Molecular Cancer最新文献

{"title":"Advances and applications of RNA vaccines in tumor treatment","authors":"Ruohan Yang, Jiuwei Cui","doi":"10.1186/s12943-024-02141-5","DOIUrl":"https://doi.org/10.1186/s12943-024-02141-5","url":null,"abstract":"Compared to other types of tumor vaccines, RNA vaccines have emerged as promising alternatives to conventional vaccine therapy due to their high efficiency, rapid development capability, and potential for low-cost manufacturing and safe drug delivery. RNA vaccines mainly include mRNA, circular RNA (circRNA), and Self-amplifying mRNA(SAM). Different RNA vaccine platforms for different tumors have shown encouraging results in animal and human models. This review comprehensively describes the advances and applications of RNA vaccines in antitumor therapy. Future directions for extending this promising vaccine platform to a wide range of therapeutic uses are also discussed.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"206 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142385474","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":"Correction: RNA m6A modification in ferroptosis: implications for advancing tumor immunotherapy","authors":"Jun-xiao Shi, Zhi-chao Zhang, Hao-zan Yin, Xian-jie Piao, Cheng-hu Liu, Qian-jia Liu, Jia-cheng Zhang, Wen-xuan Zhou, Fu-chen Liu, Fu Yang, Yue-fan Wang, Hui Liu","doi":"10.1186/s12943-024-02144-2","DOIUrl":"https://doi.org/10.1186/s12943-024-02144-2","url":null,"abstract":"<p><b>Correction:</b> <b><i>Mol Cancer</i></b> <b>23, 213 (2024)</b></p><p><b>https://doi.org/10.1186/s12943-024-02132-6</b></p><p>Following publication of the original article [1], the authors noticed that the Funding information was not indicated in the article. The details of Funding were included in the revised manuscript that was submitted by the author to production system. The Funding information is given below. The original article has been corrected.</p><p><b>Funding</b></p><p>This work was supported by the National Science and Technology Major Project (Nos. 2023ZD0500102), the National Natural Science Foundation of China (Nos. 82270634), and Clinical Young Talent Project, Eagle breeding Team of Meng Chao Tengfei Project (Eastern Hepatobiliary Surgery Hospital).</p><ol data-track-component=\"outbound reference\" data-track-context=\"references section\"><li data-counter=\"1.\"><p>Shi J, Zhang Z, Yin H, et al. RNA m6A modification in ferroptosis: implications for advancing tumor immunotherapy. Mol Cancer. 2024;23:213. https://doi.org/10.1186/s12943-024-02132-6.</p><p>Article PubMed PubMed Central Google Scholar </p></li></ol><p>Download references<svg aria-hidden=\"true\" focusable=\"false\" height=\"16\" role=\"img\" width=\"16\"><use xlink:href=\"#icon-eds-i-download-medium\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"></use></svg></p><span>Author notes</span><ol><li><p>Jun-xiao Shi, Zhi-chao Zhang, Hao-zan Yin, and Xian-jie Piao contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>The Third Department of Hepatic Surgery, Eastern Hepatobiliary Surgery Hospital, Naval Medical University, Shanghai, 200438, China</p><p>Jun-xiao Shi, Zhi-chao Zhang, Xian-jie Piao, Cheng-hu Liu, Qian-jia Liu, Jia-cheng Zhang, Wen-xuan Zhou, Fu-chen Liu, Yue-fan Wang & Hui Liu</p></li><li><p>The Department of Medical Genetics, Naval Medical University, Shanghai, 200433, China</p><p>Hao-zan Yin & Fu Yang</p></li><li><p>Key Laboratory of Biosafety Defense, Ministry of Education, Shanghai, 200433, China</p><p>Fu Yang</p></li><li><p>Shanghai Key Laboratory of Medical Biodefense, Shanghai, 200433, China</p><p>Fu Yang</p></li></ol><span>Authors</span><ol><li><span>Jun-xiao Shi</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Zhi-chao Zhang</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Hao-zan Yin</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Xian-jie Piao</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Cheng-hu Liu</span>View author publications<p>You can also search for this author in <span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Qian-jia Liu</span>View author p","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"64 