Cancer letters最新文献

{"title":"Histone acetyltransferases as promising therapeutic targets in glioblastoma resistance","authors":"Spoorthy Pathikonda,&nbsp;Farzaneh Amirmahani,&nbsp;Diya Mathew,&nbsp;Sree Deepthi Muthukrishnan","doi":"10.1016/j.canlet.2024.217269","DOIUrl":"10.1016/j.canlet.2024.217269","url":null,"abstract":"<div><div>Glioblastoma (GBM) is a fatal adult brain tumor with an extremely poor prognosis. GBM poses significant challenges for targeted therapies due to its intra- and inter-tumoral heterogeneity, a highly immunosuppressive microenvironment, diffuse infiltration into normal brain parenchyma, protection by the blood-brain barrier and acquisition of therapeutic resistance. Recent studies have implicated epigenetic modifiers as key players driving tumorigenesis, resistance, and progression of GBM. While the vast majority of GBM research on epigenetic modifiers thus far has focused predominantly on elucidating the functional roles and targeting of DNA methyltransferases and histone deacetylases, emerging evidence indicates that histone acetyltransferases (HATs) also play a key role in mediating plasticity and therapeutic resistance in GBM. Here, we will provide an overview of HATs, their dual roles and functions in cancer as both tumor suppressors and oncogenes and focus specifically on their implications in GBM resistance. We also discuss the technical challenges in developing selective HAT inhibitors and highlight their promise as potential anti-cancer therapeutics for treating intractable cancers such as GBM.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217269"},"PeriodicalIF":9.1,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342206","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":"Delivery of PARP inhibitors through 2HG-incorporated liposomes for synergistically targeting DNA repair in cancer","authors":"Zhangyi Luo,&nbsp;Yixian Huang,&nbsp;Shangyu Chen,&nbsp;Bei Zhang,&nbsp;Haozhe Huang,&nbsp;Sheida Dabiri,&nbsp;Yuang Chen,&nbsp;Anju Zhang,&nbsp;Alexis R. Andreas,&nbsp;Song Li","doi":"10.1016/j.canlet.2024.217268","DOIUrl":"10.1016/j.canlet.2024.217268","url":null,"abstract":"<div><div>PARP inhibitors (PARPi) benefit only a small subset of patients with DNA homologous recombination (HR) defects. In addition, long-term administration of a PARPi can lead to the development of drug resistance. 2-Hydroxyglutarate (2HG) has long been known as an oncometabolite but is capable of inducing an HR defect, which makes tumor cells exquisitely sensitive to PARPi. To facilitate the translation of this discovery to the treatment of both HR-deficient and HR-proficient tumors, a liposomal formulation was developed for codelivery of 2HG and veliparib, a PARPi. A sequential loading protocol was developed such that the initial loading of 2HG into liposomes greatly facilitated the subsequent, pH gradient-driven remote loading of veliparib. The liposomes co-loaded with veliparib and 2HG exhibited favorable stability, slow kinetics of drug release, and targeted delivery to the tumor. Furthermore, the veliparib/2HG liposomes demonstrated enhanced anti-tumor activity in both PARPi-resistant BRCA mutant cancer and BRCA wildtype cancer by synergistically enhancing the defect in DNA repair. Moreover, combination of veliparib and 2HG via liposomal co-delivery also augmented the function of cytotoxic T cells by activating the STING pathway and downregulating PD-L1 expression via 2HG-induced hypermethylation.