Cancer letters最新文献

{"title":"Pulsed electric field ablation as a candidate to enhance the anti-tumor immune response to immune checkpoint inhibitors","authors":"Blake M. Arciga ,&nbsp;Dustin M. Walters ,&nbsp;Eric T. Kimchi ,&nbsp;Kevin F. Staveley-O’Carroll ,&nbsp;Guangfu Li ,&nbsp;Emma Teixeiro ,&nbsp;Satyanarayana Rachagani ,&nbsp;Jussuf T. Kaifi","doi":"10.1016/j.canlet.2024.217361","DOIUrl":"10.1016/j.canlet.2024.217361","url":null,"abstract":"<div><div>Cancer ablation with pulsed electric fields (PEFs) involves the delivery of high-voltage, short-duration electrical pulses that destabilize tumor cells, leading to cellular death. Unlike most conventional ablation technologies, PEF ablation is non-thermal, allowing for safe and targeted energy delivery to the tumor without damaging surrounding tissue and critical structures. PEFs allow for specific dosing, predictable treatment zones, and preservation of the extracellular matrix and adjacent vascular tissues. Preclinical and preliminary clinical data suggest that PEF ablation may induce inflammatory changes in the tumor microenvironment (TME) that engage host innate and adaptive immune cells, stimulating an anti-tumor response. Specifically, PEF promotes local and systemic anti-tumor immune activation through immunogenic cell death and the release of damage-associated molecular patterns (DAMPs) and tumor antigens. This tumor-specific immune activation could potentially enhance response to immune checkpoint inhibitor (ICI) therapies. Furthermore, PEF ablation induces the formation of tertiary lymphoid structures (TLSs) in the TME, which are predictive biomarkers for responsiveness to ICI across several solid tumors. This combination of effects activates antigen-presenting cells and stimulates the effector T cell response, which is often inhibited in ICI-resistant cancer patients. In this review, the onco-immunological characteristics of PEF ablation are discussed, with special emphasis placed on the clinical potential of PEF ablation to induce anti-cancer immune responses and enhance responsiveness to ICI therapy in ablated and non-ablated (abscopal) tumors.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217361"},"PeriodicalIF":9.1,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142747506","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":"PAF1-mediated transcriptional reprogramming confers docetaxel resistance in advanced prostate cancer","authors":"Sakthivel Muniyan ,&nbsp;Raghupathy Vengoji ,&nbsp;Rama Krishna Nimmakayala ,&nbsp;Parthasarathy Seshacharyulu ,&nbsp;Balaji Perumalsamy ,&nbsp;Zahraa Wajih Alsafwani ,&nbsp;Sham S. Kakar ,&nbsp;Lynette M. Smith ,&nbsp;Nicole Shonka ,&nbsp;Benjamin A. Teply ,&nbsp;Subodh M. Lele ,&nbsp;Moorthy P. Ponnusamy ,&nbsp;Surinder K. Batra","doi":"10.1016/j.canlet.2024.217355","DOIUrl":"10.1016/j.canlet.2024.217355","url":null,"abstract":"<div><div>Advanced prostate cancer (PCa) remains a significant clinical challenge, and docetaxel plays a significant role in disease management. Despite the efficacy of docetaxel as a first-line chemotherapy, resistance often develops. We developed three clinically relevant in vitro PCa cell models and transcriptomic analysis identified that the Paf1/RNA polymerase II complex component (PAF1)-associated pluripotent-transcription factor (TF), SOX2, plays a crucial role in docetaxel resistance. The cancer stem cell (CSC) transcriptional master regulator PAF1 is significantly higher in PCa cell lines, tumor tissues, and docetaxel resistant (DR) PCa cells than in age-matched control cells. To determine the molecular underlying and functional characteristics of PAF1 in resistance mechanisms, we performed coimmunoprecipitation, embryonic stem cell network proteins, in vitro tumor-initiating ability, and 3D multicellular organoid growth using PAF1 knockdown cells. Tet-inducible PAF1 depletion reduced the drug-efflux phenotype, tumor-initiating frequencies, and three-dimensional organoid growth of the docetaxel-resistant PCa cell lines. Functional studies also showed restoration of docetaxel sensitivity in a 3D tumorsphere model upon PAF1 depletion. PAF1 depletion was also associated with decreased pluripotent TFs and other CSC markers. This study provides a novel regulatory mechanism of docetaxel resistance in PCa through PAF1.