mortality rates, compared to very high HDI countries. For women aged 15-44 years, cervical cancer ranked among the top three most frequent cancers in 149 countries, and among the top three causes of cancer deaths in 154 countries. If 2022 rates remain unchanged, the global burden of cervical cancer was predicted to increase to 760,082 new cases (a 14.8% increase) and 411,035 deaths (a 17.8% increase) by 2030. Our findings highlight the persistent and widening geographic and socioeconomic inequalities in the burden of cervical cancer. There is an urgent need for tailored national strategies to address these inequalities and accelerate progress towards the goal of cervical cancer elimination.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":" ","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536287","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Induction of SOX17 with stimulation of WNT, TGF-beta, and FGF signaling drives embryonal carcinomas into the yolk-sac tumor lineage resulting in increased cisplatin resistance","authors":"Mara Kotthoff,&nbsp;Margaretha A. Skowron,&nbsp;Felix Bremmer,&nbsp;Fatma Parmaksiz,&nbsp;Pia Kretschmer,&nbsp;Alexa Stephan,&nbsp;Alexander Fichtner,&nbsp;Tobias Lautwein,&nbsp;Katharina Raba,&nbsp;Janina Fuß,&nbsp;Karl Köhrer,&nbsp;Daniel Nettersheim","doi":"10.1002/ijc.35385","DOIUrl":"10.1002/ijc.35385","url":null,"abstract":"<p>Relapsing germ cell tumor (GCT) patients often harbor components of the aggressive subtype yolk-sac tumor (YST), suggesting that YST formation is an escape mechanism under therapy. Nevertheless, the molecular mechanisms inducing YST development from its stem cell-like precursor embryonal carcinoma (EC) are largely unexplored. We demonstrated that the induction of the transcription factor SOX17 together with the stimulation of WNT, TGF-beta / Activin, and FGF signaling drives EC cells into the YST lineage. Single cell RNA sequencing revealed that this cell fate switch was accompanied by the upregulation of the typical YST factors <i>AFP</i>, <i>ANKRD1</i>, <i>APOA1</i>, <i>CST1</i>, <i>FOXA2</i>, <i>GATA6</i>, and <i>GPC3</i> and microRNAs, while pluripotency-related genes <i>NANOG</i>, <i>POU5F1</i>, and <i>SOX2</i> were downregulated. Chromatin immunoprecipitation followed by sequencing analysis revealed that SOX17 may act in concert with FOXA2 and GATA factors to initiate YST formation. Xenografting of the YST-like cells into nude mice led to the growth of mixed GCT with YST components, confirming that these cells are able to form a YST in vivo. Moreover, the expression of cisplatin resistance factors was induced in a subpopulation of YST-like cells, suggesting that the formation of a YST is accompanied by the acquisition of cisplatin resistance. Indeed, the YST-like cells presented as less sensitive to cisplatin than their parental cells. Our study deciphered the molecular mechanisms forcing EC to differentiate into the YST lineage, which is accompanied by the acquisition of cisplatin resistance, confirming that YST formation is an escape mechanism for GCT under therapy. Thus, GCT patients should be screened for YST elements under therapy to identify patients at risk of developing therapy resistance.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"156 11","pages":"2210-2224"},"PeriodicalIF":5.7,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.35385","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RETRACTION: Circular RNA CEP128 Promotes Bladder Cancer Progression by Regulating Mir-145-5p/Myd88 via MAPK Signaling Pathway","authors":"","doi":"10.1002/ijc.35391","DOIUrl":"10.1002/ijc.35391","url":null,"abstract":"<p><b>RETRACTION:</b> <span>M. Sun</span>, <span>W. Zhao</span>, <span>Z. Chen</span>, <span>M. Li</span>, <span>S. Li</span>, <span>B. Wu</span> and <span>R. Bu</span>, “ <span>Circular RNA CEP128 Promotes Bladder Cancer Progression by Regulating Mir-145-5p/Myd88 via MAPK Signaling Pathway</span>,” <i>International Journal of Cancer</i> <span>145</span>, no. <span>8</span> (<span>2019</span>): <span>2170</span>–<span>2181</span>, https://doi.org/10.1002/ijc.32311.</p><p>The above article, published online on 02 April 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Christoph Plass; the Union for International Cancer Control; and John Wiley &amp; Sons, Ltd. The retraction has been agreed following an investigation into concerns raised by a third party. The investigation identified flaws and inconsistencies between the methodology described and the results presented. The authors were contacted and invited to comment on these concerns and to provide relevant supporting documentation, but they did not respond. The editors consider the results unreproducible and have therefore decided to retract this article. The authors were informed of the retraction.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"156 11","pages":"E16"},"PeriodicalIF":5.