Biomarker Research生物标志物研究
Biomarker Research(英文缩写 BIOMARK RES),ISSN 2050-7771,eISSN 2050-7771,中文译名:生物标志物研究 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
Biomarker Research 最新收录文献
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1. Cell death in ischemia-reperfusion injury: beyond a single-cell-death perspective.
1. 缺血再灌注损伤中的细胞死亡：超越单细胞死亡视角PMID:日期:2026-10-01Ischemia-reperfusion injury (IRI) contributes to the pathogenesis of major diseases, including acute kidney injury, stroke, and myocardial infarction. Multiple forms of cell death, including apoptosis, necroptosis, pyroptosis, autophagy, and ferroptosis, are key contributors to IRI. The interplay among these cell-death programs adds to the complexity of the IRI landscape. Cell-death patterns differ markedly between the ischemic and reperfusion phases and across organs, reflecting the spatiotemporal and organ-specific features of IRI. Given the complex molecular mechanisms underlying IRI, multi-target small-molecule drugs, combination regimens, and nanodelivery systems have been explored, although most remain at the preclinical stage. In this review, we summarize the major cell-death modalities involved in IRI, their interconnected molecular targets and signaling pathways, and their phase-specific and organ-specific regulation. We further discuss the coordinated roles of non-coding RNAs, metabolic reprogramming, and epigenetic alterations in regulating cell death, as well as their therapeutic potential. Finally, we propose therapeutic strategies aimed at modulating crosstalk among cell-death modalities, with potential implications for individualized IRI therapy.
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2. ZNF292 mutations impair RNA and protein biosynthesis defining an adverse prognostic subset in early-stage chronic lymphocytic leukemia.
2. ZNF292突变损害RNA和蛋白质生物合成，定义了早期慢性淋巴细胞白血病的不良预后亚群PMID:日期:2026-10-01ZNF292 alterations are recurrently detected in patients with chronic lymphocytic leukemia (CLL), occurring in 3%-6% of patients as mutations and in 2% as 6q deletions. Although preliminary evidence suggested an independent prognostic role for ZNF292 mutations, their specific clinical relevance in early-stage CLL and the underlying biological mechanisms remain poorly defined. 488 CLL patients were analyzed using targeted Next-Generation Sequencing (NGS) to characterize the landscape and clinical significance of ZNF292 mutations. CRISPR/Cas9-genome editing was employed to introduce the most prevalent ZNF292 variants into CLL cellular models. Their biological and functional implications were evaluated by integrating RNA-sequencing data from these isogenic cellular models with transcriptomic data from primary patient samples, complemented by functional validation and drug response assays. ZNF292 mutations were associated with shorter time to first treatment (TTFT; median 25 vs. 52 months, P = 0.009) and inferior overall survival (OS, median 93 vs. 148 months, P = 0.004). Importantly, when restricting the analyses to early-stage cases, ZNF292 alterations were independently associated with shorter TTFT and OS, identifying a high-risk subgroup. Mechanistically, transcriptomic analyses revealed that ZNF292 mutations suppress global protein biosynthesis and modulate cell cycle progression in both primary CLL samples and CRISPR/Cas9-edited cells. Furthermore, ZNF292 deficiency impaired replication stress responses via defective CHK1 activation, resulting in DNA damage accumulation. Evaluating potential therapeutic vulnerabilities, ZNF292-mutated cells exhibited enhanced in vitro sensitivity to ibrutinib and venetoclax. Our findings propose ZNF292 alterations as an independent prognostic factor in early-stage CLL and unveil their role in disease progression.
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3. Advances in molecular pathobiology of PCNSL - towards clinical implementation of novel diagnostics and therapeutics.
3. 原发性中枢神经系统淋巴瘤分子病理生物学进展——迈向新型诊断与治疗策略的临床转化PMID:日期:2026-10-01Primary central nervous system lymphoma (PCNSL) is a rare aggressive extranodal non-Hodgkin's lymphoma which outcomes remain poor despite therapeutic advances. Recent improvements in our understanding of the molecular diversity of aggressive diffuse large B cell lymphomas suggest that the biological refinement of PCNSL diagnostics may be enabled by an integrated multi-modal approach, augmenting clinical data with modern minimally-invasive liquid biopsy-based assays and multi-omic molecular profiling. Single cell sequencing and spatial imaging technologies dissecting the immune microenvironmental architecture of PCNSL are anticipated to further refine future diagnostics. Concurrently, several innovative strategies featuring immunomodulatory agents, oncogenic kinase inhibitors and immunotherapies including chimeric antigen receptor (CAR) T-cell therapy have emerged. In this review, we provide an update of recent advances in the understanding of the pathobiology of PCNSL focusing on clinically relevant molecular subclassifications, highlight emerging therapeutics, and discuss the translational roadmap to clinical implementation of next-generation diagnostic platforms based on novel technologies.