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217355"},"PeriodicalIF":9.1,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738488","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":"Can we utilise the circadian clock to target cancer stem cells?","authors":"Jia-Wen Lian, Shi-Yang Li, Robert B Clarke, Sacha J Howell, Qing-Jun Meng","doi":"10.1016/j.canlet.2024.217360","DOIUrl":"10.1016/j.canlet.2024.217360","url":null,"abstract":"<p><p>The 24-hourly circadian clock has been implicated in the regulation of multiple cancer hallmarks and characteristics. Cancer stem cells (CSCs) are a small but significant population of cells within many cancers, characterised by their self-renewal and clonogenic capacities. Increasing evidence points to CSCs having prominent roles in metastasis and drug resistance. However, it remains largely unknown how circadian clocks are involved with CSCs and what implications these interactions have for cancer progression and therapeutics. In this review, we examine the growing evidence on the role of circadian clocks in CSCs and discuss the potential therapeutic implications. This opens up new opportunities to target CSCs through various chronotherapeutic approaches, potentially improving clinical cancer outcomes. We propose different scenarios in which targeting circadian clocks in CSCs or their surrounding microenvironment could be developed into effective therapeutic strategies, including: (1) direct pharmacological targeting of core clock molecules, (2) optimising the timing of systemic anticancer therapies, and (3) targeting the neighbouring cells or systemic factors that influence tumour cells in a circadian-dependent manner.</p>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":" ","pages":"217360"},"PeriodicalIF":9.1,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142749562","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":"Protein profile in urinary extracellular vesicles is a marker of malignancy and correlates with muscle invasiveness in urinary bladder cancer","authors":"Loïc Steiner ,&nbsp;Maria Eldh ,&nbsp;Annemarijn Offens ,&nbsp;Rosanne E. Veerman ,&nbsp;Markus Johansson ,&nbsp;Tammer Hemdan ,&nbsp;Hans Netterling ,&nbsp;Ylva Huge ,&nbsp;Firas Abdul-Sattar Aljabery ,&nbsp;Farhood Alamdari ,&nbsp;Oskar Lidén ,&nbsp;Amir Sherif ,&nbsp;Susanne Gabrielsson","doi":"10.1016/j.canlet.2024.217352","DOIUrl":"10.1016/j.canlet.2024.217352","url":null,"abstract":"<div><div>Urinary Bladder Cancer (UBC) ranks among the most prevalent cancers worldwide, has a high recurrence rate and unpredictable treatment responses. Thus, biomarkers are urgently needed. Extracellular vesicles (EVs) are released from both cancer- and immune cells and provide a snapshot of the originating cell. They are abundant in urine and are therefore candidate biomarkers for UBC.</div><div>Isolated urinary EVs from 39 UBC patients were compared with EVs from healthy controls, prostate cancer patients and whole urine. Samples were from bladder urine at time of both transurethral resection of the bladder tumour (TURB) and cystectomy, as well as urine taken from the ureter at cystectomy. EVs were isolated by tangential flow filtration and differential ultracentrifugation and their protein composition was detected by Proximity Extension Assay (PEA; Olink, immuno-oncology panel).</div><div>In UBC patients, the proteomic signature of bladder urine EVs differed from ureter urine EVs from the same individuals, and from bladder urine derived EVs of both healthy and prostate cancer controls. Pairwise comparison was performed with matched whole urine revealing proteins solely detected in isolated vesicles. Additionally, a distinct signature was identified in bladder urine EVs correlating with muscle invasiveness, and a trained classifier could predict UBC with 92 % accuracy. Some differentially expressed proteins, HO-1 and MMP7, were analysed by bead-based flow cytometry, where HO-1 was detected on the EV surface.</div><div>Taken together, these results strengthen the rationale of using EVs as non-invasive biomarkers and prognostic tools for UBC.