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217268"},"PeriodicalIF":9.1,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142328078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular dynamics of tumor microenvironment driving immunotherapy resistance in non-small-cell lung carcinoma","authors":"Shujie Huang ,&nbsp;Jeff Yat-Fai Chung ,&nbsp;Chunjie Li ,&nbsp;Yi Wu ,&nbsp;Guibin Qiao ,&nbsp;Ka-Fai To ,&nbsp;Patrick Ming-Kuen Tang","doi":"10.1016/j.canlet.2024.217272","DOIUrl":"10.1016/j.canlet.2024.217272","url":null,"abstract":"<div><div>Immune checkpoint inhibitors (ICIs) have profoundly reshaped the treatment paradigm for non-small cell lung cancer (NSCLC). Despite these advancements, primary and secondary resistance to ICIs remain prevalent challenges in managing advanced NSCLC. Recent studies have highlighted the significant role of the tumor microenvironment (TME) in modulating treatment responses. This review aims to comprehensively examine the interactive roles of immune/stromal cells—such as T cells, B cells, neutrophils, macrophages, and CAFs within the TME, elucidating how these diverse cellular interactions contribute to immunotherapy resistance. It focuses on the dynamic interactions among diverse cell types such as the varying states of T cells under the influence of TME constituents like immune cells and cancer-associated fibroblasts (CAFs). By exploring the mechanisms involved in the complex cellular interactions, we highlight novel therapeutic targets and strategies aimed at overcoming resistance, thereby enhancing the efficacy of ICIs in NSCLC. Our synthesis of recent research provides critical insights into the multifaceted mechanisms of resistance and paves the way for the development of more effective, personalized treatment approaches.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217272"},"PeriodicalIF":9.1,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “LincRNA-ROR promotes invasion, metastasis and tumor growth in pancreatic cancer through activating ZEB1 pathway” [Cancer Lett.374 (2016) 261–271]","authors":"Han-xiang Zhan ,&nbsp;Yao Wang ,&nbsp;Ce Li ,&nbsp;Jian-wei Xu ,&nbsp;Bin Zhou ,&nbsp;Jian-kang Zhu ,&nbsp;Hai-feng Han ,&nbsp;Lei Wang ,&nbsp;Yun-shan Wang ,&nbsp;San-yuan Hu","doi":"10.1016/j.canlet.2024.217239","DOIUrl":"10.1016/j.canlet.2024.217239","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217239"},"PeriodicalIF":9.1,"publicationDate":"2024-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142342204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current status and prospect of gut and oral microbiome in pancreatic cancer: Clinical and translational perspectives","authors":"Pengyu Li ,&nbsp;Hanyu Zhang ,&nbsp;Menghua Dai","doi":"10.1016/j.canlet.2024.217274","DOIUrl":"10.1016/j.canlet.2024.217274","url":null,"abstract":"<div><div>Pancreatic cancer is a highly lethal malignancy, and its diagnosis and treatment continue to pose significant challenges. Despite advancements in surgical and comprehensive treatment methods, the five-year survival rate remains below 12 %. With the rapid development of microbiome science, the gut and oral microbiota, which are readily accessible and can be sampled non-invasively, have emerged as a novel area of interest in pancreatic cancer research. Dysbiosis in these microbial communities can induce persistent inflammatory responses and affect the host's immune system, promoting cancer development and impacting the efficacy of treatments like chemotherapy and immunotherapy. This review provides an up-to-date overview of the roles of both gut and oral microbiota in the onset, progression, diagnosis, and treatment of pancreatic cancer. It analyzes the potential of utilizing these microbiomes as biomarkers and therapeutic targets from a clinical application perspective. Furthermore, it discusses future research directions aimed at harnessing these insights to advance the diagnosis and treatment strategies for pancreatic cancer. By focusing on the microbiome's role in clinical and translational medicine, this review offers insights into improving pancreatic cancer diagnosis and treatment outcomes.