BIOMARKER RESEARCH 是一本开放获取、同行评审的期刊，涵盖了生物标志物研究的所有方面。生物标志物研究旨在发表与所有生物医学学科的生物标志物研究相关的原始发现、新概念、评论和评论。生物标志物的研究随着个性化医疗和个人健康的发展而迅速发展。在药物发现/开发以及疾病诊断、治疗、预后和预防中，生物标志物的识别和验证在基因组时代发挥着至关重要的作用。凭借从提交到出版的快速周转时间以及读者的在线反馈，BIOMARKER RESEARCH 致力于快速传播新发现和新知识。

Biomarker Research is an open access, peer-reviewed journal that covers all aspects of biomarker research. The journal aims to publish original findings, new concepts, reviews, and commentaries related to biomarker studies across all biomedical disciplines. The research on biomarkers has rapidly evolved alongside the advancements in personalized medicine and individual health. The identification and validation of biomarkers play a crucial role in drug discovery and development, as well as in disease diagnosis, treatment, prognosis, and prevention in the genomic era. Biomarker Research is committed to the rapid dissemination of new discoveries and knowledge, offering a quick turnaround time from submission to publication and encouraging online feedback from readers.

《Biomarker Research》是一本开放获取、同行评审的期刊，涵盖生物标志物研究的各个方面。该期刊旨在发表与所有生物医学学科相关的生物标志物研究的原创发现、新概念、评论和综述。随着个性化医疗和个人健康的快速发展，生物标志物的研究也在不断进步。在药物发现与开发、疾病诊断、治疗、预后和预防中，生物标志物的识别与验证在基因组时代扮演着至关重要的角色。《Biomarker Research》致力于快速传播新发现和新知识，提供从提交到出版的快速周转时间，并鼓励读者在线反馈。

Biomarker Research

Abstract Background Cerebral cavernous malformations (CCMs) are vascular abnormalities associated with deregulated angiogenesis. Their pathogenesis and optimal treatment remain unclear. This study aims to investigate the molecular signatures of cuproptosis, a newly identified type of cell death, associated with CCMs development. Methods Bulk RNA sequencing (RNA-seq) from 15 CCM and 6 control samples were performed with consensus clustering and clustered to two subtypes based on expression levels of cuproptosis-related genes (CRGs). Differentially expressed genes and immune infiltration between subtypes were then identified. Machine learning algorithms including the least absolute shrinkage and selection operator and random forest were employed to screen for hub genes for CCMs associated with cuproptosis. Furthermore, Pathway enrichment and correlation analysis were used to explore the functions of hub genes and their association with immune phenotypes in CCMs. An external dataset was then employed for validation. Finally, employing the Cellchat algorithm on a single-cell RNA-seq dataset, we explored potential mechanisms underlying the participation of these hub genes in cell-cell communication in CCMs. Results Our study revealed two distinct CCM subtypes with differential pattern of CRG expression and immune infiltration. Three hub genes (BTBD10, PFDN4, and CEMIP) were identified and validated, which may significantly associate with CCM pathogenesis. These genes were found to be significantly upregulated in CCM endothelial cells (ECs) and were validated through immunofluorescence and western blot analysis. Single-cell RNA-seq analysis revealed the cellular co-expression patterns of these hub genes, particularly highlighting the high expression of BTBD10 and PFDN4 in ECs. Additionally, a significant co-localization was also observed between BTBD10 and the pivotal cuproptosis gene FDX1 in Mki67+ tip cells, indicating the crucial role of cuproptosis for angiogenesis in CCMs. The study also explored the cell-cell communication between subcluster of ECs expressing these hub genes and immune cells, particularly M2 macrophages, suggesting a role for these interactions in CCM pathogenesis. Conclusion This study identifies molecular signatures linking cuproptosis to CCMs pathogenesis. Three hub genes—PFDN4, CEMIP, and BTBD10—may influence disease progression by modulating immunity. Further research is needed to understand their precise disease mechanisms and evaluate their potential as biomarkers or therapeutic targets for CCMs.