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217352"},"PeriodicalIF":9.1,"publicationDate":"2024-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715487","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":"Local ablation disrupts immune evasion in pancreatic cancer","authors":"Chiara Musiu ,&nbsp;Annalisa Adamo ,&nbsp;Simone Caligola ,&nbsp;Antonio Agostini ,&nbsp;Cristina Frusteri ,&nbsp;Francesca Lupo ,&nbsp;Federico Boschi ,&nbsp;Alice Busato ,&nbsp;Ornella Poffe ,&nbsp;Cristina Anselmi ,&nbsp;Antonio Vella ,&nbsp;Tian Wang ,&nbsp;Silvia Dusi ,&nbsp;Geny Piro ,&nbsp;Carmine Carbone ,&nbsp;Giampaolo Tortora ,&nbsp;Pasquina Marzola ,&nbsp;Mirko D'Onofrio ,&nbsp;Stefano Francesco Crinò ,&nbsp;Vincenzo Corbo ,&nbsp;Francesco De Sanctis","doi":"10.1016/j.canlet.2024.217327","DOIUrl":"10.1016/j.canlet.2024.217327","url":null,"abstract":"<div><h3>Background</h3><div>Pancreatic cancer (PC) is characterised by late diagnosis, tumour heterogeneity, and a peculiar immunosuppressive microenvironment, leading to poor clinical outcomes. Local ablative techniques have been proposed to treat unresectable PC patients, although their impact on activating the host immune system and overcoming resistance to immunotherapy remains elusive.</div></div><div><h3>Methods</h3><div>We dissected the immune-modulatory abilities triggered by local ablation in mouse and human PC models and human specimens, integrating phenotypic and molecular technologies with functional assays.</div></div><div><h3>Results</h3><div>Local ablation treatment performed in mice bearing orthotopic syngeneic PC tumours triggered tumour necrosis and a short-term inflammatory process characterised by the prompt increase of HMGB1 plasma levels, coupled with an enhanced amount of circulating and tumour infiltrating myeloid cells and increased MHCII expression in splenic myeloid antigen-presenting cells. Local ablation synergised with immunotherapy to restrict tumour progression and improved the survival of PC-bearing mice by evoking a T lymphocyte-dependent anti-tumour immune response. By integrating spatial transcriptomics with histological techniques, we pinpointed how combination therapy could reshape TME towards an anti-tumour milieu characterised by the preferential entrance and colocalization of activated T lymphocytes and myeloid cells endowed with antigen presentation features instead of T regulatory lymphocytes and CD206-expressing tumour-associated macrophages. In addition, treatment-dependent TME repolarization extended to neoplastic cells, promoting a shift from squamous to a more differentiated classical phenotype. Finally, we validated the immune regulatory properties induced by local ablation in PC patients and identified an association of the short-term treatment-dependent increase of neutrophils, NLR and HMGB1 with a longer time to progression.</div></div><div><h3>Conclusion</h3><div>Therefore, local ablation might overcome the current limitations of immunotherapy in PC.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217327"},"PeriodicalIF":9.1,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695304","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":"Nuclear factor I/B: Duality in action in cancer pathophysiology","authors":"Naveenkumar Perumal ,&nbsp;Prakadeeswari Gopalakrishnan ,&nbsp;Maria Burkovetskaya ,&nbsp;David Doss ,&nbsp;S. Shekar Dukkipati ,&nbsp;Ranjana K. Kanchan ,&nbsp;Sidharth Mahapatra","doi":"10.1016/j.canlet.2024.217349","DOIUrl":"10.1016/j.canlet.2024.217349","url":null,"abstract":"<div><div>The nuclear factor I (NFI) family of transcription factors plays a decisive role in organ development and maturation. Their deregulation has been linked with various diseases, most notably cancer. NFIB stands apart from the other NFI family members given its unique ability to drive both tumor suppressive and oncogenic programs. Thus, the ultimate impact of deregulated NFIB signaling is cancer-specific and strongly influenced by an intricate network of upstream regulators and downstream effectors. Deciphering the events that drive NFIB's paradoxical roles within these networks will enable us to not only understand how this critical transcription factor enacts its dual roles but also drive innovations to help us effectively target NFIB in different cancers. Here, we provide an in-depth review of NFIB. Starting with its defining role in the development of various organs, most notably the central nervous system, we highlight critical signaling pathways and the impact of deregulation on neoplastic transformation, contrasting it with the effect of silencing alone. We then provide examples of its dual roles in various cancers, identifying specific signaling networks associated with oncogenesis versus tumor suppression. We incorporate an example of a cancer type, osteosarcoma, wherein NFIB enacts its dual functions and explore which pathways influence each function. In this manner, we suggest plausible mechanisms for its role-switching from cancers sharing common triggering events in the setting of NFIB deregulation. We also review how NFIB enhances aggressiveness by driving metastasis, stemness, and chemoresistance. We conclude with a discussion on efficacious ways to target NFIB and pose some unanswered questions that may further help solidify our understanding of NFIB and facilitate clinical translation of NFIB targeting.