Journal of Biomedical Research最新文献_第2页

Unlocking the novel activation mechanism of human IL-18. 揭示人类 IL-18 的新型激活机制。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-06-25 DOI: 10.7555/JBR.38.20240154

Yingchao Hu, Yuxian Song, Shuo Yang

引用次数: 0

Timosaponin AⅢ induces drug-metabolizing enzymes by activating constitutive androstane receptor (CAR) via dephosphorylation of the EGFR signaling pathway. 噻吗皂苷 AⅢ通过表皮生长因子受体（EGFR）信号通路的去磷酸化激活组成型雄烷受体（CAR），从而诱导药物代谢酶。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-31 DOI: 10.7555/JBR.38.20240055

Muhammad Zubair Hafiz, Jie Pan, Zhiwei Gao, Ying Huo, Haobin Wang, Wei Liu, Jian Yang

{"title":"Timosaponin AⅢ induces drug-metabolizing enzymes by activating constitutive androstane receptor (CAR) via dephosphorylation of the EGFR signaling pathway.","authors":"Muhammad Zubair Hafiz, Jie Pan, Zhiwei Gao, Ying Huo, Haobin Wang, Wei Liu, Jian Yang","doi":"10.7555/JBR.38.20240055","DOIUrl":"10.7555/JBR.38.20240055","url":null,"abstract":"The current study aimed to assess the effect of timosaponin AⅢ (T-AⅢ) on drug-metabolizing enzymes during anticancer therapy. The in vivo experiments were conducted on nude and ICR mice. Following a 24-day administration of T-AⅢ, the nude mice exhibited an induction of CYP2B10, MDR1, and CYP3A11 expression in the liver tissues. In the ICR mice, the expression levels of CYP2B10 and MDR1 increased after a three-day T-AⅢ administration. The in vitro assessments with HepG2 cells revealed that T-AⅢ induced the expression of CYP2B6, MDR1, and CYP3A4, along with constitutive androstane receptor (CAR) activation. Treatment with CAR siRNA reversed the T-AⅢ-induced increases in CYP2B6 and CYP3A4 expression. Furthermore, other CAR target genes also showed a significant increase in the expression. The up-regulation of murine CAR was observed in the liver tissues of both nude and ICR mice. Subsequent findings demonstrated that T-AⅢ activated CAR by inhibiting ERK1/2 phosphorylation, with this effect being partially reversed by the ERK activator t-BHQ. Inhibition of the ERK1/2 signaling pathway was also observed in vivo. Additionally, T-AⅢinhibited the phosphorylation of EGFR at Tyr1173 and Tyr845, and suppressed EGF-induced phosphorylation of EGFR, ERK, and CAR. In the nude mice, T-AⅢ also inhibited EGFR phosphorylation. These results collectively indicate that T-AⅢ is a novel CAR activator through inhibition of the EGFR pathway.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"382-396"},"PeriodicalIF":2.2,"publicationDate":"2024-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141179665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of cell surface markers for acute myeloid leukemia prognosis based on multi-model analysis. 基于多模型分析鉴定急性髓性白血病预后的细胞表面标志物

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240065

Jiaqi Tang, Lin Luo, Bakwatanisa Bosco, Ning Li, Bin Huang, Rongrong Wu, Zihan Lin, Ming Hong, Wenjie Liu, Lingxiang Wu, Wei Wu, Mengyan Zhu, Quanzhong Liu, Peng Xia, Miao Yu, Diru Yao, Sali Lv, Ruohan Zhang, Wentao Liu, Qianghu Wang, Kening Li

{"title":"Identification of cell surface markers for acute myeloid leukemia prognosis based on multi-model analysis.","authors":"Jiaqi Tang, Lin Luo, Bakwatanisa Bosco, Ning Li, Bin Huang, Rongrong Wu, Zihan Lin, Ming Hong, Wenjie Liu, Lingxiang Wu, Wei Wu, Mengyan Zhu, Quanzhong Liu, Peng Xia, Miao Yu, Diru Yao, Sali Lv, Ruohan Zhang, Wentao Liu, Qianghu Wang, Kening Li","doi":"10.7555/JBR.38.20240065","DOIUrl":"10.7555/JBR.38.20240065","url":null,"abstract":"Given the extremely high inter-patient heterogeneity of acute myeloid leukemia (AML), the identification of biomarkers for prognostic assessment and therapeutic guidance is critical. Cell surface markers (CSMs) have been shown to play an important role in AML leukemogenesis and progression. In the current study, we evaluated the prognostic potential of all human CSMs in 130 AML patients from The Cancer Genome Atlas (TCGA) based on differential gene expression analysis and univariable Cox proportional hazards regression analysis. By using multi-model analysis, including Adaptive LASSO regression, LASSO regression, and Elastic Net, we constructed a 9-CSMs prognostic model for risk stratification of the AML patients. The predictive value of the 9-CSMs risk score was further validated at the transcriptome and proteome levels. Multivariable Cox regression analysis showed that the risk score was an independent prognostic factor for the AML patients. The AML patients with high 9-CSMs risk scores had a shorter overall and event-free survival time than those with low scores. Notably, single-cell RNA-sequencing analysis indicated that patients with high 9-CSMs risk scores exhibited chemotherapy resistance. Furthermore, PI3K inhibitors were identified as potential treatments for these high-risk patients. In conclusion, we constructed a 9-CSMs prognostic model that served as an independent prognostic factor for the survival of AML patients and held the potential for guiding drug therapy.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"397-412"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

