Critical reviews in oncology/hematology最新文献

{"title":"Tumor-educated platelets as liquid biopsy: Uncovering the mechanisms of cancer progression","authors":"Benedikt Schmidl ,&nbsp;Keyang Wei ,&nbsp;Narges Ghasemimehr ,&nbsp;Ali Bashiri Dezfouli ,&nbsp;Barbara Wollenberg","doi":"10.1016/j.critrevonc.2025.105106","DOIUrl":"10.1016/j.critrevonc.2025.105106","url":null,"abstract":"<div><div>Tumor-educated platelets (TEPs) have emerged as promising biomarkers for cancer detection, monitoring, and therapeutic evaluation. Unlike traditional tissue biopsies, liquid biopsies leveraging TEPs offer a non-invasive approach to overcome challenges posed by tumor heterogeneity and inaccessibility of certain tissues. Platelets interact dynamically with tumors, undergoing molecular and functional alterations that reflect tumor progression and metastasis. This review investigates the historical context of TEPs, their role in cancer biology, mechanisms of interaction with tumors, and also the characterization of the molecular signature by using multi-omics techniques. A comprehensive understanding of these alterations provides essential insights into tumor presence, location, and biological behavior, making TEPs a valuable diagnostic tool, which, in turn, can enhance early cancer detection and ongoing disease surveillance.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105106"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145881114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bidirectional role of neutrophils in lung cancer: Mechanisms and therapeutic implications","authors":"Jing Wang ,&nbsp;Meng Zhang ,&nbsp;Zhiyue Cui ,&nbsp;Jingjing Qu ,&nbsp;Ruimin Chang","doi":"10.1016/j.critrevonc.2025.105087","DOIUrl":"10.1016/j.critrevonc.2025.105087","url":null,"abstract":"<div><div>Lung cancer is the leading cause of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) being the predominant subtype. Despite the availability of traditional treatments such as radiation therapy, chemotherapy, and surgery, as well as emerging immunotherapies, the five-year survival rate and prognosis remain suboptimal. Tumor-associated neutrophils (TANs) are the most abundant immune cells in the tumor microenvironment (TME) of lung cancer, and understanding their role in cancer therapy is highly important. This review comprehensively discusses the dual role of TANs in lung cancer progression. First, we examined the recruitment, classification, and single-cell heterogeneity of TANs, highlighting the distinct molecular expression and functions across subpopulations. Mechanistically, TANs influence tumor behavior through direct cell<img>cell interactions and cytokine production. Additionally, neutrophils engage with other cells in the TME via metabolic reprogramming, programmed cell death, epigenetic modifications, and vesicle secretion. To date, no studies have systematically summarized and connected these mechanisms. Finally, we summarize the clinical applications and prospects of TANs in lung cancer, including their potential role in assisting in diagnosis, predicting prognosis, and targeting neutrophils to increase the efficacy of radiation, chemotherapy, and immunotherapy. We hope that this review provides insights for future research aimed at improving lung cancer prognosis through the targeting of TANs.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105087"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chinese expert consensus on precision diagnosis and treatment of refractory tumors","authors":"Lili Wang ,&nbsp;Yu Zhang ,&nbsp;Yanhong Shang ,&nbsp;Yuanzhi Lu ,&nbsp;Hailong Hu ,&nbsp;Gang Wang ,&nbsp;Haitao Wang ,&nbsp;China Consortium for Precision Diagnosis and Therapeutics in Refractory Tumors (CCPT)","doi":"10.1016/j.critrevonc.2025.105109","DOIUrl":"10.1016/j.critrevonc.2025.105109","url":null,"abstract":"<div><div>Refractory tumors, including rare and treatment-resistant malignancies, pose major challenges due to genomic and intra- and inter-tumoral heterogeneity. The Molecular Tumor Board provides a multidisciplinary model for precision oncology. To address the lack of consensus, the China Consortium for Precision Diagnosis and Therapeutics in Refractory Tumors (CCPT) developed evidence-based guidelines. Building on established frameworks and clinical expertise, CCPT also introduced a Chinese-specific classification system, together with recommendations on multi-omics testing, personalized therapy, combination strategies, dose optimization, and data-sharing, to standardize practice and advance integrated precision care.