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142384151","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":"Proapoptotic activity of JNK-sensitive BH3-only proteins underpins ovarian cancer response to replication checkpoint inhibitors","authors":"Annapoorna Venkatachalam, Cristina Correia, Kevin L. Peterson, Xianon Hou, Paula A. Schneider, Annabella R. Strathman, Karen S. Flatten, Chance C. Sine, Emily A. Balczewski, Cordelia D. McGehee, Melissa C. Larson, Laura N. Duffield, X. Wei Meng, Nicole D. Vincelette, Husheng Ding, Ann L. Oberg, Fergus J. Couch, Elizabeth M. Swisher, Hu Li, S. John Weroha, Scott H. Kaufmann","doi":"10.1186/s12943-024-02125-5","DOIUrl":"https://doi.org/10.1186/s12943-024-02125-5","url":null,"abstract":"Recent studies indicate that replication checkpoint modulators (RCMs) such as inhibitors of CHK1, ATR, and WEE1 have promising monotherapy activity in solid tumors, including platinum-resistant high grade serous ovarian cancer (HGSOC). However, clinical response rates are generally below 30%. While RCM-induced DNA damage has been extensively examined in preclinical and clinical studies, the link between replication checkpoint interruption and tumor shrinkage remains incompletely understood. Here we utilized HGSOC cell lines and patient-derived xenografts (PDXs) to study events leading from RCM treatment to ovarian cancer cell death. These studies show that RCMs increase CDC25A levels and CDK2 signaling in vitro, leading to dysregulated cell cycle progression and increased replication stress in HGSOC cell lines independent of homologous recombination status. These events lead to sequential activation of JNK and multiple BH3-only proteins, including BCL2L11/BIM, BBC3/PUMA and the BMF, all of which are required to fully initiate RCM-induced apoptosis. Activation of the same signaling pathway occurs in HGSOC PDXs that are resistant to poly(ADP-ribose) polymerase inhibitors but respond to RCMs ex vivo with a decrease in cell number in 3-dimensional culture and in vivo with xenograft shrinkage or a significantly diminished growth rate. These findings identify key cell death-initiating events that link replication checkpoint inhibition to antitumor response in ovarian cancer.\u0000","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"12 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142383732","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":"Artificial intelligence alphafold model for molecular biology and drug discovery: a machine-learning-driven informatics investigation","authors":"Song-Bin Guo, Yuan Meng, Liteng Lin, Zhen-Zhong Zhou, Hai-Long Li, Xiao-Peng Tian, Wei-Juan Huang","doi":"10.1186/s12943-024-02140-6","DOIUrl":"https://doi.org/10.1186/s12943-024-02140-6","url":null,"abstract":"AlphaFold model has reshaped biological research. However, vast unstructured data in the entire AlphaFold field requires further analysis to fully understand the current research landscape and guide future exploration. Thus, this scientometric analysis aimed to identify critical research clusters, track emerging trends, and highlight underexplored areas in this field by utilizing machine-learning-driven informatics methods. Quantitative statistical analysis reveals that the AlphaFold field is enjoying an astonishing development trend (Annual Growth Rate = 180.13%) and global collaboration (International Co-authorship = 33.33%). Unsupervised clustering algorithm, time series tracking, and global impact assessment point out that Cluster 3 (Artificial Intelligence-Powered Advancements in AlphaFold for Structural Biology) has the greatest influence (Average Citation = 48.36 ± 184.98). Additionally, regression curve and hotspot burst analysis highlight “structure prediction” (s = 12.40, R2 = 0.9480, p = 0.0051), “artificial intelligence” (s = 5.00, R2 = 0.8096, p = 0.0375), “drug discovery” (s = 1.90, R2 = 0.7987, p = 0.0409), and “molecular dynamics” (s = 2.40, R2 = 0.8000, p = 0.0405) as core hotspots driving the research frontier. More importantly, the Walktrap algorithm further reveals that “structure prediction, artificial intelligence, molecular dynamics” (Relevance Percentage[RP] = 100%, Development Percentage[DP] = 25.0%), “sars-cov-2, covid-19, vaccine design” (RP = 97.8%, DP = 37.5%), and “homology modeling, virtual screening, membrane protein” (RP = 89.9%, DP = 26.1%) are closely intertwined with the AlphaFold model but remain underexplored, which implies a broad exploration space. In conclusion, through the machine-learning-driven informatics methods, this scientometric analysis offers an objective and comprehensive overview of global AlphaFold research, identifying critical research clusters and hotspots while prospectively pointing out underexplored critical areas.