SEMINARS IN CANCER BIOLOGY肿瘤生物学专题综述

SEMINARS IN CANCER BIOLOGY(英文缩写 SEMIN CANCER BIOL),ISSN 1044-579X,eISSN 1096-3650,中文译名:肿瘤生物学专题综述 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。

2026 年数据 · 影响因子
20.300
JCR 分区
Q1
CAS 分区
B2
近一年发文量
86
本站 PubMed 收录统计

发文量统计区间:2025-09-27 至 2026-09-27,按本站收录文献的发表日期统计。

ISSN: 1044-579X · eISSN: 1096-3650 · 缩写: SEMIN CANCER BIOL ·中文: 肿瘤生物学专题综述

期刊介绍

选择期刊介绍栏目

期刊简介

Seminars in Cancer Biology 是一本以专题综述为核心的肿瘤学学术期刊,聚焦癌症生物学的基础机制与转化研究。每期围绕特定主题,邀请领域内专家撰写系统性综述,涵盖肿瘤发生、微环境、信号通路、免疫治疗及分子靶向等方向。读者群主要为肿瘤学研究者、临床肿瘤医师及生物医学研究生,适合快速把握某一专题的研究现状与前沿争议。

研究方向

主要发表肿瘤生物学领域的综述与专题评论,主题包括癌基因与抑癌基因、细胞周期与凋亡、肿瘤微环境与转移、免疫逃逸、代谢重编程、表观遗传调控及新型治疗策略。论文类型以邀约综述为主,也包含少量观点性文章,强调对已有证据的整合与批判性分析,而非原始实验数据。

期刊特色

研究取向偏重机制整合与概念梳理,论文通常由活跃在该领域的学者撰写,篇幅较长、引用充分,适合作为专题入门或教学参考。对希望系统了解某一癌症生物学方向、寻找研究切入点或撰写基金背景部分的读者尤为有用,也适合作为研究生课程补充读物。

投稿难度

投稿难度整体较高,但并非仅由分区决定。该刊多为邀约或经预审的综述,自由投稿需先以提案说明主题新颖性与必要性。准备时应聚焦一个明确且尚存争议的科学问题,避免泛泛罗列文献,并突出对领域概念或治疗思路的整合价值。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
202117.012Q1
202214.500Q1
202312.100Q1
202415.700Q1
202520.300Q1

SEMINARS IN CANCER BIOLOGY 最新收录文献

  1. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    1. Metabolic Drivers of Bidirectional Heart-Cancer Crosstalk: From a Relatively Tumor-Restrictive Myocardium to Therapeutic Decoupling.

    作者:
    Zili Tang, Rong Luo, Wanfeng Zhang, Xin Cao, Shun Lu, Xiaoping Li
    日期:
    2026-09-24

    Cardio-oncology has traditionally centered on treatment-related cardiotoxicity, yet cancer and cardiovascular disease influence one another before, during, and after therapy. This Review develops a direction-weighted staged framework for their metabolic interaction. We propose the healthy adult myocardium as a relatively tumor-restrictive environment in which metabolic reserve operates alongside mechanical, vascular, stromal, and immune constraints. Cancer can erode this reserve before overt cardiotoxicity through substrate redistribution, cachexia, mitochondrial stress, and circulating metabolites. Once metabolically injured, the heart can reshape immune, neurohumoral, metabolic, and vesicular signaling in ways that promote tumor progression; this heart-to-tumor direction constitutes reverse cardio-oncology within the broader bidirectional model. The proposed trajectory-from tumor-driven reserve loss to heart-derived reinforcement and subsequent stabilization or amplification-is common but not universal and may be reshaped by pre-existing cardiac disease or anticancer therapy. Evidence maturity differs across hubs: D-2-hydroxyglutarate provides the clearest source-defined tumor-to-heart proof of concept, whereas lactate handling and ferroptosis-related lipid-iron stress represent broader, testable, but less clinically resolved pathways. We translate these pathways into metabolic endotypes, provisional measurable criteria, and paired cardiac-oncologic endpoints to support therapeutic decoupling without compromising cancer control.

  2. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    2. Precision oncology in GI-cancers: Mechanisms of action, indications and ongoing strategies to overcome primary and secondary resistance.