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105109"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145901935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The microbiome in head and neck squamous cell carcinoma: Biological drivers, therapeutic interactions, and emerging clinical applications","authors":"A. Di Bello ,&nbsp;A. Scala ,&nbsp;R. Gili ,&nbsp;R. Falcicchia ,&nbsp;A. Bassolino ,&nbsp;S. Polidori ,&nbsp;F. D’Auria ,&nbsp;G. Tortora ,&nbsp;P. Bossi ,&nbsp;A. Cassano","doi":"10.1016/j.critrevonc.2025.105108","DOIUrl":"10.1016/j.critrevonc.2025.105108","url":null,"abstract":"<div><div>Head and neck squamous cell carcinoma (HNSCC) develops within a biologically complex niche shaped by epithelial, immune, environmental, and microbial interactions. Growing evidence indicates that microbial communities influence HNSCC initiation, progression, therapeutic response, and toxicity. This narrative review synthesizes current knowledge on microbiome composition in healthy mucosa, oral potentially malignant disorders, and established HNSCC, emphasizing how dysbiosis characterized by enrichment of periodontitis-associated taxa such as <em>Fusobacterium</em> and <em>Porphyromonas</em> and depletion of protective genera including <em>Corynebacterium</em> and <em>Kingella</em> may drive carcinogenesis through inflammation, genotoxic metabolites, immune modulation, and metabolic alterations. We also examine microbiome-mediated effects on systemic treatments, including chemotherapy, radiotherapy-induced mucositis, and immune checkpoint inhibitor (ICI) response, and review emerging approaches to therapeutically modulate microbial communities. Although several microbial signatures show potential as biomarkers or therapeutic targets, no reproducible microbiome-based tools are yet ready for clinical implementation. Standardized methodologies and prospective interventional studies will be essential to translate these findings into precision oncology for HNSCC.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105108"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145901866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"What’s missing in patient-reported outcome reporting? A scoping review and aggregated trial-level analysis of completion rates in oncology randomized controlled trials","authors":"Daniela Krepper ,&nbsp;Niclas J. Hubel ,&nbsp;Samuel M. Vorbach ,&nbsp;Lotte van der Weijst ,&nbsp;Abigirl Machingura ,&nbsp;Claudia Seidl ,&nbsp;Johannes M. Giesinger ,&nbsp;Monika Sztankay ,&nbsp;Scottie Kern ,&nbsp;Deborah Fitzsimmons ,&nbsp;Madeline Pe ,&nbsp;Bernhard Holzner ,&nbsp;Jens Lehmann ,&nbsp;on behalf of the EORTC Quality of Life Group","doi":"10.1016/j.critrevonc.2025.105100","DOIUrl":"10.1016/j.critrevonc.2025.105100","url":null,"abstract":"<div><h3>Background</h3><div>Missing patient-reported outcome (PRO) data undermine the ability to draw robust conclusions from PRO endpoints included in cancer randomized controlled trials (RCTs). This review aimed to systematically evaluate PRO completion rates and identify trial characteristics associated with completion.</div></div><div><h3>Methods</h3><div>We conducted a scoping review searching for RCTs published on PubMed between 2019 and 2023. We searched for RCTs evaluating biomedical interventions in patients with solid tumors (breast, bladder, colorectal, gynecological, prostate, or lung). Trials were eligible if they used commonly applied cancer-specific PRO measures and reported information on completion. For each trial, we extracted or calculated completion rates at baseline and first post-baseline assessment, reasons for missingness, and trial characteristics. We used regression models to examine associations between trial characteristics and completion.</div></div><div><h3>Findings</h3><div>We identified 222 eligible trials from 9331 screened references. Mean baseline PRO completion rates were 91·3 % (control) and 92·1 % (intervention), declining to 82·1 % and 82·9 % at the first post-baseline assessment. Reasons for missing PRO data were documented in only 18 % of trials. Industry-sponsored trials exhibited significantly higher completion rates compared to non-industry-sponsored trials. Trials with double-blind designs had higher completion rates than open-label trials, while no difference between treatment arms was found. Electronic PRO assessment was not significantly associated with higher completion rates.</div></div><div><h3>Interpretation</h3><div>PRO completion rates in cancer RCTs remain challenging as they vary across settings, particularly beyond baseline, and reporting on missing data is often inadequate. These findings highlight the need for improved reporting and greater prioritization of PRO completion regardless of trial design.