Chengwei Chen

Yuting Bao

Sihan Ju

Conglin Jiang

Xiang Zou

Xin Zhang

Liang Chen

Single-cell and bulk RNA-seq unveils the immune infiltration landscape associated with cuproptosis in cerebral cavernous malformations

单细胞和批量RNA测序揭示了与脑动静脉畸形相关的铜死亡免疫浸润景观

Abstract Background and objective Breast cancer is a leading cause of morbidity and mortality among women worldwide. This study aimed to assess the global burden of breast cancer and identify attributable risk factors across 204 countries and territories from 1990 to 2021. Methods Using data from the Global Burden of Disease Study 2021, we analyzed the incidence, mortality, disability-adjusted life years (DALYs), and risk factors associated with breast cancer. We obtained and analyzed the age-standardized incidence rate (ASIR), age-standardized death rate (ASDR), and age-standardized DALYs rate from 1990 to 2021. We assessed geographical variations and the impact of the Socio-demographic Index (SDI) using regression analysis and stratification by SDI quintiles. Additionally, we estimated the risk factors attributable to breast cancer deaths and DALYs using the comparative risk assessment framework of the GBD study. Results Globally, breast cancer incident cases increased from 875,657 in 1990 to 2,121,564 in 2021. The ASIR rose from 16.42 to 26.88 per 100,000 (95% CI: 1.54–1.60). High SDI regions showed the highest ASIR (66.89 per 100,000 in 2021), while Low SDI regions had the lowest (6.99 per 100,000 in 2021). The global ASDR decreased from 10.42 to 8.54 per 100,000, and the age-standardized DALYs rate decreased from 313.36 to 261.5 per 100,000 between 1990 and 2021. However, these improvements were not uniform across SDI regions. Risk factors included high body-mass index, alcohol use, tobacco, and high fasting plasma glucose, with variations across SDI regions. Conclusion The global burden of breast cancer has increased significantly from 1990 to 2021, with disparities observed across SDI regions. While high SDI areas show improvements in mortality and DALYs, lower SDI regions face increasing burdens. Targeted interventions addressing modifiable risk factors and improving healthcare access in less developed regions are crucial for reducing the global impact of breast cancer.

Rui Sha

Xiang-meng Kong

Xin-yu Li

Ya-bing Wang

Global burden of breast cancer and attributable risk factors in 204 countries and territories, from 1990 to 2021: results from the Global Burden of Disease Study 2021

204个国家和地区1990年至2021年乳腺癌的全球负担及可归因风险因素：2021年全球疾病负担研究结果

Immunotherapy has shown promising anti-tumor effects across various tumors, yet it encounters challenges from the inhibitory tumor immune microenvironment (TIME). Infiltrating regulatory T cells (Tregs) are important contributors to immunosuppressive TIME, limiting tumor immunosurveillance and blocking effective anti-tumor immune responses. Although depletion or inhibition of systemic Tregs enhances the anti-tumor immunity, autoimmune sequelae have diminished expectations for the approach. Herein, we summarize emerging strategies, specifically targeting tumor-infiltrating (TI)-Tregs, that elevate the capacity of organisms to resist tumors by reprogramming their phenotype. The regulatory mechanisms of Treg reprogramming are also discussed as well as how this knowledge could be utilized to develop novel and effective cancer immunotherapies.

Zhaokai Zhou

Jiaxin Xu

Shutong Liu

Yingying Lv

Ruiqi Zhang

Xing Zhou

Yuyuan Zhang

Siyuan Weng

Hui Xu

Yuhao Ba

Anning Zuo

Xinwei Han

Zaoqu Liu

Biomark Res

Infiltrating treg reprogramming in the tumor immune microenvironment and its optimization for immunotherapy

肿瘤免疫微环境中浸润性调节性T细胞的重编程及其在免疫治疗中的优化

Abstract Ferroptosis is a novel form of programmed cell death caused by damage to lipid membranes due to the accumulation of lipid peroxides in response to various stimuli, such as high levels of iron, oxidative stress, metabolic disturbance, etc. Sugar, lipid, amino acid, and iron metabolism are crucial in regulating ferroptosis. The solute carrier transporters (SLCs) family, known as the “metabolic gating” of cells, is responsible for transporting intracellular nutrients and metabolites. Recent studies have highlighted the significant role of SLCs family members in ferroptosis by controlling the transport of various nutrients. Here, we summarized the function and mechanism of SLCs in ferroptosis regulated by ion, metabolic control of nutrients, and multiple signaling pathways, with a focus on SLC–related transporters that primarily transport five significant components: glucose, amino acid, lipid, trace metal ion, and other ion. Furthermore, the potential clinical applications of targeting SLCs with ferroptosis inducers for various diseases, including tumors, are discussed. Overall, this paper delves into the novel roles of the SLCs family in ferroptosis, aiming to enhance our understanding of the regulatory mechanisms of ferroptosis and identify new therapeutic targets for clinical applications.