p53 exerts anticancer effects by regulating enhancer formation and activity. p53 通过调节增强子的形成和活性发挥抗癌作用。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230206

Shuhan Chen, Xuchun Wang, Nan Yang, Yuechi Song, He Cheng, Yujie Sun

{"title":"p53 exerts anticancer effects by regulating enhancer formation and activity.","authors":"Shuhan Chen, Xuchun Wang, Nan Yang, Yuechi Song, He Cheng, Yujie Sun","doi":"10.7555/JBR.37.20230206","DOIUrl":"10.7555/JBR.37.20230206","url":null,"abstract":"The abnormality of the p53 tumor suppressor is crucial in lung cancer development, because p53 regulates target gene promoters to combat cancer. Recent studies have shown extensive p53 binding to enhancer elements. However, whether p53 exerts a tumor suppressor role by shaping the enhancer landscape remains poorly understood. In the current study, we employed several functional genomics approaches to assess the enhancer activity at p53 binding sites throughout the genome based on our established TP53 knockout (KO) human bronchial epithelial cells (BEAS-2B). A total of 943 active regular enhancers and 370 super-enhancers (SEs) disappeared upon the deletion of p53, indicating that p53 modulates the activity of hundreds of enhancer elements. We found that one p53-dependent SE, located on chromosome 9 and designated as KLF4-SE, regulated the expression of the Krüppel-like factor 4 ( KLF4) gene. Furthermore, the deletion of p53 significantly decreased the KLF4-SE enhancer activity and the KLF4 expression, but increased colony formation ability in the nitrosamines 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone-induced cell transformation model. Subsequently, in TP53 KO cells, the overexpression of KLF4 partially reversed the increased clonogenic capacity caused by p53 deficiency. Consistently, KLF4 expression also decreased in lung cancer tissues and cell lines. It appeared that overexpression of KLF4 significantly suppressed the proliferation and migration of lung cancer cells. Collectively, our results suggest that the regulation of enhancer formation and activity by p53 is an integral component of the p53 tumor suppressor function. Therefore, our findings offer some novel insights into the regulation mechanism of p53 in lung oncogenesis and introduce a new strategy for screening therapeutic targets.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"334-347"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phase separation and transcriptional regulation in cancer development. 癌症发展过程中的相分离和转录调控。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230214

Yan Gu, Ke Wei, Jun Wang

引用次数: 0

Genetic variants in C1GALT1 are associated with gastric cancer risk by influencing immune infiltration. C1GALT1 基因变异与胃癌风险和免疫浸润有关。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230161

Mengfan Guo, Jingyuan Liu, Yujuan Zhang, Jingjing Gu, Junyi Xin, Mulong Du, Haiyan Chu, Meilin Wang, Hanting Liu, Zhengdong Zhang

{"title":"Genetic variants in C1GALT1 are associated with gastric cancer risk by influencing immune infiltration.","authors":"Mengfan Guo, Jingyuan Liu, Yujuan Zhang, Jingjing Gu, Junyi Xin, Mulong Du, Haiyan Chu, Meilin Wang, Hanting Liu, Zhengdong Zhang","doi":"10.7555/JBR.37.20230161","DOIUrl":"10.7555/JBR.37.20230161","url":null,"abstract":"Core 1 synthase glycoprotein-N-acetylgalactosamine 3-β-galactosyltransferase 1 (C1GALT1) is known to play a critical role in the development of gastric cancer, but few studies have elucidated associations between genetic variants in C1GALT1 and gastric cancer risk. By using the genome-wide association study data from the database of Genotype and Phenotype (dbGAP), we evaluated such associations with a multivariable logistic regression model and identified that the rs35999583 G>C in C1GALT1 was associated with gastric cancer risk (odds ratio, 0.83; 95% confidence interval [CI], 0.75-0.92; P = 3.95 × 10 -4). C1GALT1 mRNA expression levels were significantly higher in gastric tumor tissues than in normal tissues, and gastric cancer patients with higher C1GALT1 mRNA levels had worse overall survival rates (hazards ratio, 1.33; 95% CI, 1.05-1.68; P log-rank = 1.90 × 10 -2). Furthermore, we found that C1GALT1 copy number differed in various immune cells and that C1GALT1 mRNA expression levels were positively correlated with the infiltrating levels of CD4 + T cells and macrophages. These results suggest that genetic variants of C1GALT1 may play an important role in gastric cancer risk and provide a new insight for C1GALT1 into a promising predictor of gastric cancer susceptibility and immune status.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"348-357"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300523/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells via regulating β-catenin activation and EMT pathways. 环肽moroidin通过调节β-catenin激活和EMT通路抑制胶质母细胞瘤细胞形成的血管生成模拟。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240015