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"1 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142377365","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":"Pharmacological targeting of P300/CBP reveals EWS::FLI1-mediated senescence evasion in Ewing sarcoma.","authors":"Erdong Wei, Ana Mitanoska, Quinn O'Brien, Kendall Porter, MacKenzie Molina, Haseeb Ahsan, Usuk Jung, Lauren Mills, Michael Kyba, Darko Bosnakovski","doi":"10.1186/s12943-024-02115-7","DOIUrl":"10.1186/s12943-024-02115-7","url":null,"abstract":"<p><p>Ewing sarcoma (ES) poses a significant therapeutic challenge due to the difficulty in targeting its main oncodriver, EWS::FLI1. We show that pharmacological targeting of the EWS::FLI1 transcriptional complex via inhibition of P300/CBP drives a global transcriptional outcome similar to direct knockdown of EWS::FLI1, and furthermore yields prognostic risk factors for ES patient outcome. We find that EWS::FLI1 upregulates LMNB1 via repetitive GGAA motif recognition and acetylation codes in ES cells and EWS::FLI1-permissive mesenchymal stem cells, which when reversed by P300 inhibition leads to senescence of ES cells. P300-inhibited senescent ES cells can then be eliminated by senolytics targeting the PI3K signaling pathway. The vulnerability of ES cells to this combination therapy suggests an appealing synergistic strategy for future therapeutic exploration.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"23 1","pages":"222"},"PeriodicalIF":27.7,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11453018/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142375659","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":"Deciphering resistance mechanisms in cancer: final report of MATCH-R study with a focus on molecular drivers and PDX development.","authors":"Damien Vasseur, Ludovic Bigot, Kristi Beshiri, Juan Flórez-Arango, Francesco Facchinetti, Antoine Hollebecque, Lambros Tselikas, Mihaela Aldea, Felix Blanc-Durand, Anas Gazzah, David Planchard, Ludovic Lacroix, Noémie Pata-Merci, Catline Nobre, Alice Da Silva, Claudio Nicotra, Maud Ngo-Camus, Floriane Braye, Sergey I Nikolaev, Stefan Michiels, Gérôme Jules-Clement, Ken André Olaussen, Fabrice André, Jean-Yves Scoazec, Fabrice Barlesi, Santiago Ponce, Jean-Charles Soria, Benjamin Besse, Yohann Loriot, Luc Friboulet","doi":"10.1186/s12943-024-02134-4","DOIUrl":"10.1186/s12943-024-02134-4","url":null,"abstract":"<p><strong>Background: </strong>Understanding the resistance mechanisms of tumor is crucial for advancing cancer therapies. The prospective MATCH-R trial (NCT02517892), led by Gustave Roussy, aimed to characterize resistance mechanisms to cancer treatments through molecular analysis of fresh tumor biopsies. This report presents the genomic data analysis of the MATCH-R study conducted from 2015 to 2022 and focuses on targeted therapies.</p><p><strong>Methods: </strong>The study included resistant metastatic patients (pts) who accepted an image-guided tumor biopsy. After evaluation of tumor content (TC) in frozen tissue biopsies, targeted NGS (10 < TC < 30%) or Whole Exome Sequencing and RNA sequencing (TC > 30%) were performed before and/or after the anticancer therapy. Patient-derived xenografts (PDX) were established by implanting tumor fragments into NOD scid gamma mice and amplified up to five passages.