Li-Li Sun

Hai-Yan He

Wei Li

Wei-Lin Jin

Yi-Ju Wei

The solute carrier transporters (SLCs) family in nutrient metabolism and ferroptosis

溶质载体转运蛋白（SLCs）家族在营养代谢和铁死亡中的作用

Treatment based on immune checkpoint blockade has revolutionized cancer therapy. Despite the remarkable success achieved and the preclinical development of multiple checkpoint inhibitors targeting other checkpoints, only antibodies targeting the PD-1/PD-L1 axis and CTLA-4 have been approved for patient treatment, especially in solid tumors. Currently, with the approval of relatlimab, a LAG-3 blocking antibody, a third player, has been used in the fight against cancer. The endorsement of relatlimab marks a significant milestone in cancer immunotherapy, opening new avenues for combination therapies and enhancing treatment outcomes. However, the complex biology of LAG-3 may hinder its full development as a therapeutic alternative. In this review, we provide in-depth insight into the biology of LAG-3 and its current and future development in cancer treatment.

Alejandra Martínez-Pérez

Rocío Granda-Díaz

Candelaria Aguilar-García

Christian Sordo-Bahamonde

Segundo Gonzalez

Deciphering LAG-3: unveiling molecular mechanisms and clinical advancements

解密LAG-3：揭示分子机制与临床进展

Abstract The leukocyte immunoglobulin-like receptor B (LILRB) proteins, characterized by their transmembrane nature and canonical immunoreceptor tyrosine-based inhibitory motifs (ITIM) signaling, play a pivotal role in maintaining immune homeostasis and are implicated in the pathogenesis of various disease states. This comprehensive review will focus on the intricate involvement of the LILRB family in hematologic malignancies. These receptors have emerged as valuable diagnostic and prognostic biomarkers in leukemia, lymphoma, and myeloma. Beyond their prognostic implications, LILRBs actively shape the immune microenvironment and directly influence the disease pathogenesis of hematologic malignancies. Furthermore, their identification as potential therapeutic targets offer a promising avenue for precision medicine strategies in the treatment of these disorders. Currently, multiple LILRB directed therapies are in the preclinical and clinical trial pipelines. This review underscores the multifaceted role of the LILRB family in hematologic malignancies, highlighting their significance from diagnostic and prognostic perspectives to their broader impact on disease pathophysiology and as valuable therapeutic targets.

Alan Hodges

Rachel Dubuque

Shu-Hsia Chen

Ping-Ying Pan

The LILRB family in hematologic malignancies: prognostic associations, mechanistic considerations, and therapeutic implications

血液系统恶性肿瘤中的LILRB家族：预后关联、机制考量及治疗意义

Abstract Harnessing the power of the immune system to target cancer cells is one of the most appealing approaches for cancer therapy. Among these immunotherapies, messenger ribonucleic acid (mRNA) cancer vaccines are worthy of consideration, as they have demonstrated promising results in clinical trials. These vaccines have proven to be safe and well-tolerated. They can be easily mass-produced in a relatively short time and induce a systemic immune response effective against both the primary tumor and metastases. Transcripts encoding immunomodulatory molecules can also be incorporated into the mRNA, enhancing its efficacy. On the other hand, there are some challenges associated with their application, including mRNA instability, insufficient uptake by immune cells, and intrinsic immunogenicity, which can block mRNA translation. Many innovations have been suggested to overcome these obstacles, including structural modification (such as 5’ cap modification), optimizing delivery vehicles (especially dendritic cells (DCs) and nanoparticles), and using antigens that can enhance immunogenicity by circumventing tolerance mechanisms. A popular approach is to combine mRNA cancer vaccines with traditional and novel cancer treatments like chemotherapy, radiotherapy, and immune checkpoint blockade (ICB). They are most efficacious when combined with other therapies like ICBs. There is still a long way to go before these vaccines enter the standard of care for cancer patients, but with the incredible pace of development in this field, their clinical application will soon be witnessed. This review highlights the recent advances and challenges of mRNA cancer vaccines. Finally, some of the most prominent clinical applications of these vaccines will be reviewed.