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217349"},"PeriodicalIF":9.1,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709211","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":"MHC class I upregulation contributes to the therapeutic response to radiotherapy in combination with anti-PD-L1/anti-TGF-β in squamous cell carcinomas with enhanced CD8 T cell memory-driven response","authors":"Hanne T. Lind ,&nbsp;Spencer C. Hall ,&nbsp;Alexander A. Strait ,&nbsp;Jack B. Goon ,&nbsp;John D. Aleman ,&nbsp;Samantha M.Y. Chen ,&nbsp;Sana D. Karam ,&nbsp;Christian D. Young ,&nbsp;Jing H. Wang ,&nbsp;Xiao-Jing Wang","doi":"10.1016/j.canlet.2024.217347","DOIUrl":"10.1016/j.canlet.2024.217347","url":null,"abstract":"<div><div>Radiation therapy (RT), a mainstay treatment for head and neck squamous cell carcinoma (HNSCC), kills cancer cells and modulates the tumor immune microenvironment. We sought to assess the effect of RT in combination with PD-L1/TGF-β dual blockade in squamous cell carcinomas (SCC) and analyze the underlying mechanisms. We transplanted mouse SCC cells derived from keratin-15 (K15) stem cells harboring Kras^G12D/Smad4^−/− mutations into syngeneic recipients and irradiated tumors followed by PD-L1/TGF-β dual blockade. We identified a responder line and a non-responder line to this combination therapy. Responder hosts eradicated SCCs by the combined therapy and rejected re-transplanted SCC cells 6 months post tumor eradication, which correlated with clonotype expansions of splenic CD8 T cells and effector memory gene expression identified by single cell sequencing of TCR and transcriptomes, respectively. Mechanistically, RT upregulated MHC-I (major histocompatibility complex I) and its transcriptional regulators including NLRC5, in SCCs of the responders but not non-responders. These data are consistent with the TCGA HNSCC database in which NLRC5 correlated to MHC-I genes and CD8 T cell gene expression. Functional contribution of MHC-I to PD-L1/TGF-β blockade response was confirmed by knocking out beta-2-microglobulin in responder cells that attenuated the response to the same therapy. Thus, the therapeutic effectiveness appeared to largely depend on cancer-cell MHC-I expression, triggering CD8 T cell effector memory-driven responses against tumor cell antigens. Identifying the differential RT response to MHC-I induction may serve as a predictive marker for stratifying patients that are most likely to benefit from this combination therapy.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"608 ","pages":"Article 217347"},"PeriodicalIF":9.1,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142695311","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":"Integrating machine learning-predicted circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) in metastatic breast cancer: A proof of principle study on endocrine resistance profiling","authors":"Lorenzo Gerratana ,&nbsp;Andrew A. Davis ,&nbsp;Lorenzo Foffano ,&nbsp;Carolina Reduzzi ,&nbsp;Tania Rossi ,&nbsp;Arielle Medford ,&nbsp;Katherine Clifton ,&nbsp;Ami N. Shah ,&nbsp;Leslie Bucheit ,&nbsp;Marko Velimirovic ,&nbsp;Sara Bandini ,&nbsp;Charles S. Dai ,&nbsp;Firas Wehbe ,&nbsp;William J. Gradishar ,&nbsp;Amir Behdad ,&nbsp;Paola Ulivi ,&nbsp;Cynthia X. Ma ,&nbsp;Fabio Puglisi ,&nbsp;Aditya Bardia ,&nbsp;Massimo Cristofanilli","doi":"10.1016/j.canlet.2024.217325","DOIUrl":"10.1016/j.canlet.2024.217325","url":null,"abstract":"<div><div>The study explored endocrine resistance by leveraging machine learning to establish the prognostic stratification of predicted Circulating tumor cells (CTCs), assessing its integration with circulating tumor DNA (ctDNA) features and contextually evaluate the potential of CTCs-based transcriptomics. 