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Macrophage-directed therapeutic strategies in cancer. 巨噬细胞导向的癌症治疗策略。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-21 DOI: 10.1016/j.trecan.2026.08.006
Shweta Joshi, Judith Varner
{"title":"Macrophage-directed therapeutic strategies in cancer.","authors":"Shweta Joshi, Judith Varner","doi":"10.1016/j.trecan.2026.08.006","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.006","url":null,"abstract":"<p><p>Tumor-associated macrophages (TAMs) are a major component of the tumor microenvironment and exhibit remarkable functional plasticity, acting as either immunosuppressive cells that promote tumor progression or immunostimulatory cells that can support antitumor immunity, depending on the prevailing microenvironmental cues. These cells promote angiogenesis, metastasis, immune suppression, and therapy resistance. However, when appropriately reprogrammed, TAMs can directly kill or phagocytose cancer cells and/or activate antitumor T cell and natural killer cell responses. In this article, we review current therapeutic strategies targeting TAMs, including approaches directed against macrophage-associated receptors, signaling pathways, and epigenetic and metabolic regulators. We also discuss emerging TAM-targeted therapeutic modalities, including cytokine-based therapies, cell-based therapies, bispecific antibodies, macrophage-targeted nanoplatforms, and anti-TAM chimeric antigen receptor T-cell approaches, highlighting their potential to enhance antitumor immunity and improve clinical outcomes.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017531","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}
引用次数: 0
Next-generation tumor-agnostic targets on the horizon. 新一代肿瘤不可知论靶点即将出现。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-21 DOI: 10.1016/j.trecan.2026.08.009
Niamh Coleman, Jia Liu, Juliana Beal, Vivek Subbiah
{"title":"Next-generation tumor-agnostic targets on the horizon.","authors":"Niamh Coleman, Jia Liu, Juliana Beal, Vivek Subbiah","doi":"10.1016/j.trecan.2026.08.009","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.009","url":null,"abstract":"<p><p>Tumor-agnostic drug development reframes oncology around shared molecular dependencies rather than tissue origin, enabling efficient development for rare, actionable drivers across tumors. Since the first tumor-agnostic approval in 2017 for immunotherapy in microsatellite instability-high or mismatch repair-deficient tumors, the regulatory paradigm has expanded to high tumor mutation burden (TMB-H) cancers, oncogene-directed kinase inhibitors, such as NTRK, rearranged during transfection (RET), BRAF valine-to-glutamic acid substitution at codon 600 (BRAF V600E), and antibody-drug conjugate targeting Her2 overexpression, establishing proof of principle across modalities. In this review, we examine current tumor-agnostic approvals and emerging targets with pan-cancer potential: Kirsten rat sarcoma viral oncogene homolog (KRAS) variants [glycine-to-cysteine substitution at codon 12 (G12C), glycine-to-aspartic acid substitution at codon 12 (G12D), and active GTP-bound RAS (RAS(ON)) inhibitors; degraders; and chimeric antigen receptor T-cell (CAR-T)], methylthioadenosine phosphorylase (MTAP) loss (methylthioadenosine (MTA)-cooperative protein arginine methyltransferase 5 (PRMT5) and methionine adenosyltransferase 2A (MAT2A) inhibition), tumor protein p53 (TP53) tyrosine-to-cysteine substitution at codon 220 (Y220C) allele-specific reactivation, and fibroblast growth factor receptor 2 (FGFR2) and neuregulin (NRG) fusions. We explore critical challenges including standardized assays, endpoints, infrastructure, and access limitations. Finally, we outline features shaping next-generation programs: novel basket-trial designs, real-world evidence integration, and international collaborative frameworks. With molecules, infrastructure, and trial designs advancing in parallel, tumor-agnostic strategies are poised to deliver equitable benefit across cancers, realizing precision medicine without borders.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017538","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}
引用次数: 0
Lkb1 loss links dietary lipids to cancer cachexia. Lkb1的丢失将饮食脂质与癌症恶病质联系起来。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-15 DOI: 10.1016/j.trecan.2026.08.011
Xiaolin Liu, Jiayi Shen, Gaofei Wei
{"title":"Lkb1 loss links dietary lipids to cancer cachexia.","authors":"Xiaolin Liu, Jiayi Shen, Gaofei Wei","doi":"10.1016/j.trecan.2026.08.011","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.011","url":null,"abstract":"<p><p>Cancer cachexia involves more than a caloric deficit. A recent study by Cross et al. in Science shows that dietary lipid composition exacerbates cachexia in LKB1/STK11-deficient lung cancer through local prostaglandin E<sub>2</sub> production and pulmonary sensory neuron activation. By linking local lipid metabolism to anorexia and wasting, these findings support precision nutritional interventions for cancer cachexia.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148978215","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}