    作者:
    Laia Aceituno, Elena Valenzi, Oreste Segatto, Anna Saborowski, Arndt Vogel
    日期:
    2026-09-20

    Gastrointestinal (GI) cancers remain a leading cause of cancer mortality, with durable benefit from current therapies limited to a subset of patients. Precision oncology is expanding options by targeting recurrent, actionable alterations, most notably in cholangiocarcinoma (CCA), in genes such as FGFR2, IDH1, KRAS, BRAF and ERBB2. Here, we review the evolving therapeutic landscape, emphasizing clinical efficacy, and indications for various treatment modalities. Key therapies include FGFR inhibitors (first and next-generation; both covalent and FGFR2-selective agents), IDH1 inhibitors, KRAS and BRAF inhibitors combined with EGFR blockade and/or chemotherapy, and HER2-targeted monoclonal antibodies, tyrosine kinase inhibitors (TKIs), and antibody-drug conjugates (ADCs). Central mechanisms of both primary and secondary resistance are detailed, with a focus on on-target mutations and convergent off-target MAPK signaling pathways. Finally, we discuss drug-tolerant persister cells, residual tumor cell states that survive therapy without canonical genetic resistance alterations and may contribute to relapse and secondary resistance.

  3. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    3. Recent advances in unlocking T cell signatures in cancer through deep learning.

    作者:
    Norman Teik Wei Yap, Kesong Wu, Linlin Li, Sen Wang, Zewen Kelvin Tuong
    日期:
    2026-09-18

    T-cell receptors (TCRs) recognize antigens, including cancer antigens, offering a promising avenue for immunological profiling and early detection. As cancer diagnostics increasingly shift towards less invasive methods, deep learning has emerged as a powerful tool in facilitating this transition. The identification of cancer-associated TCRs (caTCRs) from peripheral blood samples presents a compelling alternative to traditional biopsy-based approaches, enabling more scalable and non-invasive cancer screening. In this review, we examine twelve state-of-the-art caTCR detection frameworks, detailing their conceptual innovations and method workflows. We also perform a limited external benchmarking of a subset of publicly available pre-trained models on our own data and analyze their performance. We further discuss the biological and methodological constraints of caTCRs and their detection methods, and assess their ability to be adopted within clinical settings. By highlighting both recent advances and remaining limitations, this manuscript aims to provide a balanced perspective on the field and to inform future research towards more robust, interpretable, and clinically relevant caTCR-based diagnostic tools.

  4. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    4. Physical exercise as an adjunctive therapy in obesity-associated cancer: From biological rationale to a pragmatic clinical framework.

    作者:
    Giuseppe Annunziata, Elisabetta Camajani, Massimiliano Caprio, Antonio Paoli, Luigi Barrea
    日期:
    2026-09-04

    Obesity represents a well-established risk factor for numerous cancers, contributing substantially to the global burden of this disease. In parallel, accumulating evidence supports the relevant biological effects of physical activity in counteracting the pathological mechanisms linking obesity to carcinogenesis and tumor progression, including chronic low-grade inflammation, adipocyte dysfunction, and insulin resistance, which collectively promote the establishment of a pro-tumorigenic microenvironment. Despite the growing body of evidence on the benefits of physical activity in oncological patients, its translation into practical recommendations for individuals with both obesity and cancer remains limited, representing a critical clinical and scientific gap. The present review aims to provide a critical overview of the biological basis and available evidence, with the goal of proposing a pragmatic evidence-informed clinical framework for the integration and prescription of physical exercise in the management of patients with cancer and obesity. Major international guidelines on physical activity in oncology will be analyzed, highlighting areas of convergence and operational gaps, with particular emphasis on the absence of specific recommendations for this dual pathological condition. Exercise modality, dose, progression, and timing will be discussed, with attention to the most relevant individual and systemic barriers. Collectively, the available evidence supports the integration of individualized exercise prescription as a core component of multidisciplinary care for patients with obesity-associated cancer, while highlighting the urgent need for dedicated clinical trials and consensus recommendations specifically addressing this high-risk population.

  5. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    5. Extracellular chromatin fragments as biomarkers for cancer screening.

    作者:
    Manlio Vinciguerra, Desislava K Tsoneva
    日期:
    2026-09-03

    Extracellular chromatin fragments, including cell-free DNA (cfDNA) and histones, have emerged as promising non-invasive biomarkers for cancer screening and monitoring. While aberrant DNA methylation patterns in cfDNA are already established hallmarks of cancer and are increasingly used in liquid biopsy assays, circulating histones and nucleosomes reflect complementary aspects of tumor-associated epigenetic dysregulation and chromatin remodeling. This review integrates current knowledge on intracellular and extracellular histones in cancer, highlighting their release via necrosis, apoptosis, or neutrophil extracellular traps (NETs), and their dual roles as damage-associated molecular patterns and modulators of the tumor microenvironment. We discuss the intricate mechanistic links between DNA methylation and histone modifications, histone variants, and post-translational modifications, including the bidirectional crosstalk mediated by enzymes such as DNMTs, UHRF1, and PAD4. Special emphasis is placed on NETosis and its epigenetic regulation, which further connects histone citrullination with DNA methylation machinery and tumor progression. We evaluate the clinical potential of combining cfDNA methylation profiling with circulating histone levels, histone variants, and nucleosome-associated post-translational modifications. Evidence from multiple cancer types demonstrates that multimodal epigenetic approaches, incorporating fragmentomics, histone marks, and methylation signatures, significantly improve diagnostic accuracy, tissue-of-origin identification, and early detection compared to single-modality or conventional protein biomarkers in several cancer types. Fragmentomics, reflecting nucleosome positioning and chromatin accessibility, adds a functional layer to methylation-based assays. Collectively, extracellular chromatin components offer a rich, biologically interconnected source of information. Their integrated analysis holds substantial promise for advancing precision oncology through improved screening, prognosis, treatment monitoring, and development of safer epigenetic therapies.