1118 patients with a diagnosis of luminal-like Metastatic Breast Cancer (MBC) were characterized for ctDNA through NGS before treatment start, predicted CTCs were computed through a K nearest neighbor algorithm. Differences across subgroups were analyzed through chi square or Fisher’s exact test according to sample size and corrected for False Discovery Rate. Differences in survival were tested by log-rank test and uni- and multivariable Cox regression. CTCs transcriptomics was performed through RNAseq after sorting with DEPArray NxT. Univariable and multivariable analysis adjusted for ctDNA alterations revealed a significant impact of CTCs predictive stratification on both progression-free survival (PFS) and overall survival (OS). Alterations in <em>RTK</em> and <em>ER</em> pathways were significantly correlated with predicted-Stage IV_aggressive. The combined impact of CTCs stratification and RTK/ER pathway alterations influenced patient outcomes, with predicted-Stage IV_aggressive having a negative impact on PFS regardless of the mutational status. The pilot exploratory CTCs transcriptomics analysis showed transcriptional changes linked to cell proliferation such as under expression of <em>MALAT1</em> and overexpression of <em>GREM1</em>, <em>GPR85</em> and <em>OCM</em>. Our data underline the potential of an integration between ctDNA and CTCs, both through quantification and transcriptomic analysis, for a deeper understanding of tumor biology and treatment response in HR-positive, HER2-negative MBC.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217325"},"PeriodicalIF":9.1,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142692748","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":"Exploring bile acid transporters as key players in cancer development and treatment: Evidence from preclinical and clinical studies","authors":"Bintee Bintee ,&nbsp;Ruchira Banerjee ,&nbsp;Mangala Hegde ,&nbsp;Ravichandran Vishwa ,&nbsp;Mohammed S. Alqahtani ,&nbsp;Mohamed Abbas ,&nbsp;Athba Alqahtani ,&nbsp;Latha Rangan ,&nbsp;Gautam Sethi ,&nbsp;Ajaikumar B. Kunnumakkara","doi":"10.1016/j.canlet.2024.217324","DOIUrl":"10.1016/j.canlet.2024.217324","url":null,"abstract":"<div><div>Bile acid transporters (BATs) are integral membrane proteins belonging to various families, such as solute carriers, organic anion transporters, and ATP-binding cassette families. These transporters play a crucial role in bile acid transportation within the portal and systemic circulations, with expression observed in tissues, including the liver, kidney, and small intestine. Bile acids serve as signaling molecules facilitating the absorption and reabsorption of fats and lipids. Dysregulation of bile acid concentration has been implicated in tumorigenesis, yet the role of BATs in this process remains underexplored. Emerging evidence suggests that BATs may modulate various stages of cancer progression, including initiation, development, proliferation, metastasis, and tumor microenvironment regulation. Targeting BATs using siRNAs, miRNAs, and small compound inhibitors in preclinical models and their polymorphisms are well-studied for transporters like BSEP, MDR1, MRP2, OATP1A2, etc., and have shed light on their involvement in tumorigenesis, particularly in cancers such as those affecting the liver and gastrointestinal tract. While BATs' role in diseases like Alagille syndrome, biliary atresia, and cirrhosis have been extensively studied, their implications in cancer warrant further investigation. This review highlights the expression and function of BATs in cancer development and emphasizes the potential of targeting these transporters as a novel therapeutic strategy for various malignancies.</div></div>","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"609 ","pages":"Article 217324"},"PeriodicalIF":9.1,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686227","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":"Embracing innovation and collaboration: A message from the new Editor-in-Chief","authors":"Min Li","doi":"10.1016/j.canlet.2024.217338","DOIUrl":"10.1016/j.canlet.2024.217338","url":null,"abstract":"","PeriodicalId":9506,"journal":{"name":"Cancer letters","volume":"607 ","pages":"Article 217338"},"PeriodicalIF":9.1,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667045","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}