Pengxiang Min, Yingying Li, Cuirong Wang, Junting Fan, Shangming Liu, Xiang Chen, Yamin Tang, Feng Han, Aixia Zhang, Lili Feng

{"title":"Cyclopeptide moroidin inhibits vasculogenic mimicry formed by glioblastoma cells via regulating β-catenin activation and EMT pathways.","authors":"Pengxiang Min, Yingying Li, Cuirong Wang, Junting Fan, Shangming Liu, Xiang Chen, Yamin Tang, Feng Han, Aixia Zhang, Lili Feng","doi":"10.7555/JBR.38.20240015","DOIUrl":"10.7555/JBR.38.20240015","url":null,"abstract":"Glioblastoma (GBM) is a highly vascularized malignant brain tumor with poor clinical outcomes. Vasculogenic mimicry (VM) formed by aggressive GBM cells is an alternative approach for tumor blood supply and contributes to the failure of anti-angiogenic therapy. To date, there is still a lack of effective drugs that target VM formation in GBM. In the present study, we evaluated the effects of the plant cyclopeptide moroidin on VM formed by GBM cells and investigated its underlying molecular mechanisms. Moroidin significantly suppressed cell migration, tube formation, and the expression levels of α-smooth muscle actin and matrix metalloproteinase-9 in human GBM cell lines at sublethal concentrations. The RNA sequencing data suggested the involvement of the epithelial-mesenchymal transition (EMT) pathway in the mechanism of moroidin. Exposure to moroidin led to a concentration-dependent decrease in the expression levels of the EMT markers N-cadherin and vimentin in GBM cells. Moreover, moroidin significantly reduced the level of phosphorylated extracellular signal-regulated protein kinase (p-ERK) and inhibited the activation of β-catenin. Finally, we demonstrated that the plant cyclopeptide moroidin inhibited VM formation by GBM cells through inhibiting the ERK/β-catenin-mediated EMT. Therefore, our study indicates a potential application of moroidin as an anti-VM agent in the treatment of GBM.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"322-333"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161372","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic variation of circHIBADH enhances prostate cancer risk through regulating HNRNPA1-related RNA splicing. circHIBADH的基因变异通过调节HNRNPA1相关的RNA剪接提高了患前列腺癌的风险。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240030

Yifei Cheng, Rongjie Shi, Shuai Ben, Silu Chen, Shuwei Li, Junyi Xin, Meilin Wang, Gong Cheng

{"title":"Genetic variation of circHIBADH enhances prostate cancer risk through regulating HNRNPA1-related RNA splicing.","authors":"Yifei Cheng, Rongjie Shi, Shuai Ben, Silu Chen, Shuwei Li, Junyi Xin, Meilin Wang, Gong Cheng","doi":"10.7555/JBR.38.20240030","DOIUrl":"10.7555/JBR.38.20240030","url":null,"abstract":"The current study aimed to investigate associations of circRNAs and related genetic variants with the risk of prostate cancer (PCa) as well as to elucidate biological mechanisms underlying the associations. We first compared expression levels of circRNAs between 25 paired PCa and adjacent normal tissues to identify risk-associated circRNAs by using the MiOncoCirc database. We then used logistic regression models to evaluate associations between genetic variants in candidate circRNAs and PCa risk among 4662 prostate cancer patients and 3114 healthy controls, and identified circHIBADH rs11973492 T>C as a significant risk-associated variant (odds ratio = 1.20, 95% confidence interval: 1.08-1.34, P = 7.06 × 10 -4) in a dominant genetic model, which altered the secondary structure of the corresponding RNA chain. In the in silico analysis, we found that circHIBADH sponged and silenced 21 RNA-binding proteins (RBPs) enriched in the RNA splicing pathway, among which HNRNPA1 was identified and validated as a hub RBP using an external RNA-sequencing data as well as the in-house (four tissue samples) and publicly available single-cell transcriptomes. Additionally, we demonstrated that HNRNPA1 influenced hallmarks including MYC target, DNA repair, and E2F target signaling pathways, thereby promoting carcinogenesis. In conclusion, genetic variants in circHIBADH may act as sponges and inhibitors of RNA splicing-associated RBPs including HNRNPA1, playing an oncogenic role in PCa.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"358-368"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mycobacterium smegmatis enhances shikonin-induced immunogenic cell death-an efficient in situ tumor vaccine strategy. 烟肉分枝杆菌可增强志贺宁诱导的免疫原性细胞死亡--一种高效的原位肿瘤疫苗策略。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.38.20240049