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105100"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145835557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sequential use of targeted radioligand therapies in metastatic castration-resistant prostate cancer: A case report and systematic review","authors":"Hatice Bölek ,&nbsp;Mine Araz ,&nbsp;Cigdem Soydal ,&nbsp;Emre Yekedüz ,&nbsp;Nuriye Özlem Küçük ,&nbsp;Yüksel Ürün","doi":"10.1016/j.critrevonc.2025.105088","DOIUrl":"10.1016/j.critrevonc.2025.105088","url":null,"abstract":"<div><h3>Background</h3><div>The treatment landscape of metastatic castration-resistant prostate cancer (mCRPC) has evolved with the introduction of novel therapies, including targeted radioligand therapies (RLTs). However, data about sequential use of RLT remains limited.</div></div><div><h3>Objective</h3><div>This study aims to present a case report on the sequential use of RLTs and to investigate the efficacy of administering different RLTs in sequence.</div></div><div><h3>Methods</h3><div>A systematic review of the literature was conducted following PRISMA guidelines. Studies reporting on patients who received sequential RLT agents for mCRPC and included efficacy data for the subsequent agent were included in the study.</div></div><div><h3>Results</h3><div>A total of 16 studies met the inclusion criteria. Among these, nine studies reported the use of Lutetium-177 PSMA (¹⁷⁷Lu‑PSMA) following Radium-223 (²²³Ra), seven studies reported Actinium‑225 PSMA (²²⁵Ac‑PSMA) after ¹ ⁷⁷Lu‑PSMA, two studies reported ²²⁵Ac‑PSMA following ²²³Ra, and one study investigated Terbium-161 PSMA (¹⁶¹Tb‑PSMA) after ¹ ⁷⁷Lu‑PSMA. For patients receiving ¹ ⁷⁷Lu‑PSMA following ²²³Ra, the reported median progression-free survival (PFS) ranged from 3 to 10 months, while overall survival (OS) ranged from 11.1 to 18 months. In those treated with ²²⁵Ac‑PSMA after prior ¹ ⁷⁷Lu‑PSMA, the median PFS ranged from 3.1 to 10 months, and OS ranged from 7.7 to 16 months. Treatment was generally well tolerated; hematologic toxicities were the most reported adverse events.</div></div><div><h3>Conclusion</h3><div>Sequential administration of RLTs may provide sustained clinical benefit in patients with mCRPC. However, the existing evidence is limited, heterogeneous, and predominantly derived from retrospective analyses.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105088"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic approaches to prostate cancer: Present landscape and future prospects","authors":"Konstantinos Mesiakaris,&nbsp;Efthalia Kontogianni,&nbsp;Souzana Logotheti,&nbsp;Vasiliki Tzelepi","doi":"10.1016/j.critrevonc.2025.105083","DOIUrl":"10.1016/j.critrevonc.2025.105083","url":null,"abstract":"<div><div>Genetic profiles alone do not fully describe the development and evolution of prostate cancer (PCa), whereas epigenetic alterations are emerging as promising therapeutic targets. This review explores FDA-approved and experimental epigenetic strategies, including DNA methyltransferase inhibitors (DNMTis), histone deacetylase inhibitors (HDACis), histone methyltransferase inhibitors, bromodomain and extra-terminal domain inhibitors (BETi), non-coding RNA therapies, antisense oligonucleotides, and future prospects such as chromatin remodeling, DNA hydroxymethylation, and RNA methylation. Although DNMTis and HDACis have historically dominated clinical trials, mainly in hematologic cancers, the 2020 approval of an epigenetic therapy for a solid tumor marked an important breakthrough. Despite this, epigenetic drugs remain underexplored in PCa: among 2254 clinical studies of such agents, only 58 (2.57 %) included PCa patients. This disparity highlights an urgent need for novel therapeutic approaches beyond chemotherapy and androgen deprivation. By assessing current progress and outlining opportunities in drug repositioning and novel targets, this review underscores epigenetics as a critical frontier for advancing PCa treatment.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105083"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145770169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application and potential of the tumor microenvironment, ferroptosis, cuproptosis, and disulfidptosis in cancer treatment and monitoring","authors":"Dehuan Zhang ,&nbsp;Yuehan Zhao,&nbsp;Dandan Guo","doi":"10.1016/j.critrevonc.2025.105066","DOIUrl":"10.1016/j.critrevonc.2025.105066","url":null,"abstract":"<div><div>The interplay between the tumor microenvironment and metabolic cell death pathways has emerged as a critical focus in contemporary cancer research. This comprehensive review examines the mechanistic interactions between these processes and evaluates their therapeutic and diagnostic implications in cancer management. Following Hanahan and Weinberg's seminal characterization of cancer hallmarks in 2011, substantial experimental and clinical evidence has accumulated, expanding our understanding of tumor biology. This review specifically addresses several key aspects: metabolic perturbations within the TME and their interactions with ferroptosis, cuproptosis, and disulfidptosis pathways; therapeutic agents and combinatorial approaches targeting these distinct metabolic cell death mechanisms; advanced delivery systems, particularly nanocarrier-based platforms, for enhancing metabolic cell death-inducing therapeutic strategies. It also points out the limitations of various therapeutic approaches that induce metabolic death in tumor cells, and predicts the directions that can be focused on exploring in the future.