引用次数: 0
From fixed antibody-drug conjugates to programmable therapeutics. 从固定抗体-药物偶联物到可编程疗法。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-14 DOI: 10.1016/j.trecan.2026.08.012
Xinlei Zhuang, Liqiang Pan
{"title":"From fixed antibody-drug conjugates to programmable therapeutics.","authors":"Xinlei Zhuang, Liqiang Pan","doi":"10.1016/j.trecan.2026.08.012","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.012","url":null,"abstract":"<p><p>Antibody-drug conjugates have long been designed as fixed therapeutic entities. In Nature, Simó et al. introduce in vivo molecular assembly as an alternative strategy, prompting a broader question: could future cancer therapeutics be engineered by programming molecular interactions within patients rather than constructing increasingly complex drugs beforehand?</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148971501","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}
引用次数: 0
Fusion-product control in hematologic cancers. 血液学癌症的融合产物控制。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-14 DOI: 10.1016/j.trecan.2026.08.008
Min Zhang, Li Yu
{"title":"Fusion-product control in hematologic cancers.","authors":"Min Zhang, Li Yu","doi":"10.1016/j.trecan.2026.08.008","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.008","url":null,"abstract":"<p><p>Oncogenic fusions both drive hematologic cancers and enable precise measurable residual disease tracking, yet whether residual fusion products can be therapeutically controlled remains incompletely defined. Emerging genomic, RNA, and proteostasis strategies now frame fusion control as a layer-matched therapeutic strategy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148971466","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}
引用次数: 0
Heterotypic tumor microenvironments mirror dynamic wound-healing process. 异型肿瘤微环境反映了动态的伤口愈合过程。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-09 DOI: 10.1016/j.trecan.2026.08.007
Liqun Yu, Xiang H-F Zhang
{"title":"Heterotypic tumor microenvironments mirror dynamic wound-healing process.","authors":"Liqun Yu, Xiang H-F Zhang","doi":"10.1016/j.trecan.2026.08.007","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.007","url":null,"abstract":"<p><p>Tumors co-opt normal wound-healing programs to shape their immune microenvironment, yet how distinct immune states arise and influence therapy remains unclear. Here, we synthesize emerging evidence that tumors become locked in either proinflammatory or pro-resolution phases, defined by neutrophil- or macrophage-dominated ecosystems. These states not only remodel local tissues but also systemically reprogram hematopoiesis, creating self-reinforcing immune circuits that drive progression, metastasis, and treatment resistance. We highlight recent advances linking epithelial-mesenchymal plasticity, lipid metabolism, and myeloid dynamics into an integrated 'wound-healing clock' model. This framework provides a conceptual basis for patient stratification and suggests that therapeutically redirecting immune states may unlock new strategies to overcome resistance across cancer types.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148921019","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}
引用次数: 0
Cancer-associated synonymous mutations target mRNA structures and protein activity. 癌症相关的同义突变靶向mRNA结构和蛋白质活性。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-07 DOI: 10.1016/j.trecan.2026.08.005
Robin Fahraeus
{"title":"Cancer-associated synonymous mutations target mRNA structures and protein activity.","authors":"Robin Fahraeus","doi":"10.1016/j.trecan.2026.08.005","DOIUrl":"https://doi.org/10.1016/j.trecan.2026.08.005","url":null,"abstract":"<p><p>The role of adaptive mRNA structures in regulating gene expression in mammalian cells remains poorly understood. Synonymous mutations have been linked to a range of diseases, including cancer, yet their impact on cell biology remains largely unexplored. This opinion focuses on how cancer-associated synonymous mutations (CASMs) in the TP53 mRNA disrupt signal-induced mRNA structures and alter the activity of the encoded protein. CASM203 induces conformational changes that recapitulate those driven by PERK during the unfolded protein response, promoting expression of the p53/p47 isoform. By contrast, CASM22 and CASM34 interfere with DNA damage-induced RNA structures and affect full-length p53 activity. Together, these examples illustrate an underappreciated regulatory axis in which dynamic mRNA structures interface between upstream signalling pathways and downstream effector functions, with direct implications for tumour biology.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148907209","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}