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4. Megakaryocytes in myelofibrosis: mechanisms of fibrotic niche remodeling and therapeutic implications.
4. 骨髓纤维化中的巨核细胞：纤维化微环境重塑机制及治疗意义PMID:日期:2026-09-29Myelofibrosis is a clonal myeloproliferative neoplasm characterized by progressive remodeling of the bone marrow microenvironment. Megakaryocyte (MK) abnormalities are defining histological features of prefibrotic and overt primary myelofibrosis and contribute to disease pathogenesis. Dysplastic MKs can directly modify the pericellular extracellular matrix (ECM), but their main fibrogenic influence comes from coordinating stromal, immune, and endothelial responses. This Review synthesizes evidence linking abnormal MK biology to fibrotic progression and examines its implications for biomarkers and therapy. In normal bone marrow, MKs regulate hematopoietic stem cell quiescence, organize the ECM and vascular niches, and participate in immune regulation. Hematopoiesis driven by mutations in JAK2, CALR, or MPL, together with chronic inflammation, disrupts these functions. Dysplastic MKs release or activate transforming growth factor-β1 (TGF-β1), platelet factor 4 (PF4/CXCL4), and other profibrotic mediators and interact with neutrophils, monocytes, mesenchymal stromal cells, and endothelial cells. These interactions promote stromal activation, monocyte-to-fibrocyte differentiation, vascular and osteogenic remodeling, and ECM accumulation. As disease progresses, collagen cross-linking and altered bone marrow mechanics help stabilize the remodeled niche. Janus kinase inhibitors reduce splenomegaly and symptoms, but pharmacological therapies have not been shown to consistently reverse established bone marrow fibrosis. Durable disease modification will likely require sustained suppression of mutant progenitors and dysplastic MK production together with inhibition of stromal activation, inflammatory signaling, and matrix deposition or cross-linking. Clinical improvement, suppression of abnormal megakaryopoiesis, reduction in profibrotic signaling, and regression of bone marrow fibrosis should therefore be assessed separately using measures matched to each therapeutic mechanism.
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5. A biomarker-driven approach to targeting polyamine depletion in triple negative breast cancer.
5. 针对三阴性乳腺癌中多胺耗竭的生物标志物驱动方法PMID:日期:2026-09-29Triple negative breast cancer (TNBC) is the most aggressive and heterogenous breast cancer subtype. Polyamines are essential for TNBC growth and proliferation; however, therapeutic strategies targeting polyamine metabolism have shown limited efficacy in TNBC. In this study, we demonstrate a biomarker-driven approach to treating TNBC through polyamine depletion. As the rate limiting catabolic enzyme in the polyamine pathway, spermidine/spermine N-acetlytransferase (SAT1) reduces polyamines and generates the metabolite, diacetylspermine. TNBC cell lines, ex vivo tumor slices, and in vivo patient-derived xenograft (PDX) models with low, moderate and high baseline levels of SAT1 were used to determine whether the efficacy of polyamine depletion therapy depends on their SAT1 metabolic phenotype. TNBC with high baseline SAT1 expression was sensitive to the SAT1 agonist N, N-diethylnorspermine (DENSpm) resulting in reduced cell viability, polyamine depletion and elevated diacetylspermine production. Cell viability in moderate baseline SAT1 expressing TNBC was further reduced by combining DENSpm with both therapeutic and subtherapeutic doxorubicin treatment. In vivo, the addition of DENSpm to doxorubicin treatment further attenuated tumor growth in moderate SAT1 expressing TNBC-PDX, which corresponded to a sustained increase in urine diacetylspermine as a biomarker of treatment effectiveness. Mechanism delineating experiments demonstrated that doxorubicin induces SAT1 expression while DENSpm promotes productive splicing, effectively increasing and sustaining SAT1 function, depleting polyamines and increasing diacetylspermine production. In conclusion, these findings suggest that an SAT1-defined metabolic phenotype may enable a precision-guided strategy to effectively target polyamine depletion as a TNBC treatment and that treatment effectiveness may be monitored through evaluation of urine diacetylspermine as a non-invasive biomarker of treatment response.