Alireza Shariati

Pouria Khani

Farzad Nasri

Hamed Afkhami

Arya Khezrpour

Sina Kamrani

Fatemeh Shariati

Sajad Alavimanesh

Mohammad Hossein Modarressi

mRNA cancer vaccines from bench to bedside: a new era in cancer immunotherapy

从实验室到临床：癌症免疫治疗的新时代——mRNA癌症疫苗

Abstract The TAM receptor tyrosine kinase family member AXL plays critical roles in tissue homeostasis, survival, chemoresistance, and motility. This study investigates the receptor expression in six AML cell lines and bone marrow myeloblasts from 25 patients with myeloid neoplasms. We found that AXL expression was generally absent or very low in AML myeloblasts. These findings suggest that the efficacy of AXL inhibitors may not depend on AXL positivity but rather on alternative therapeutic mechanisms, such as inducing significant immune responses.

Pia Aehnlich

Katharina Leuchte

Claudia Schöllkopf

Sara Fresnillo Salo

Tina J. Seremet

Estrid Høgdall

Özcan Met

Kirsten Grønbaek

Per thor Straten

AXL in myeloid malignancies – an elusive target?

髓系恶性肿瘤中的AXL——一个难以捉摸的目标？

Xingliang Qin

Ruoxi Niu

Yongyao Tan

Yuxin Huang

Weishu Ren

Weiwei Zhou

Huiquan Wu

Junlong Zhang

Mingze Xu

Xiang Zhou

Hongyu Guan

Xun Zhu

Yu Chen

Kaiyuan Cao

Correction: Exosomal PSM-E inhibits macrophage M2 polarization to suppress prostate cancer metastasis through the RACK1 signaling axis

更正：外泌体PSM-E通过RACK1信号轴抑制巨噬细胞M2极化以抑制前列腺癌转移

Abstract Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) technology is a groundbreaking and dynamic molecular tool for DNA and RNA “surgery”. CRISPR/Cas9 is the most widely applied system in oncology research. It is a major advancement in genome manipulation due to its precision, efficiency, scalability and versatility compared to previous gene editing methods. It has shown great potential not only in the targeting of oncogenes or genes coding for immune checkpoint molecules, and in engineering T cells, but also in targeting epigenomic disturbances, which contribute to cancer development and progression. It has proven useful for detecting genetic mutations, enabling the large-scale screening of genes involved in tumor onset, progression and drug resistance, and in speeding up the development of highly targeted therapies tailored to the genetic and immunological profiles of the patient’s tumor. Furthermore, the recently discovered Cas12 and Cas13 systems have expanded Cas9-based editing applications, providing new opportunities in the diagnosis and treatment of cancer. In addition to traditional cis-cleavage, they exhibit trans-cleavage activity, which enables their use as sensitive and specific diagnostic tools. Diagnostic platforms like DETECTR, which employs the Cas12 enzyme, that cuts single-stranded DNA reporters, and SHERLOCK, which uses Cas12, or Cas13, that specifically target and cleave single-stranded RNA, can be exploited to speed up and advance oncological diagnostics. Overall, CRISPR platform has the great potential to improve molecular diagnostics and the functionality and safety of engineered cellular medicines. Here, we will emphasize the potentially transformative impact of CRISPR technology in the field of oncology compared to traditional treatments, diagnostic and prognostic approaches, and highlight the opportunities and challenges raised by using the newly introduced CRISPR-based systems for cancer diagnosis and therapy.

Emma Di Carlo

Carlo Sorrentino

State of the art CRISPR-based strategies for cancer diagnostics and treatment

基于CRISPR的癌症诊断和治疗最新策略

Abbreviation	Biomark Res
Journal Impact	9.36
Quartiles(Global)	ONCOLOGY(Q1)

ISSN	2050-7771
h-index	48

Publication Information	Publisher: BioMed Central Ltd，Publishing cycle: ，Journal Type: journal，Open Access Journals: Yes
Basic data	Year of publication: 2013，Proportion of original research papers: 37.04%，Self Citation Rate:1.10%， Gold OA Rate: 100.00%
Journal Fees	$3690Details
Average review cycle	网友分享经验：10 Weeks

Biomarker Research

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