  6. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    6. Evolutionary and resistance dynamics in oligometastatic and oligoprogressive cancer treated with stereotactic radiotherapy and systemic therapies: A systematic review and focused meta-analysis.

    作者:
    Marilina García-Aranda, Juan Zafra-Martín, Alba Rodríguez-Martínez, Antonio Rueda-Domínguez, Isabel Barragán
    日期:
    2026-09-01

    Oligometastatic and oligoprogressive disease treated with stereotactic ablative radiotherapy (SABR) represents a clinically heterogeneous entity. Increasing evidence suggests that anatomical definitions alone may not adequately capture underlying biological diversity. This systematic review aimed to synthesize translational evidence exploring evolutionary dynamics, resistance mechanisms, and biomarker-driven stratification in patients treated with SABR. A systematic literature review was performed including prospective and retrospective studies evaluating translational biomarkers in oligometastatic or oligoprogressive settings treated with SABR. Studies assessing genomic, transcriptomic, circulating or immune-related biomarkers were included. Data were summarized qualitatively according to predefined translational domains: (i) evolutionary dynamics under systemic therapy pressure, (ii) baseline biological stratification, (iii) longitudinal circulating biomarkers, and (iv) systemic immune remodeling. Exploratory quantitative visual syntheses were performed using reported hazard ratios when conceptually comparable endpoints were available. 19 studies comprising 1527 patients were included. Across tumor types and treatment contexts, translational analyses consistently indicated that anatomically defined oligometastatic states encompass biologically distinct subgroups with different risks of systemic progression. Studies evaluating oligoprogression under ongoing systemic therapy suggested a distinction between spatially constrained resistance and systemic molecular escape, supported by circulating tumor DNA and tissue- or plasma-based molecular profiling (including genomic and transcriptomic analyses). Baseline biological features, including adverse genomic signatures and circulating biomarkers, were associated with inferior progression outcomes despite metastasis-directed therapy. Longitudinal biomarkers provided early signals of treatment response and systemic control. Immune remodeling after SABR showed context-dependent effects, both systemic immune activation and treatment-related immunosuppression reported across studies.

  7. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    7. Unveiling tumor heterogeneity by single cell RNA-sequencing: From basic considerations to clinical applications.

    作者:
    Tina Fuchs, Michael Menzel, Katharina Mößinger, Daniel Kazdal, Andy Kahles, Jan Budczies, Albrecht Stenzinger
    日期:
    2026-09-01

    Tumor heterogeneity-encompassing diverse cellular phenotypes, genomic alterations, and microenvironmental contexts-is a principal barrier to effective cancer therapy. Single-cell RNA sequencing (scRNA-seq) has transformed our ability to resolve this complexity by capturing transcriptomes at single-cell resolution. Here, we review the technical foundations required for high-quality scRNA-seq studies. We then trace the evolution of scRNA-seq platforms from manual micromanipulation to high-throughput systems, and describe the computational pipelines that enable reliable data interpretation. The application of scRNA-seq is exemplarily shown in the context of lung cancer, where single-cell profiling has revealed (i) the clonal and sub-clonal architecture of tumors, (ii) extensive remodeling of the immune microenvironment, iii) key mechanisms underlying resistance to targeted agents and immune-checkpoint blockade, and (iv) the dynamics of neo-antigen-specific T-cell responses. Integrating machine-learning techniques-such as deep-learning classifiers and graph-based models-with single-cell transcriptomic data has markedly sped up biomarker discovery, produced more accurate risk-stratification scores, and enabled the generation of patient-specific therapeutic predictions. We surveyed the major trial registry ClinicalTrials.gov and identified ∼380 ongoing or completed studies that explicitly incorporate scRNA-seq as a correlative or pharmacodynamic endpoint. Overall, the analysis shows that scRNA-seq becomes an increasingly important component of modern trials, providing high-resolution cellular and molecular readouts that complement conventional imaging and bulk-omics endpoints. While key challenges remain, ranging from costs, scalability and need for rigorous validation before routine clinical deployment, ongoing technological advances continue to expand the potential of scRNA-seq as a cornerstone of precision medicine.

  8. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    8. Intraclonal heterogeneity in mature B-cell malignancies: The perspective of immunogenetics.