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6. Genetic orchestration of the primary central nervous system lymphoma microenvironment.
PMID:日期:2026-09-29Primary central nervous system lymphoma (PCNSL) of the CNS is a distinct entity of diffuse large B-cell lymphoma (DLBCL). CNS lymphomas primarily occur in immune-privileged sites and tend to be confined to extranodal locations such as the brain, spinal cord, meninges, and/or eyes. Due to the presence of the blood-brain barrier and the inherent "immune privilege" characteristics of brain tissue, the tumor microenvironment (TME) of PCNSL exhibits unique features. Additionally, genetic factors originating from the lymphoma cells themselves significantly influence the TME. Substantial evidence has demonstrated that PCNSL exhibits highly characteristic molecular genetic alterations, with a mutational profile distinctly different from that of systemic DLBCL. These unique genetic variations collectively shape the malignant biological behavior of PCNSL, including activation of signal transduction, evasion of immune surveillance, and promotion of malignant progression. Here, we synthesize current evidence to conceptualize the genetic-TME axis as a unifying framework for PCNSL biology, wherein tumor-intrinsic genetic alterations and the specialized CNS microenvironment interact bidirectionally to shape immune evasion, tumor evolution, and therapeutic response. We review the distinctive genetic landscape of PCNSL, the cellular and molecular architecture of its TME, and the reciprocal mechanisms linking these compartments during disease progression. Integrating these dimensions may refine molecular stratification, facilitate biomarker-guided therapeutic selection, and inform more rational treatment strategies for PCNSL.
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7. Neural-tumor interactions: bidirectional regulatory mechanisms and nervous system-targeted tumor therapeutic strategies.
PMID:日期:2026-09-24Neural-tumor crosstalk has emerged as a critical frontier in tumor microenvironment research. Central to this field is the dynamic, bidirectional regulatory network between the nervous system and tumor cells that orchestrates malignant progression. This review focuses on tumors arising outside the central nervous system and their bidirectional interactions with peripheral nerves, summarizing the current evidence on the molecular mechanisms underlying these reciprocal interactions. We first examine how neural components modulate tumorigenesis through the release of neuroactive molecules and proteins that activate oncogenic signaling pathways. In particular, neurons and Schwann cells can transmit protumorigenic signals via paracrine signaling, exosome-mediated communication, and the formation of functional neuroneoplastic synapses. Conversely, tumors can actively "hijack" and remodel their neural architecture to promote axonogenesis and neural infiltration while contributing to complications such as cancer pain and paraneoplastic neurological syndromes. We further highlight the pivotal role of neural signaling in reshaping the tumor microenvironment across three interconnected dimensions: the spatial dimension (neural niches), the signaling dimension (bidirectional communication mediated by neuroactive molecules), and the functional dimension (immunometabolic reprogramming). Together, these processes contribute to tumor progression and immune evasion. Building on these insights, therapeutic strategies targeting the neural-tumor interface have shown promising clinical potential. Further characterization of these regulatory networks may identify context-specific drivers of tumorigenesis and progression and inform the development of novel therapeutics targeting neural pathways.
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8. Metabolic-inflammatory index CTI identifies high-risk early-stage natural killer/T-cell lymphoma and informs a novel prognostic model.