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217274"},"PeriodicalIF":9.1,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Spliceosomal vulnerability of MYCN-amplified neuroblastoma is contingent on PRMT5-mediated regulation of epitranscriptomic and metabolomic pathways","authors":"Jodie Bojko ,&nbsp;Madhu Kollareddy ,&nbsp;Marianna Szemes ,&nbsp;Jacob Bellamy ,&nbsp;Evon Poon ,&nbsp;Ahmad Moukachar ,&nbsp;Danny Legge ,&nbsp;Emma E. Vincent ,&nbsp;Nicholas Jones ,&nbsp;Sally Malik ,&nbsp;Alexander Greenhough ,&nbsp;Alex Paterson ,&nbsp;Ji Hyun Park ,&nbsp;Kelli Gallacher ,&nbsp;Louis Chesler ,&nbsp;Karim Malik","doi":"10.1016/j.canlet.2024.217263","DOIUrl":"10.1016/j.canlet.2024.217263","url":null,"abstract":"<div><div>Approximately 50 % of poor prognosis neuroblastomas arise due to <em>MYCN</em> over-expression. We previously demonstrated that MYCN and PRMT5 proteins interact and PRMT5 knockdown led to apoptosis of <em>MYCN</em><em>-</em>amplified (MNA) neuroblastoma. Here we evaluate the highly selective first-in-class PRMT5 inhibitor GSK3203591 and its <em>in vivo</em> analogue GSK3326593 as targeted therapeutics for MNA neuroblastoma. Cell-line analyses show MYCN-dependent growth inhibition and apoptosis, with approximately 200-fold greater sensitivity of MNA neuroblastoma lines. RNA sequencing of three MNA neuroblastoma lines treated with GSK3203591 reveal deregulated MYCN transcriptional programmes and altered mRNA splicing, converging on key regulatory pathways such as DNA damage response, epitranscriptomics and cellular metabolism. Stable isotope labelling experiments in the same cell lines demonstrate that glutamine metabolism is impeded following GSK3203591 treatment, linking with disruption of the MLX/Mondo nutrient sensors via intron retention of <em>MLX</em> mRNA. Interestingly, glutaminase (GLS) protein decreases after GSK3203591 treatment despite unchanged transcript levels. We demonstrate that the RNA methyltransferase METTL3 and cognate reader YTHDF3 proteins are lowered following their mRNAs undergoing GSK3203591-induced splicing alterations, indicating epitranscriptomic regulation of GLS; accordingly, we observe decreases of GLS mRNA m6A methylation following GSK3203591 treatment, and decreased GLS protein following YTHDF3 knockdown. <em>In vivo</em> efficacy of GSK3326593 is confirmed by increased survival of <em>Th-MYCN</em> mice, with drug treatment triggering splicing events and protein decreases consistent with <em>in vitro</em> data. Together our study demonstrates the PRMT5-dependent spliceosomal vulnerability of MNA neuroblastoma and identifies the epitranscriptome and glutamine metabolism as critical determinants of this sensitivity.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217263"},"PeriodicalIF":9.1,"publicationDate":"2024-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142307151","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":"Localized ablative immunotherapy enhances antitumor immunity by modulating the transcriptome of tumor-infiltrating Gamma delta T cells","authors":"Kaili Liu ,&nbsp;Ashley R. Hoover ,&nbsp;Lin Wang ,&nbsp;Yuanhong Sun ,&nbsp;Trisha I. Valerio ,&nbsp;Coline Furrer ,&nbsp;Jacob Adams ,&nbsp;Jingxuan Yang ,&nbsp;Min Li ,&nbsp;Wei R. Chen","doi":"10.1016/j.canlet.2024.217267","DOIUrl":"10.1016/j.canlet.2024.217267","url":null,"abstract":"<div><div>Gamma delta T cells (γδT cells) play crucial roles in the immune response against tumors, yet their functional dynamics under different cancer therapies remain poorly understood. Laser Ablative Immunotherapy (LAIT) is a novel cancer treatment modality combining local photothermal therapy (PTT) and intratumoral injection of an immunostimulant, N-dihydrogalactochitosan (glycated chitosan, GC). LAIT has been shown to induce systemic antitumor immune responses in pre-clinical studies and clinical trials, eradicating both treated local tumors and untreated distant metastases. In