引用次数: 0
Exploiting DNA damage tolerance for precision oncology. 利用DNA损伤耐受性进行精准肿瘤学研究。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-05 DOI: 10.1016/j.trecan.2026.08.003
Audesh Bhat, Ganesh P Lahane, Raj K Pandita, Albino Bacolla, Bettina Hoden, Kenneth S Ramos, Sunil Krishnan, Partha S Sarkar, Arti Dhar, John A Tainer, Tej K Pandita
{"title":"Exploiting DNA damage tolerance for precision oncology.","authors":"Audesh Bhat, Ganesh P Lahane, Raj K Pandita, Albino Bacolla, Bettina Hoden, Kenneth S Ramos, Sunil Krishnan, Partha S Sarkar, Arti Dhar, John A Tainer, Tej K Pandita","doi":"10.1016/j.trecan.2026.08.003","DOIUrl":"10.1016/j.trecan.2026.08.003","url":null,"abstract":"<p><p>Unresolved DNA lesions trigger replication stress, forcing cancer cells to hijack DNA damage tolerance (DDT) networks, specifically translesion synthesis (TLS) and template switching, to sustain replication. While DDT prevents lethal fork collapse, error-prone TLS drives mutagenesis, tumor evolution, chemoresistance and radioresistance. Proliferating cell nuclear antigen post-translational modifications dynamically govern pathway selection. Cancer cells exploit this plasticity, creating actionable vulnerabilities such as postreplicative single-stranded DNA gaps. Emerging inhibitors targeting TLS polymerases, upstream regulators such as ubiquitin-specific peptidase 1 (USP1), and critical protein-protein interactions offer unprecedented opportunities for precision oncology. By integrating DDT inhibition with biomarkers such as homologous recombination deficiency and tumor mutational burden, we can drive synthetic lethality, sensitize tumors to genotoxic agents, suppress treatment-induced mutagenesis, and potentially enhance responses to immunotherapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":21.6,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13552213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148892469","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}
引用次数: 0
Microbiome: a driver of pancreatic inflammation and tumorigenesis. 微生物组：胰腺炎症和肿瘤发生的驱动因素。
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-01 Epub Date: 2026-05-13 DOI: 10.1016/j.trecan.2026.04.006
Aftab Alam, Shyamananda Singh Mayengbam, Sharon Senchanthisai, Elif Irmak Bektas, Prasenjit Dey
{"title":"Microbiome: a driver of pancreatic inflammation and tumorigenesis.","authors":"Aftab Alam, Shyamananda Singh Mayengbam, Sharon Senchanthisai, Elif Irmak Bektas, Prasenjit Dey","doi":"10.1016/j.trecan.2026.04.006","DOIUrl":"10.1016/j.trecan.2026.04.006","url":null,"abstract":"<p><p>The human microbiome plays a crucial role in regulating various physiological processes, including immune responses, inflammation, gut permeability, and overall homeostasis. Recent studies have identified bacterial and fungal components in the tumor microenvironment of multiple malignancies, including pancreatic ductal adenocarcinoma (PDAC). These intratumoral microbiomes drive tumorigenesis by activating oncogenic signaling cascades and reprogramming both innate and adaptive immune responses, ultimately establishing a protumorigenic niche. In this review, we highlight the advances, limitations, and challenges of studying the intratumoral microbiome and its cellular products in PDAC tumorigenesis, with a specific focus on their modulation of the immune axis. Finally, we evaluate existing and emerging therapeutic strategies, including microbiome-targeted drugs, antibiotics, probiotics, and engineered microbes, to disrupt protumorigenic microbial influences and improve clinical outcomes.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"877-888"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13178113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147933890","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}
引用次数: 0
Aging: Barrier or catalyst of cancer? 衰老：癌症的屏障还是催化剂？
IF 21.6 1区 医学
Trends in cancer Pub Date : 2026-09-01 Epub Date: 2026-06-12 DOI: 10.1016/j.trecan.2026.05.007
Anda Huna, Nadine Martin, David Bernard
{"title":"Aging: Barrier or catalyst of cancer?","authors":"Anda Huna, Nadine Martin, David Bernard","doi":"10.1016/j.trecan.2026.05.007","DOIUrl":"10.1016/j.trecan.2026.05.007","url":null,"abstract":"<p><p>Aging is a major risk factor for cancer, yet its role in cancer biology remains largely unexplored and often overlooked. Interestingly, studies assessing the impact of aging on oncogenic Kras<sup>G12D</sup>-driven lung tumor initiation, early progression, and metastasis have reported both pro- or antitumoral effects, which are presented and discussed herein.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"798-801"},"PeriodicalIF":21.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148240434","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}
引用次数: 0
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