PMID:日期:2026-09-16The prognostic heterogeneity of early-stage natural killer/T-cell lymphoma (NKTCL) remains inadequately defined. This study aimed to investigate the prognostic value and potential biological relevance of the metabolic-inflammatory biomarkers in early-stage NKTCL. We conducted a secondary analysis on 166 patients with early-stage NKTCL from a multicenter clinical trial (NCT02631239). C-reactive protein-triglyceride-glucose Index (CTI) was calculated as: 0.412* Ln (CRP [mg/L]) + Ln (TG [mg/dL] × FPG [mg/dL])/2. Cox proportional hazards models and restricted cubic spline analyses were applied to assess the association and dose-response relationship between CTI and overall survival (OS). Mechanistic insights were explored through animal experiments and clinical lymphocyte-subset analyses. Independent prognostic factors were identified using multivariable Cox regression, and a composite prognostic model incorporating CTI, body mass index (BMI), and albumin (ALB) was subsequently developed and internally evaluated. High CTI was independently associated with inferior OS in patients with early-stage NKTCL, with a significant linear dose-response relationship. Patients with high CTI had a higher incidence of B symptoms and elevated lactate dehydrogenase and β2-microglobulin levels. A simplified CTI-BMI-ALB prognostic model demonstrated moderate predictive performance for 1-, 3-, and 5-year OS, with AUCs of 0.71, 0.71, and 0.69, respectively, and an overall C-index of 0.69 (95% CI: 0.59-0.79). In the present cohort, the CTI-BMI-ALB model showed improved discriminative performance compared with conventional prognostic indices and provided additional survival stratification among patients classified as low-risk or favorable-risk by these indices within this cohort. In vivo experiments showed that the Gubra-Amylin NASH diet-induced metabolic-inflammatory state with elevated CTI levels was associated with accelerated lymphoma progression, reduced intratumoral CD8 T-cell infiltration, and increased proportions of Tregs and M2 macrophages. Consistently, clinical lymphocyte-subset analysis confirmed Treg enrichment in patients with high CTI and a positive association between CTI and the proportion of Tregs. CTI is an independent prognostic biomarker in early-stage NKTCL, reflecting systemic metabolic-inflammatory and immune dysregulation. The CTI-BMI-ALB model, which integrates inflammatory, nutritional, and metabolic dimensions, showed potential for complementary risk stratification beyond conventional prognostic indices and warrants further validation before broader clinical application.
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9. Biohybrid M13 phage backpacks for active blood-brain barrier traversal and precision central nervous system leukemia treatment.
PMID:日期:2026-09-16Central nervous system (CNS) leukemia remains a major clinical challenge in acute lymphoblastic leukemia, largely due to the restrictive nature of the blood-brain barrier (BBB), which severely limits therapeutic delivery and contributes to high relapse rates and poor prognosis. Here, we report ALB-phage, a bioengineered anti-leukemia backpack-phage system designed for active BBB navigation and intracranial drug delivery. M13 bacteriophages were genetically engineered to display BBB-homing ligands, forming a high-aspect-ratio biological transport platform (BTP). A leukemia-targeting therapeutic backpack (L-Pak) was constructed by encapsulating methotrexate within lipid nanoparticles fused with leukemia cell membranes, enabling homotypic targeting. The L-Pak was conjugated to the BTP via a matrix metalloproteinase-responsive PLGVR linker, allowing selective cleavage within the cerebrospinal fluid. Owing to its filamentous morphology, ALB-phage achieved efficient BBB translocation predominantly through energy-dependent macropinocytosis with an additional contribution from clathrin-mediated endocytosis. Both in vitro and in vivo studies demonstrate that ALB-phage effectively penetrates the BBB and selectively eradicates leukemia blasts, resulting in marked tumor suppression and a significant extension of median survival from 29 to 40 days in cell-line-derived xenograft models. Collectively, this M13 bacteriophage-based all-in-one platform integrates targeted BBB penetration with homology-mediated cytotoxicity, offering a promising strategy for the treatment of CNS leukemia and other central nervous system malignancies.
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10. Cellular crosstalk of fibroblast-myofibroblast transition in intestinal homeostasis and disease.
10. 肠道稳态与疾病中成纤维细胞-肌成纤维细胞转变的细胞串扰PMID:日期:2026-09-16Fibroblasts are central components of the intestinal microenvironment and can acquire a myofibroblast phenotype through fibroblast-to-myofibroblast transition (FMT), a process linked to increased tissue mechanosensitivity and active extracellular matrix (ECM) remodeling. In this way, FMT participates in normal intestinal homeostasis and repair, but it can also contribute to fibrosis and tumor-associated stromal remodeling when sustained. More importantly, FMT is not a passive process but an active reprogramming event in response to physiological demands or pathological conditions. Its regulation is highly complicated by the temporal and spatial coordination of various intestinal cell types, ultimately determining disease onset and progression. In this context, targeting cellular interaction networks and remodeling the pathological microenvironment may provide opportunities to limit or redirect disease-associated stromal remodeling. In this review, we summarize the key intercellular dialogs that regulate FMT during the onset and progression of intestinal disorders and further analyze their regulatory mechanisms. Moreover, we discuss emerging therapies targeting cellular interaction networks to provide a new framework and research focus for treating inflammatory bowel disease (IBD), intestinal fibrosis, and related tumors.