Zhaoye Qian, Zhe Zhang, Lanqi Cen, Yaohua Ke, Jie Shao, Manman Tian, Baorui Liu

{"title":"Mycobacterium smegmatis enhances shikonin-induced immunogenic cell death-an efficient in situ tumor vaccine strategy.","authors":"Zhaoye Qian, Zhe Zhang, Lanqi Cen, Yaohua Ke, Jie Shao, Manman Tian, Baorui Liu","doi":"10.7555/JBR.38.20240049","DOIUrl":"10.7555/JBR.38.20240049","url":null,"abstract":"Tumor vaccines are a promising avenue in cancer immunotherapy. Despite the progress in targeting specific immune epitopes, tumor cells lacking these epitopes can evade the treatment. Here, we aimed to construct an efficient in situ tumor vaccine called Vac-SM, utilizing shikonin (SKN) to induce immunogenic cell death (ICD) and Mycobacterium smegmatis as an immune adjuvant to enhance in situ tumor vaccine efficacy. SKN showed a dose-dependent and time-dependent cytotoxic effect on the tumor cell line and induced ICD in tumor cells as evidenced by the CCK-8 assay and the detection of the expression of relevant indicators, respectively. Compared with the control group, the in situ Vac-SM injection in mouse subcutaneous metastatic tumors significantly inhibited tumor growth and distant tumor metastasis, while also improving survival rates. Mycobacterium smegmatis effectively induced maturation and activation of bone marrow-derived dendritic cells (DCs), and in vivo tumor-draining lymph nodes showed an increased maturation of DCs and a higher proportion of effector memory T-cell subsets with the Vac-SM treatment, based on flow cytometry analysis results. Collectively, the Vac-SM vaccine effectively induces ICD, improves antigen presentation by DCs, activates a specific systemic antitumor T-cell immune response, exhibits a favorable safety profile, and holds the promise for clinical translation for local tumor immunotherapy.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"369-381"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300524/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Potential clinical application of microRNAs in bladder cancer. 微RNA在膀胱癌中的潜在临床应用。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-05-29 DOI: 10.7555/JBR.37.20230245

Pei Wang, Xiaowei Wei, Xiaojun Qu, Yefei Zhu

{"title":"Potential clinical application of microRNAs in bladder cancer.","authors":"Pei Wang, Xiaowei Wei, Xiaojun Qu, Yefei Zhu","doi":"10.7555/JBR.37.20230245","DOIUrl":"10.7555/JBR.37.20230245","url":null,"abstract":"Bladder cancer (BC) is the tenth most prevalent malignancy globally, presenting significant clinical and societal challenges because of its high incidence, rapid progression, and frequent recurrence. Presently, cystoscopy and urine cytology serve as the established diagnostic methods for BC. However, their efficacy is limited by their invasive nature and low sensitivity. Therefore, the development of highly specific biomarkers and effective non-invasive detection strategies is imperative for achieving a precise and timely diagnosis of BC, as well as for facilitating an optimal tumor treatment and an improved prognosis. microRNAs (miRNAs), short noncoding RNA molecules spanning around 20-25 nucleotides, are implicated in the regulation of diverse carcinogenic pathways. Substantially altered miRNAs form robust functional regulatory networks that exert a notable influence on the tumorigenesis and progression of BC. Investigations into aberrant miRNAs derived from blood, urine, or extracellular vesicles indicate their potential roles as diagnostic biomarkers and prognostic indicators in BC, enabling miRNAs to monitor the progression and predict the recurrence of the disease. Simultaneously, the investigation centered on miRNA as a potential therapeutic agent presents a novel approach for the treatment of BC. This review comprehensively analyzes biological roles of miRNAs in tumorigenesis and progression, and systematically summarizes their potential as diagnostic and prognostic biomarkers, as well as therapeutic targets for BC. Additionally, we evaluate the progress made in laboratory techniques within this field and discuss the prospects.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"289-306"},"PeriodicalIF":2.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11300522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0