BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER生物化学与生物物理学报-癌症评论
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER(英文缩写 BBA-REV CANCER),ISSN 0304-419X,eISSN 1879-2561,中文译名:生物化学与生物物理学报-癌症评论 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。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 11.414 | Q1 |
| 2022 | 11.200 | Q1 |
| 2023 | 9.700 | Q1 |
| 2024 | 8.300 | Q1 |
| 2025 | 11.200 | Q1 |
BIOCHIMICA ET BIOPHYSICA ACTA-REVIEWS ON CANCER 最新收录文献
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1. Lipid metabolic regulation and targeting strategies in the brain metastasis tumor microenvironment.
1. 脑转移瘤微环境中的脂质代谢调控及靶向策略PMID:日期:2026-10-02Brain metastasis is a major contributor to poor prognosis in cancer patients, with therapeutic efficacy severely constrained by the blood-brain barrier and the complex brain microenvironment. Although lipid metabolic reprogramming has been linked to tumor progression across multiple cancer types, its mechanistic involvement in brain metastasis, particularly its reciprocal interactions with central nervous system microenvironmental cells, remains insufficiently defined. This review synthesizes existing evidence to elucidate how lipid metabolic reprogramming promotes tumor cell colonization and growth in the brain and to evaluate its therapeutic relevance. Current findings indicate that metastatic tumor cells adapt to the brain microenvironment via increased de novo lipogenesis, altered cholesterol metabolism, reduced fatty acid oxidation, and enhanced uptake of exogenous lipids. Emerging evidence further indicates reciprocal lipid-metabolic interactions between metastatic tumor cells and central nervous system-resident cells; however, the directionality, cell-type specificity, and underlying molecular mechanisms of this metabolic crosstalk remain insufficiently characterized. Such interactions may promote immunosuppressive microenvironmental remodeling and facilitate metastatic progression. Significant heterogeneity is observed among primary tumor types in their use of lipid metabolism associated mechanisms. Targeting critical nodes at the interface of lipid metabolic reprogramming and microenvironmental interactions may therefore help overcome current therapeutic limitations in brain metastasis. Future studies using advanced multi-omics approaches are expected to define spatial heterogeneity and support the development of combination strategies capable of crossing the blood-brain barrier, ultimately informing improved clinical management strategies.
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2. The endothelial cell-neutrophil axis: Mechanisms and therapeutic perspectives in colitis-associated carcinogenesis.
2. 内皮细胞-中性粒细胞轴：结肠炎相关癌变中的机制与治疗前景PMID:日期:2026-09-30Endothelial dysfunction coupled with neutrophil infiltration drives colitis-associated carcinogenesis (CAC). Vascular endothelial cells sustain homeostasis and immune surveillance. In CAC, endothelial impairment increases vascular permeability, recruits neutrophils, aggravates inflammation, and further stimulates angiogenesis, thereby promoting tumor proliferation and metastasis. Targeting endothelial signaling cascades, including the VEGF and MAPK axes, represents a promising strategy for suppressing inflammatory responses and tumor outgrowth. Blockade of adhesion molecules such as VCAM-1 and ICAM-1 curtails neutrophil recruitment and mitigates intestinal inflammatory lesions. Anti-VEGF and MAPK-targeted interventions have been investigated in cancer and inflammatory diseases, and emerging work on neutrophil extracellular traps opens new therapeutic directions. Despite these mechanistic and translational advances, a systematic overview of the interplay between endothelial cells and neutrophils during CAC remains lacking. Here we describe the central contribution of endothelial dysfunction to the multistep progression of CAC, discuss how therapeutic modulation of the endothelial cell-neutrophil axis could optimize clinical outcomes, and highlight vascular endothelium-targeted interventions as promising strategies for limiting CAC progression.
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3. Macrophage-mesenchymal crosstalk in recurrent glioblastoma: a perspective for therapeutic strategies.
PMID:日期:2026-09-28Glioblastoma (GBM) remains one of the most lethal cancers, with recurrence in nearly all patients despite standard therapy. However, the biological mechanisms governing recurrence remain incompletely understood. Increasing evidence suggests that recurrence is driven not only by tumor-intrinsic resistance, but also by dynamic reciprocal interactions between tumor cell plasticity and the tumor microenvironment (TME). Here, we integrate these dynamic interactions into a unifying ecological framework in which therapeutic stress induces proneural-to-mesenchymal transition (PMT), a phenotypic shift associated with increased invasiveness, inflammatory signaling, and treatment tolerance. Mesenchymal tumor states remodel the TME by promoting the recruitment and functional reprogramming of monocyte-derived macrophages (MDMs), which become increasingly enriched in recurrent tumors. In turn, macrophage-derived cytokines, including IL-6 and TGF-β, together with metabolites such as lactate and cholesterol derivatives, reinforce mesenchymal transcriptional programs and stabilize tumor cell states through immunometabolic interactions. We highlight how this bidirectional crosstalk forms a macrophage-mesenchymal feedback loop that sustains the recurrent tumor ecosystem. Fundamentally metabolism acts as a key regulatory layer that links immune polarization to tumor cell plasticity. Finally, we outline therapeutic strategies aimed at disrupting this circuit, emphasizing combination approaches that concurrently target phenotypic plasticity, macrophage recruitment and function, and metabolic crosstalk. A circuit-informed perspective provides a conceptual basis for designing more effective interventions against recurrent GBM.