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105066"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"\"THE ENDS IN THE BEGINNINGS” age-related mechanisms of Telomere maintenance in pediatric and AYA-group Neuroblastoma.","authors":"Ugo Rovigatti","doi":"10.1016/j.critrevonc.2025.105047","DOIUrl":"10.1016/j.critrevonc.2025.105047","url":null,"abstract":"<div><div>This review focuses on the different Telomere Maintenance Mechanisms (TMMs), which take place in High-Risk Neuroblastoma (HR-NB) and vary according to age: 1. Reactivation of Telomerase (TEL+) in approximately 70–75 % of cases and 2. Alternative Lengthening of Chromosomes (ALT+) present in 25–30 % -mostly older-cases. ALT+ is based on homologous recombination and replication, but it is poorly understood. A seminal paper by Cheung et al. at MSKCC in 2012 initially discovered a skewed distribution of ALT+ pathway, with 0 % incidence in Infants and 100 % presence in the Adolescent/ Young Adults (AYA) group. This is critically evaluated and corrected in a less dichotomized fashion, thanks to more sophisticated NGS technologies. In contrast to the current interpretation for the skewed values -i.e. that aging creates very different oncogene dependencies, leading to different clonal expansions- this analysis underlines that (similarly to what happens in childhood leukemia/lymphoma) aging in neural crest cells causes remodelling of nuclear chromatin sites. Therefore, different genomic sites are susceptible to mutagenesis/rearrangements according to patients age and to clastogenic events. This second explanation better fits intra- and inter-tumor heterogeneity (TH) and the Micro-Foci inducing Virus (MFV) model as a clastogenic hit. Special discussion is on ATRX mutations of the ALT+ pathway, since very recent work from the Netherlands suggests that it may affect ribosomal genes and biogenesis. Previous work from the author showed that MFV may cause such ALT+ pathways as well as the reactivation of the Telomerase (hTERT) and that the target of GD2 immunotherapy corresponds indeed the MFV immediate-receptor.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105047"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145696420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pseudogenes in breast cancer pathogenesis and their clinical utility","authors":"Isabel Kannampuzha ,&nbsp;Farhad Ghasemi ,&nbsp;Armen Parsyan","doi":"10.1016/j.critrevonc.2025.105078","DOIUrl":"10.1016/j.critrevonc.2025.105078","url":null,"abstract":"<div><div>Breast cancer remains as one of the leading causes of mortality and morbidity among women worldwide, underscoring the need for a better understanding of breast cancer etiopathogenesis, effective new therapeutics and clinically actionable biomarkers. Pseudogenes, traditionally seen as nonfunctional sequences of DNA, are increasingly recognized to have important functions in physiology and disease, including in various cancers. Recently accumulating and expanding body of data has emphasized the potential role of pseudogenes in multiple aspects of breast cancer pathogenesis including their function as oncogenes or tumor suppressors to influence cellular proliferation, migration, invasion, apoptosis, angiogenesis, immune modulation, and maintenance of cancer stem cell properties. Moreover, expression of many pseudogenes has been shown to correlate with patient survival parameters and clinicopathologic characteristics of the tumor, making them excellent candidates as prognostic biomarkers. Pseudogene expression can also modulate responses of breast cancer to chemotherapeutic agents and antihormonal treatments, as well as radiotherapy, indicating their potential as treatment response biomarkers. Given their functions in breast cancer biology, pseudogenes can serve as novel targets for treatment. Here, the roles of pseudogenes in breast cancer are discussed in detail.</div></div>","PeriodicalId":11358,"journal":{"name":"Critical reviews in oncology/hematology","volume":"218 ","pages":"Article 105078"},"PeriodicalIF":5.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145727856","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}