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.35391","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biopsy-derived organoids in personalised early breast cancer care: Challenges of tumour purity and normal cell overgrowth cap their practical utility","authors":"Paul Schwerd-Kleine,&nbsp;Roberto Würth,&nbsp;Tasneem Cheytan,&nbsp;Laura Michel,&nbsp;Verena Thewes,&nbsp;Ewgenija Gutjahr,&nbsp;Huriye Seker-Cin,&nbsp;Daniel Kazdal,&nbsp;Sarah-Jane Neuberth,&nbsp;Vera Thiel,&nbsp;Jonas Schwickert,&nbsp;Tim Vorberg,&nbsp;Jennifer Wischhusen,&nbsp;Albrecht Stenzinger,&nbsp;Marc Zapatka,&nbsp;Peter Lichter,&nbsp;Andreas Schneeweiss,&nbsp;Andreas Trumpp,&nbsp;Martin R. Sprick","doi":"10.1002/ijc.35386","DOIUrl":"10.1002/ijc.35386","url":null,"abstract":"<p>The ability to establish organoids composed exclusively of tumour rather than healthy cells is essential for their implementation into clinical practice. Organoids have recently emerged as a powerful tool to expand patient material in culture and generate modifiable 3D models derived from humans or animal models. For translational research, they enable the creation of model systems for an ever-increasing number of cell types and diseases. And in personalised medicine, they potentially allow for functional drug testing with high predictive power in certain settings. We found that using biopsy material from untreated, early-stage primary breast cancer patients poses significant challenges for consistently culturing tumour cells as organoids. Specifically, we observed frequent outgrowth of genetically normal, non-cancerous epithelial cells. We analysed &gt;100 biopsy samples from early-stage breast cancer and present our large collection of &gt;70 organoid lines. We also show methods of assessing successful tumour cell culture in a time, and cost-efficient manner, proving a high rate (&gt;85%) of normal cell overgrowth in early-stage breast cancer organoids. Finally, we show a number of successful attempts to culture cancer organoids from mastectomy-derived tissue of advanced, metastatic breast cancer. We conclude that the usefulness of organoids from early breast cancer for translational research and personalised medicine, especially guidance of adjuvant or post-surgical maintenance therapy, is strongly limited by the low success rate of culturing cancerous cells under organoid conditions.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"156 11","pages":"2200-2209"},"PeriodicalIF":5.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.35386","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143530878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pirtobrutinib in Chinese patients with relapsed or refractory B-cell malignancies: A single-arm, open-label, phase 2, multicenter trial","authors":"Yanyan Liu,&nbsp;Ningjing Lin,&nbsp;Shuhua Yi,&nbsp;Huiqiang Huang,&nbsp;Ye Guo,&nbsp;Qingyuan Zhang,&nbsp;Haiyan Yang,&nbsp;Huilai Zhang,&nbsp;Liling Zhang,&nbsp;Ru Feng,&nbsp;Yijiao Qian,&nbsp;Jiankun Zhu,&nbsp;Yuqin Song,&nbsp;Jun Zhu","doi":"10.1002/ijc.35339","DOIUrl":"10.1002/ijc.35339","url":null,"abstract":"<p>Pirtobrutinib, a highly selective, noncovalent (reversible) Bruton tyrosine kinase inhibitor (BTKi), demonstrated clinically meaningful antitumor responses in covalent BTKi pretreated mantle cell lymphoma (MCL) and chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) in the global phase 1/2 BRUIN study. In this multi-center, open-label, phase 2 trial, we investigated the efficacy and safety of pirtobrutinib in Chinese patients with BTKi pretreated relapsed/refractory (R/R) MCL, CLL/SLL, or other B-cell malignancies. All patients received pirtobrutinib once daily in continuous 28-day cycles. The primary endpoint was the overall response rate (ORR). Efficacy was assessed in patients with MCL and CLL/SLL with prior BTKi treatment and safety in all enrolled patients who received at least one dose of pirtobrutinib. Among 35 patients with covalent BTKis (cBTKi) pretreated MCL, the ORR was 62.9% (95% CI: 44.9, 78.5), the median duration of response (DOR) was not reached, and the 12-month DOR rate was 59.7% (95% CI: 35.3, 77.5). Among 11 patients with cBTKi pretreated CLL/SLL, the ORR was 63.6% (95% CI: 30.8, 89.1), and the 12-month DOR rate was 83.3% (95% CI: 27.3, 97.5). The most common adverse events in the safety population (<i>n</i> = 87) were anemia (32.2%) and neutrophil count decreased (31.0%). Grade ≥3 hemorrhage occurred in 2.3% of patients and there were no cases of atrial fibrillation/flutter. Pirtobrutinib demonstrated clinically meaningful efficacy in Chinese patients with cBTKi pretreated R/R MCL, preliminary antitumor activity in Chinese patients with cBTKi pretreated R/R CLL/SLL and was generally well-tolerated with no new safety signals observed.</p>","PeriodicalId":180,"journal":{"name":"International Journal of Cancer","volume":"156 11","pages":"2158-2168"},"PeriodicalIF":5.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ijc.35339","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}