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4. The cGAS-STING signaling in hepatocellular carcinoma: A spatiotemporally gated immune switch linking pro-tumorigenic immune evasion and anti-tumor therapeutic response.
PMID:日期:2026-09-27Hepatocellular carcinoma (HCC) arises from chronic inflammation and immune tolerance, posing substantial challenges for immunotherapy. The cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling is a central immunological hub linking innate immune sensing to adaptive immune responses in tumors. In HCC, cGAS-STING signaling exhibits a context-dependent dual role across multiple hepatic cell types, including hepatocytes, hepatic stellate cells and immune cells, orchestrating both anti-tumor immunity and pro-tumorigenic inflammation. While acute activation enhances dendritic cell maturation, antigen presentation, and CD8+ T-cell priming to boost anti-tumor immunity, sustained or dysregulated cGAS-STING signaling promotes chronic inflammation and subsequently remodels an immunosuppressive tumor microenvironment (TME) to promote tumorigenesis. This dual functionality positions the cGAS-STING signaling as both a therapeutic opportunity and a critical constraint in HCC immunotherapy. Recent advances highlight the translational potential of STING-targeted strategies, including synthetic agonists, combination regimens with targeted therapies, immune checkpoint inhibitors (ICIs) as well as nanomaterial-based delivery systems. At the same time, clinical translation remains constrained by systemic inflammatory toxicity, context-dependent tumor-promoting inflammation, pathway refractoriness or silencing, and the lack of validated biomarkers for patient selection. In this review, we summarize the molecular mechanisms, cell-type-specific functions and intercellular crosstalk of cGAS-STING signaling in HCC, and discuss therapeutic strategies and translational challenges. We propose future directions focusing on spatiotemporal activation, precision delivery, and biomarker-guided interventions to exploit the therapeutic potential of targeting the cGAS-STING signaling in HCC.
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5. Ubiquitination in DNA double-strand break repair: Mechanisms, regulation, and therapeutic implications.
PMID:日期:2026-09-26DNA double-strand break (DSB) repair depends on tightly coordinated signaling that controls damage recognition, chromatin remodeling, pathway choice, and repair termination. Among the regulatory layers involved, ubiquitination functions as a central organizing axis of the DNA damage response (DDR), directing the ordered assembly, retention, and turnover of repair factors at damaged chromatin. The RNF8-RNF168 ubiquitin cascade represents a core signaling module that amplifies DSB signals and licenses downstream repair programs. In this review, we summarize recent advances in ubiquitin-dependent regulation of DSB repair, focusing on how ubiquitination governs repair factor dynamics and the balance between classical non-homologous end joining (cNHEJ) and homologous recombination (HR). We further discuss SUMO modification as a tightly coupled regulatory layer that cooperates with ubiquitin signaling to fine-tune signal amplitude and duration through coordinated SUMO-ubiquitin interactions and SUMO-targeted ubiquitination. In addition to ubiquitin-centered regulation, emerging crosstalk with phosphorylation, methylation, acetylation, and PARylation further shapes repair timing, pathway commitment, and signal resolution. Finally, we discuss the translational implications of ubiquitin- and SUMO-centered DDR regulation, highlighting how adaptive repair states and acquired resistance to genotoxic therapies create exploitable therapeutic vulnerabilities.
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6. Tertiary lymphoid structures for anti-tumor immunotherapy.
6. 三级淋巴结构用于抗肿瘤免疫治疗PMID:日期:2026-09-24Tertiary lymphoid structures (TLSs) are transient ectopic lymphoid-like structures potentiating the adaptive anti-tumor immunotherapy efficiency. They have been observed across diverse malignancies since they were initially found to correlate with favorable prognosis in non-small cell lung cancer. Importantly, TLSs could systematically enhance immune responses efficiency by optimizing the immune ecology of the tumor microenvironmen (TME). They have attracted considerable interest as predictive biomarkers for anti-tumor treatment responses, including immune checkpoint blockade (ICB) and potential chemotherapy. However, TLSs formation within tumor is poorly controllable, and lacks effective strategies for precisely modulating their formation and function. In this comprehensive review, we first summarize the composition and formation mechanism of TLSs. Second, we address the role of TLSs in enhancing anti-tumor immunotherapy efficiency. Third, we explore the advanced methods to modulate TLSs formation. Finally, we summarize novel multifunctional materials in facilitating TLSs formation to enhance anti-tumor immunotherapy both in basic and clinical. Deep understanding of the formation mechanism and role of TLSs could provide insights into modulation of TLSs for improving anti-tumor immunotherapy efficiency.
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7. Radiotherapy-induced PD-L1 conversion in esophageal squamous cell carcinoma: From multidimensional mechanisms to clinical rescue strategies.