this study, we used LAIT to treat breast tumors in a mouse model and investigated the effects of LAIT on tumor-infiltrating γδT cells using single-cell RNA sequencing (scRNAseq). We characterized the γδT cells from tumors in control, PTT, GC, and LAIT (PTT + GC) groups, by identifying six distinct subtypes: activated, cytotoxic, cycling cytotoxic, IFN-enriched, antigen-presenting, and IL17-producing γδT cells. Differential gene expression analysis revealed that LAIT significantly upregulated genes associated with T cell activation, leukocyte adhesion, and interferon signaling in treated tumor tissues while downregulating genes involved in protein folding and stress responses. LAIT also uniquely increased the proportion of IL17-producing γδT cells, which correlated with prolonged survival in breast cancer patients, as analyzed using TCGA data. Furthermore, the transcriptomic profiles of γδT cells in LAIT-treated tumors closely resembled those in immune checkpoint inhibitor (ICI)-treated patients, suggesting potential synergistic effects. Our findings indicate that LAIT modulates the γδT cell transcriptome, enhancing their antitumor capabilities and providing a basis for combining LAIT with ICI therapy to improve cancer treatment outcomes.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217267"},"PeriodicalIF":9.1,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0304383524006621/pdfft?md5=b135bdab5a4a51c7f7a7b5c98e179023&pid=1-s2.0-S0304383524006621-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280535","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 ROCK-1/2 inhibitor RKI-1447 blocks N-MYC, promotes cell death, and emerges as a synergistic partner for BET inhibitors in neuroblastoma","authors":"Adena Pepich ,&nbsp;Conny Tümmler ,&nbsp;Sara Abu Ajamieh ,&nbsp;Diana Treis ,&nbsp;Ammelie Svea Boje ,&nbsp;Quinty Vellema ,&nbsp;Ioanna Tsea ,&nbsp;Emma Åkerlund ,&nbsp;Brinton Seashore-Ludlow ,&nbsp;Shahrzad Shirazi Fard ,&nbsp;Per Kogner ,&nbsp;John Inge Johnsen ,&nbsp;Malin Wickström","doi":"10.1016/j.canlet.2024.217261","DOIUrl":"10.1016/j.canlet.2024.217261","url":null,"abstract":"<div><div>High-risk neuroblastoma has a poor prognosis despite intensive treatment, highlighting the need for new therapeutic strategies. Genetic alterations in activators and inactivators of Rho GTPase have been identified in neuroblastoma suggested to activate Rho/Rho-kinase (ROCK) signaling. ROCK has also been implicated in therapy resistance. Therefore, we have explored the efficacy of the dual ROCK inhibitor RKI-1447 in neuroblastoma, emphasizing combination strategies. Treatment with RKI-1447 resulted in decreased growth, increased cell death, and inhibition of N-MYC <em>in vitro</em> and <em>in vivo</em>. A combination screen revealed enhanced effects between RKI-1447 and BET inhibitors. Synergistic effects from RKI-1447 and the BET inhibitor, ABBV-075, were confirmed in various neuroblastoma models, including zebrafish. Interestingly, ABBV-075 increased phosphorylation of both myosin light chain 2 and cofilin, downstream effectors of ROCK, increases that were blocked by adding RKI-1447. The combination treatment also augmented an inhibitory effect on C-MYC and, less pronounced, N-MYC protein expression. BET inhibitors have shown preclinical efficacy against neuroblastoma, but acquired resistance has limited their therapeutic benefit. We reveal that the combination of ROCK and BET inhibitors offers a promising treatment approach that can potentially mitigate resistance to BET inhibitors and reduce toxicity.