Biomedicine & Pharmacotherapy最新文献_第10页

Empagliflozin attenuates hypoxia-induced heart failure of zebrafish embryos via influencing MMP13 expression Empagliflozin 通过影响 MMP13 的表达减轻缺氧诱发的斑马鱼胚胎心力衰竭

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-26 DOI: 10.1016/j.biopha.2024.117453

{"title":"Empagliflozin attenuates hypoxia-induced heart failure of zebrafish embryos via influencing MMP13 expression","authors":"","doi":"10.1016/j.biopha.2024.117453","DOIUrl":"10.1016/j.biopha.2024.117453","url":null,"abstract":"<div><h3>Background</h3><div>Today, sodium glucose co-transporter 2 (SGLT2) inhibitors are more than diabetes drugs. They are also indicated in chronic heart failure (HF) treatment in both diabetic and non-diabetic patients, independently of the ejection fraction. Multiple mechanisms have been suggested behind the cardioprotective effects of SGLT2 inhibitors. However, the underlying mechanisms still remain largely unexplored. Here, we used a zebrafish embryo model to search for new potential players whereby SGLT2 inhibitors attenuate HF.</div></div><div><h3>Methods</h3><div>HF in zebrafish embryos was caused exposing them to chemically induced hypoxia. As a SGLT2 inhibitor, we used empagliflozin. Its effect on hypoxia-induced HF of the embryos was evaluated using video microscopy and calculation of fractional shortening (FS) of embryos´ hearts. RT-qPCR of brain natriuretic peptide (<em>bnp</em>) expression was also used to examine empagliflozin´s effect on HF. Transcriptome analysis of total RNA of the embryos was performed to search for new potential mechanisms contributing to the beneficial effect of empagliflozin on HF.</div></div><div><h3>Results</h3><div>Empagliflozin significantly attenuated hypoxia-induced HF of zebrafish embryos as shown with improved FS of the hearts and decreased <em>bnp</em> expression. Transcriptome analysis revealed that the improvement of HF in response to empagliflozin was accompanied with decreased <em>matrix metalloproteinase 13a</em> (<em>mmp13a</em>) expression. Treatment of hypoxia-induced embryos with MMP13 inhibitor ameliorated the impaired heart function accordingly to the effect of empagliflozin. MMP13 inhibitor was not toxic to the embryos.</div></div><div><h3>Conclusions</h3><div>Our study shows that empagliflozin´s favorable effect on attenuating HF is mediated via MMP13. MMP13 provides a novel option when developing new therapeutics for HF treatment.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142322041","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Targeting mast cell activation alleviates anti-MHC I antibody and LPS-induced TRALI in mice by pharmacologically blocking the TLR3 and MAPK pathway 通过药理阻断 TLR3 和 MAPK 通路，以肥大细胞活化为目标，缓解抗 MHC I 抗体和 LPS 引起的小鼠 TRALI

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117456

{"title":"Targeting mast cell activation alleviates anti-MHC I antibody and LPS-induced TRALI in mice by pharmacologically blocking the TLR3 and MAPK pathway","authors":"","doi":"10.1016/j.biopha.2024.117456","DOIUrl":"10.1016/j.biopha.2024.117456","url":null,"abstract":"<div><div>Transfusion-related lung injury (TRALI) poses a significant risk following blood transfusion and remains the primary cause of transfusion-related morbidity and mortality, primarily driven by the activation of immune cells through anti-major histocompatibility complex class I (anti-MHC I) antibody. However, it remains to be defined how immune microenvironmental cue contributes to TRALI. Here, we uncover that activated mast cells within the immune microenvironment promote lung inflammation and injury in antibody-mediated TRALI, both <em>in vitro</em> and <em>in vivo.</em> This was demonstrated by co-culturing lipopolysaccharide (LPS)-pretreated mast cell line with anti-MHC I antibody and establishing a “two-hit” TRALI mouse model through intratracheal injection of LPS followed by tail-vein injection of anti-MHC I antibody. Importantly, mast cell-deficient <em>Kit</em><sup>W-sh/W-sh</sup> mice exhibited markedly reduced lung inflammation and injury responses in antibody-mediated TRALI compared with wild-type mice. Mechanistically, activation of toll-like receptor 3 (TLR3)/mitogen-activated protein kinase (MAPK) signaling pathway in mast cells contributes to the enhanced production of proinflammatory factors. These excessive proinflammatory factors produced by activated mast cells contribute to lung inflammation and injury in antibody-mediated TRALI. Pharmacologically targeting the TLR3/MAPK pathway to inhibit mast cell activation normalizes the proinflammatory microenvironment and alleviates lung inflammation and injury in the preclinical TRALI mouse model. Overall, we find that activation of mast cells via the TLR3/MAPK pathway contributes to lung inflammation and injury in antibody-mediated TRALI, providing novel insights into its underlying mechanisms. Furthermore, targeting activated mast cells and the associated pathway offers potential therapeutic strategies for antibody-mediated TRALI.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