PMID:日期:2026-09-23Esophageal squamous cell carcinoma (ESCC) remains a formidable malignancy, with patients harboring programmed death ligand-1 (PD-L1)-negative tumors frequently exhibiting an "immune desert" phenotype and poor response to immune checkpoint blockade (ICB). Radiotherapy (RT), traditionally utilized for localized cytoreduction, acts as an in situ vaccine capable of remodeling the tumor immune microenvironment. A potential contributor to RT-ICB synergy is RT-associated modulation of PD-L1 expression, including possible conversion from a PD-L1-negative to a PD-L1-positive state. This review synthesizes ESCC-specific evidence and cross-tumor mechanistic data regarding cGAS-STING-mediated DNA sensing, eIF2α/ATF4-driven translational stress, epigenetic de-repression, metabolic-stromal signaling, and vesicular PD-L1 dissemination. While RT-induced PD-L1 upregulation serves as an adaptive resistance mechanism that can be therapeutically exploited, significant clinical barriers remain. Notable challenges include radiation-induced lymphopenia and overlapping toxicities, despite high pathological complete response rates in recent neoadjuvant RT-ICB trials. To address the needs of the PD-L1-negative population, we evaluate current clinical evidence and ongoing trial strategies. We emphasize the need to refine, rather than replace, existing radiotherapy paradigms through precision-oriented strategies, including careful optimization of spatiotemporal sequencing, cautious exploration of immunomodulatory low-dose radiotherapy, and structural preservation approaches such as tumor-draining lymph node sparing. By modulating stromal and metabolic resistance through refined RT parameters, localized radiation may be effectively translated into durable, systemic antitumor immunity.
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8. WNT/β-catenin signaling: implications for homeostasis and tumorigenesis in the esophagus.
PMID:日期:2026-09-23The WNT/β-catenin signaling pathway plays a central role in the development, homeostasis, and tumorigenesis of the gastrointestinal tract. During embryonic development, dynamic regulation of β-catenin activity is essential for foregut formation and for the transition of the esophageal epithelium from columnar to stratified squamous morphology, with inhibitory signals ensuring proper lineage specification. In the adult esophagus, however, the precise role of WNT/β-catenin signaling in basal progenitor cell proliferation and differentiation remains incompletely understood, although dysregulation of this pathway, including overexpression of WNT ligands and downregulation of WNT inhibitors, has been observed in Barrett's esophagus (BE) and esophageal cancer. This review highlights recent insights into the roles of WNT signaling in esophageal development, epithelial homeostasis, and disease pathogenesis.
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9. Metabolic reprogramming in T-cell acute lymphoblastic leukemia: Mechanisms of therapy resistance and clinical applications.
PMID:日期:2026-09-17T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy in which therapy resistance remains a major cause of treatment failure and relapse. Increasing evidence indicates that metabolic reprogramming and metabolic plasticity can contribute to T-ALL persistence under therapeutic pressure, rather than reflecting a single uniform metabolic phenotype. In this review, we examine the reprogramming of glucose, amino acid, lipid, and nucleotide metabolism, as well as metabolic adaptations within the tumor microenvironment, and their associations with therapy resistance in T-ALL. We further discuss the regulatory roles of oncogenic signaling pathways and metabolism-epigenetics crosstalk in metabolic adaptation. Emerging metabolism-targeted strategies are also reviewed, with particular attention to their potential therapeutic vulnerabilities and the evidence supporting their use in different experimental and clinical contexts. Major barriers to clinical translation include metabolic heterogeneity, compensatory metabolic rewiring, and toxicity arising from metabolic dependencies shared with normal tissues. Future metabolic-directed therapies require precise metabolic subtyping guided by multi-omics approaches, the development of novel targeted drugs, and the implementation of rational combination therapies.
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10. Advances in the regulation of vascular function by stromal cells in the tumour microenvironment of tongue squamous cell carcinoma and prospects for treatment.
10. 舌鳞状细胞癌肿瘤微环境中基质细胞调控血管功能的研究进展及治疗前景PMID:日期:2026-09-16Tongue squamous cell carcinoma (TSCC) is a highly aggressive subtype of oral squamous cell carcinoma, characterised by a high risk of local recurrence and cervical lymph node metastasis; its development is closely associated with the continuous remodelling of the tumour microenvironment (TME). A growing body of evidence suggests that the malignant progression of TSCC is not solely driven by tumour cells, but is highly dependent on the dynamic interactions between stromal cells and abnormal vascular networks within the tumour microenvironment. This article reviews recent research on the regulation of vascular dysfunction by stromal cells in TSCC, outlining how they modulate tumour angiogenesis, maturation, permeability and perfusion through intercellular communication, paracrine signalling, extracellular matrix remodelling and extracellular vesicle-mediated molecular delivery, thereby further influencing TSCC invasion, metastasis, immune evasion and treatment response. Building upon this, the paper summarises key molecular mechanisms underlying the stromal-vascular axis and explores therapeutic strategies targeting this axis, particularly the theoretical basis, practical limitations and future prospects of the combined application of anti-angiogenic therapy and immunotherapy, with the aim of providing new research perspectives and translational evidence for precision interventions in TSCC.