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"605 ","pages":"Article 217261"},"PeriodicalIF":9.1,"publicationDate":"2024-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280548","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 splicing factor QKI inhibits metastasis by modulating alternative splicing of E-Syt2 in papillary thyroid carcinoma","authors":"Mengya Zhao ,&nbsp;Yu Jin ,&nbsp;Zhongyi Yan ,&nbsp;Chunyan He ,&nbsp;Wenhua You ,&nbsp;Zilong Zhu ,&nbsp;Ren Wang ,&nbsp;Yun Chen ,&nbsp;Judong Luo ,&nbsp;Yuan Zhang ,&nbsp;Yao Yao","doi":"10.1016/j.canlet.2024.217270","DOIUrl":"10.1016/j.canlet.2024.217270","url":null,"abstract":"<div><div>Alternative splicing (AS) plays a crucial role in the hallmarks of cancer and can open new avenues for targeted therapies. However, the aberrant AS events and the metastatic cascade in papillary thyroid carcinoma (PTC) remain largely unclear. Here, we identify the splicing factor, quaking protein (QKI), which was significantly downregulated in PTC and correlated with poor survival outcomes in patients with PTC. Functional studies indicated that low expression of QKI promoted the PTC cell growth and metastasis <em>in vitro</em> and <em>in vivo</em>. Mechanistically, low QKI induced exon 14 retention of extended synaptotagmin 2 (E-Syt2) and produced a long isoform transcript (termed E-Syt2L) that acted as an important oncogenic factor of PTC metastasis. Notably, overexpression of long non-coding RNA eosinophil granule ontogeny transcript (EGOT) physically binds to QKI and suppressed its activity by inhibiting ubiquitin specific peptidase 25 (USP25) mediated deubiquitination and subsequent degradation of QKI. Collectively, these data demonstrate the novel mechanistic links between the splicing factor QKI and splicing event in <span>PTC</span> metastasis and support the potential utility of targeting splicing events as a therapeutic strategy for <span>PTC</span>.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217270"},"PeriodicalIF":9.1,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian disruption in cancer hallmarks: Novel insight into the molecular mechanisms of tumorigenesis and cancer treatment","authors":"Zhaokai Zhou ,&nbsp;Ruiqi Zhang ,&nbsp;Yuyuan Zhang ,&nbsp;Yudi Xu ,&nbsp;Ruizhi Wang ,&nbsp;Shuang Chen ,&nbsp;Yingying Lv ,&nbsp;Yifeng Chen ,&nbsp;Yuqing Ren ,&nbsp;Peng Luo ,&nbsp;Quan Cheng ,&nbsp;Hui Xu ,&nbsp;Siyuan Weng ,&nbsp;Anning Zuo ,&nbsp;Yuhao Ba ,&nbsp;Shutong Liu ,&nbsp;Xinwei Han ,&nbsp;Zaoqu Liu","doi":"10.1016/j.canlet.2024.217273","DOIUrl":"10.1016/j.canlet.2024.217273","url":null,"abstract":"<div><div>Circadian rhythms are 24-h rhythms governing temporal organization of behavior and physiology generated by molecular clocks composed of autoregulatory transcription-translation feedback loops (TTFLs). Disruption of circadian rhythms leads to a spectrum of pathologies, including cancer by triggering or being involved in different hallmarks. Clock control of phenotypic plasticity involved in tumorigenesis operates in aberrant dedifferentiating to progenitor-like cell states, generation of cancer stem cells (CSCs) and epithelial-to-mesenchymal transition (EMT) events. Circadian rhythms might act as candidates for regulatory mechanisms of cellular senescent and functional determinants of senescence-associated secretory phenotype (SASP). Reciprocal control between clock and epigenetics sheds light on post-transcriptional regulation of circadian rhythms and opens avenues for novel anti-cancer strategies. Additionally, disrupting circadian rhythms influences microbiota communities that could be associated with altered homeostasis contributing to cancer development. Herein, we summarize recent advances in support of the nexus between disruptions of circadian rhythms and cancer hallmarks of new dimensions, thus providing novel perspectives on potentially effective treatment approaches for cancer management.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"604 ","pages":"Article 217273"},"PeriodicalIF":9.1,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142280532","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}