    作者:
    Anastasia Iatrou, Athanasios Roussos, Thomas Chatzikonstantinou, Anastasia Chatzidimitriou, Kostas Stamatopoulos, Andreas Agathangelidis
    日期:
    2026-08-22

    Intraclonal heterogeneity is increasingly recognized as a central determinant of evolutionary fitness in B-cell malignancies. Since these tumors arise from lineages that naturally diversify through V(D)J recombination, somatic hypermutation (SHM), and class switch recombination (CSR), their malignant counterparts retain and/or aberrantly reactivate these processes, generating antigen receptor repertoires with complex subclonal architectures. Advances in next-generation and single-cell immunogenetics have revealed that intraclonal heterogeneity arising from variations in IG genes is neither random nor incidental: it reflects ongoing antigenic engagement, microenvironmental pressures, and selection for functional B-cell receptor immunoglobulin (BcR IG) configurations that promote survival and, conceivably, also therapy escape. Here, we provide an overview of BcR IG intraclonal heterogeneity across malignancies of mature B cells, focusing on how it may relate to tumor evolution, immune surveillance, and treatment-induced bottlenecks. We also highlight methodological breakthroughs enabling high-resolution reconstruction of subclonal trajectories and discuss how intraclonal heterogeneity can be leveraged to refine risk stratification, measurable residual disease (MRD) assessment, and individualized treatment strategies.

  9. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    9. Clonal dynamics on the road to hematological malignancy (MBL, MGUS, CH).

    作者:
    Xie Zhuoer, Sekar Aswin, Ghia Paolo, Kumar Shaji, A Parikh Sameer
    日期:
    2026-08-09

    Monoclonal gammopathy of undetermined significance (MGUS), monoclonal B-cell lymphocytosis (MBL), and clonal hematopoiesis (CH) of indeterminate potential represent highly prevalent, age-associated precursor states characterized by detectable serological, cellular, or genetic alterations in otherwise asymptomatic individuals. The advent of high-sensitivity technologies, including mass spectrometry, multiparametric flow cytometry, and next-generation sequencing, has revealed that these conditions are far more widespread than previously appreciated, yet only a minority of affected individuals progress to overt malignancies such as multiple myeloma, chronic lymphocytic leukemia, or myeloid neoplasms. Across these entities, a unifying paradigm is emerging in which malignant transformation is governed not simply by the presence of driver lesions, but by dynamic clonal evolution shaped by intrinsic fitness, temporal acquisition of alterations, and selective pressures imposed by the aging microenvironment. In CH, mutation-specific growth kinetics and inflammation-driven selection define both hematologic and systemic risks. In MBL, antigenic stimulation, immune dysfunction, and genetic complexity modulate progression to CLL. In MGUS, disease evolution reflects a gradual co-evolution between plasma cell clones and a progressively permissive niche. Aging-associated inflammation and tissue remodeling act as common denominators, fostering a competitive landscape that selectively advantages aberrant clones while suppressing normal hematopoiesis. In turn, these clones actively remodel their microenvironment, establishing feed-forward loops that sustain clonal expansion and malignant potential. Integrating insights across CH, MBL, and MGUS highlights shared biological principles and supports a shift toward "precision prevention" strategies aimed at intercepting high-risk trajectories while minimizing unnecessary surveillance in low-risk individuals.

  10. JCR分区: Q1 CAS分区: B2 影响因子: 20.3

    10. Beyond the traditional dish: Advanced 3D ex vivo culture platforms for tumor modelling.

    作者:
    Konstantina Strepi, Roos F Koppenol, Jos Jonkers, Julia M Houthuijzen
    日期:
    2026-07-24

    The tumor microenvironment (TME) and its complex, dynamic interactions play a pivotal role in cancer development, progression and therapy response. However, faithful recapitulation of the diverse cellular and structural components of the TME in vitro remains a major challenge in cancer research. Traditional 2D cancer cell cultures fail to preserve TME interactions and tissue organization that critically impacts tumor behavior, while advanced 3D systems, including organoids, 3D-bioprinted structures and microfluidic platforms capture only selected aspects of TME complexity and host physiology. Recent advances in the culture of primary tumor specimens with minimal disruption to tissue architecture has led to a rapidly evolving set of model systems that benefit TME research. These ex vivo cultures (EVCs), as we collectively refer to them here, are established from fresh primary tumor tissue and preserve the native tumor architecture, extracellular matrix composition, immune and stromal compartments and their multilayered crosstalk within a physiologically relevant context. This review outlines the historical evolution of 2D and 3D model systems in oncology, followed by a comprehensive overview of current EVC methodologies. Furthermore, we address their applications in fundamental cancer research, personalized medicine and drug discovery, while highlighting their advances and challenges for the future.

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指标接近的期刊