</p><p><strong>Results: </strong>A total of 1,120 biopsies were collected from 857 pts with the most frequent tumor types being lung (38.8%), digestive (16.3%) and prostate (14.1%) cancer. Molecular targetable driver were identified in 30.9% (n = 265/857) of the patients, with EGFR (41.5%), FGFR2/3 (15.5%), ALK (11.7%), BRAF (6.8%), and KRAS (5.7%) being the most common altered genes. Furthermore, 66.0% (n = 175/265) had a biopsy at progression on targeted therapy. Among resistant cases, 41.1% (n = 72/175) had no identified molecular mechanism, 32.0% (n = 56/175) showed on-target resistance, and 25.1% (n = 44/175) exhibited a by-pass resistance mechanism. Molecular profiling of the 44 patients with by-pass resistance identified 51 variants, with KRAS (13.7%), PIK3CA (11.8%), PTEN (11.8%), NF2 (7.8%), AKT1 (5.9%), and NF1 (5.9%) being the most altered genes. Treatment was tailored for 45% of the patients with a resistance mechanism identified leading to an 11 months median extension of clinical benefit. A total of 341 biopsies were implanted in mice, successfully establishing 136 PDX models achieving a 39.9% success rate. PDX models are available for EGFR (n = 31), FGFR2/3 (n = 26), KRAS (n = 18), ALK (n = 16), BRAF (n = 6) and NTRK (n = 2) driven cancers. These models closely recapitulate the biology of the original tumors in term of molecular alterations and pharmacological status, and served as valuable models to validate overcoming treatment strategies.</p><p><strong>Conclusion: </strong>The MATCH-R study highlights the feasibility of on purpose image guided tumor biopsies and PDX establishment to characterize resistance mechanisms and guide personalized therapies to improve outcomes in pre-treated metastatic patients.</p>","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"23 1","pages":"221"},"PeriodicalIF":27.7,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11451117/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372358","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":"Correction: Nac1 promotes stemness and regulates myeloid‑derived cell status in triple‑negative breast cancer.","authors":"Chrispus Ngule, Ruyi Shi, Xingcong Ren, Hongyan Jia, Felix Oyelami, Dong Li, Younhee Park, Jinhwan Kim, Hami Hemati, Yi Zhang, Xiaofang Xiong, Andrew Shinkle, Nathan L Vanderford, Sara Bachert, Binhua P Zhou, Jianlong Wang, Jianxun Song, Xia Liu, Jin-Ming Yang","doi":"10.1186/s12943-024-02143-3","DOIUrl":"10.1186/s12943-024-02143-3","url":null,"abstract":"","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"23 1","pages":"220"},"PeriodicalIF":27.7,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11448293/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142365874","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":"Editorial expression of concern: miR-630 targets IGF1R to regulate response to HER-targeting drugs and overall cancer cell progression in HER2 over-expressing breast cancer","authors":"Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty, Irene M Ghobrial, John Crown, Lorraine O’Driscoll","doi":"10.1186/s12943-024-02139-z","DOIUrl":"https://doi.org/10.1186/s12943-024-02139-z","url":null,"abstract":"&lt;p&gt;&lt;b&gt;Correction:&lt;/b&gt;&lt;b&gt;&lt;i&gt;Mol Cancer&lt;/i&gt;&lt;/b&gt;&lt;b&gt; 13&lt;/b&gt;, &lt;b&gt;71 (2014)&lt;/b&gt;&lt;/p&gt;&lt;p&gt;&lt;b&gt;https://doi.org/10.1186/1476-4598-13-71&lt;/b&gt;&lt;/p&gt;&lt;p&gt;&lt;b&gt;Published: 24 March 2014&lt;/b&gt;&lt;/p&gt;&lt;p&gt;After the publication of this article, the publisher was alerted to an apparent panel duplication and frameshift in Fig. 4B migration (ii) SKBR3-LR NC mimic and 4 C invasion (ii) SKBR3-LR NC mimic. Because the issue was detected ten years after publication, the original images for the study are no longer available. The panel has not been replaced. Readers are urged to take caution when interpreting the content and conclusions of this article.&lt;/p&gt;&lt;h3&gt;Authors and Affiliations&lt;/h3&gt;&lt;ol&gt;&lt;li&gt;&lt;p&gt;School of Pharmacy and Pharmaceutical Sciences &amp; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland&lt;/p&gt;&lt;p&gt;Claire Corcoran, Sweta Rani, Susan Breslin, Martina Gogarty &amp; Lorraine O’Driscoll&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Department of Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA&lt;/p&gt;&lt;p&gt;Irene M Ghobrial&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;p&gt;Department of Oncology, St. Vincent’s University Hospital, Dublin 4, Ireland&lt;/p&gt;&lt;p&gt;John Crown&lt;/p&gt;&lt;/li&gt;&lt;/ol&gt;&lt;span&gt;Authors&lt;/span&gt;&lt;ol&gt;&lt;li&gt;&lt;span&gt;Claire Corcoran&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Sweta Rani&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Susan Breslin&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Martina Gogarty&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Irene M Ghobrial&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;John Crown&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;li&gt;&lt;span&gt;Lorraine O’Driscoll&lt;/span&gt;View author publications&lt;p&gt;You can also search for this author in &lt;span&gt;PubMed&lt;span&gt; &lt;/span&gt;Google Scholar&lt;/span&gt;&lt;/p&gt;&lt;/li&gt;&lt;/ol&gt;&lt;h3&gt;Corresponding author&lt;/h3&gt;&lt;p&gt;Correspondence to Lorraine O’Driscoll.&lt;/p&gt;&lt;h3&gt;Publisher’s note&lt;/h3&gt;&lt;p&gt;Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.&lt;/p&gt;&lt;p&gt;The online version of the original article can be found at https://doi.org/10.1186/1476-4598-13-71.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Open Access&lt;/b&gt; This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed mater","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"7 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360352","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":"Traditional Chinese medicine for the treatment of cancers of hepatobiliary system: from clinical evidence to drug discovery","authors":"Junyu Wu, Guoyi Tang, Chien-Shan Cheng, Ranna Yeerken, Yau-Tuen Chan, Zhiwen Fu, Yi-Chao Zheng, Yibin Feng, Ning Wang","doi":"10.1186/s12943-024-02136-2","DOIUrl":"https://doi.org/10.1186/s12943-024-02136-2","url":null,"abstract":"Hepatic, biliary, and pancreatic cancer pose significant challenges in the field of digestive system diseases due to their highly malignant nature. Traditional Chinese medicine (TCM) has gained attention as a potential therapeutic approach with long-standing use in China and well-recognized clinical benefits. In this review, we systematically summarized the clinical applications of TCM that have shown promising results in clinical trials in treating hepatic, biliary, and pancreatic cancer. We highlighted several commonly used TCM therapeutics with validated efficacy through rigorous clinical trials, including Huaier Granule, Huachansu, and Icaritin. The active compounds and their potential targets have been thoroughly elucidated to offer valuable insights into the potential of TCM for anti-cancer drug discovery. We emphasized the importance of further research to bridge the gap between TCM and modern oncology, facilitating the development of evidence-based TCM treatment for these challenging malignancies. ","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"58 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360304","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":"Chinese herbal medicine for the treatment of intestinal cancer: preclinical studies and potential clinical applications","authors":"Juan Zhang, Yulin Wu, Yuanyang Tian, Hongxi Xu, Zhi-Xiu Lin, Yan-Fang Xian","doi":"10.1186/s12943-024-02135-3","DOIUrl":"https://doi.org/10.1186/s12943-024-02135-3","url":null,"abstract":"Intestinal cancer (IC) poses a significant global health challenge that drives continuous efforts to explore effective treatment modalities. Conventional treatments for IC are effective, but are associated with several limitations and drawbacks. Chinese herbal medicine (CHM) plays an important role in the overall cancer prevention and therapeutic strategies. Recent years have seen a growing body of research focus on the potential of CHM in IC treatment, showing promising results in managing IC and mitigating the adverse effects of radiotherapy and chemotherapy. This review provides updated information from preclinical research and clinical observation on CHM’s role in treatment of IC, offering insights into its comprehensive management and guiding future prevention strategies and clinical practice.","PeriodicalId":19000,"journal":{"name":"Molecular Cancer","volume":"27 1","pages":""},"PeriodicalIF":37.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360534","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}