PPARγ antagonism as a new tool for preventing or overcoming endocrine resistance in luminal A breast cancers 将 PPARγ 拮抗作用作为预防或克服管腔 A 型乳腺癌内分泌抗药性的新工具

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117461

{"title":"PPARγ antagonism as a new tool for preventing or overcoming endocrine resistance in luminal A breast cancers","authors":"","doi":"10.1016/j.biopha.2024.117461","DOIUrl":"10.1016/j.biopha.2024.117461","url":null,"abstract":"<div><h3>Purpose</h3><div>This research investigates the role of PPARγ in the complex molecular events underlying the acquisition of resistance to tamoxifen (Tam) in luminal A breast cancer (BC) cells. Furthermore, it focuses on evaluating the possibility of repurposing Imatinib mesylate, an FDA-approved anticancer agent recently recognized also as a PPARγ antagonist, for the personalized therapy of endocrine-resistant BC with increased PPARγ expression.</div></div><div><h3>Methods</h3><div>Differential gene expression between parental and Tam-resistant MCF7 cells was assessed by RNA-seq followed by bioinformatics analysis and validation by RT-qPCR. PPARγ was downregulated by esiRNAs or inhibited by the antagonist GW9662. Cell viability and proliferation were measured by MTT and colony formation assays. Spheroids were prepared from parental and Tam-resistant MCF7 cells. Other luminal A BC cell lines resistant to Tam were generated.</div></div><div><h3>Results</h3><div>In MCF7-TamR cells, PPARγ and several of its target genes were significantly upregulated. Increased PPARγ expression was due to the modulation of its positive/negative transcriptional regulators. Downregulating PPARγ with esiRNAs or GW9662 effectively killed parental and Tam-resistant cells and spheroids. Imatinib revealed to be as effective as GW9662 in restoring Tam susceptibility of these cells. PPARγ overexpression was also observed in the newly-selected Tam-resistant luminal A BC cells, in which GW9662 and Imatinib restored their susceptibility to Tam.</div></div><div><h3>Conclusion</h3><div>Our findings demonstrate that the overexpression of PPARγ is a frequent occurrence during acquisition of Tam resistance in luminal A BC cells, and that PPARγ antagonism represents an alternative therapeutic approach for the personalized treatment of BC showing dysregulation of this nuclear receptor.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Enhancing targeted therapy by combining PI3K and AKT inhibitors with or without cisplatin or vincristine in medulloblastoma cell lines in vitro 在体外髓母细胞瘤细胞系中，通过将 PI3K 和 AKT 抑制剂与顺铂或长春新碱联合使用或不联合使用，增强靶向治疗效果

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117500

{"title":"Enhancing targeted therapy by combining PI3K and AKT inhibitors with or without cisplatin or vincristine in medulloblastoma cell lines in vitro","authors":"","doi":"10.1016/j.biopha.2024.117500","DOIUrl":"10.1016/j.biopha.2024.117500","url":null,"abstract":"<div><h3>Aim</h3><div>Despite current intensive therapy, survival rates of medulloblastoma (MB) greatly vary according to molecular subgroup, so new therapies are needed. Recently, we showed that combining phosphoinositide 3-kinase (PI3K), fibroblast growth factor receptor and cyclin-dependent-kinase-4/6 inhibitors (BYL719, JNJ-42756493 and PD-0332991, respectively) or poly (ADP-ribose) polymerase (PARP) and WEE-1 inhibitors (BMN673 and MK1775 respectively) had synergistic effects on MB. Here, in continuation, we investigated the effects of single and combined administrations of PI3K and AKT inhibitors, with/without cisplatin or vincristine on adherent or suspension cultures of different MB subgroups as well as in a spheroid culture of one MB line.</div></div><div><h3>Material and methods</h3><div>MB cell lines DAOY, UW228–3, D425, Med8A, and D283 were treated with single and combined administrations of BYL719, AZD5363, cisplatin or vincristine and followed for viability, cell confluence, cytotoxicity, and cell migration. DAOY was also tested as a spheroid culture.</div></div><div><h3>Key findings</h3><div>Single BYL719, AZD5363, cisplatin, or vincristine administrations gave dose-dependent responses with regard to inhibition of viability and cell confluence. Combining AZD5363 with BYL719, cisplatin or vincristine resulted in synergistic effects with regard to inhibition of viability in all cell lines, and confluence and migration in all tested cell lines. The administration of single and combined treatments to DAOY spheroids produced largely similar effects.</div></div><div><h3>Significance</h3><div>This study provides pre-clinical evidence that AKT inhibitors combined with PI3K inhibitors, cisplatin, or vincristine exhibit additive/synergistic anti-MB activity, and lower doses could be used. The latter also applied to one MB line grown as spheroids, further supporting their future potential use.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320224","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

In situ crosslinked injectable chondroitin sulfate hydrogel for preventing postoperative adhesion 用于防止术后粘连的原位交联可注射硫酸软骨素水凝胶

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117495

{"title":"In situ crosslinked injectable chondroitin sulfate hydrogel for preventing postoperative adhesion","authors":"","doi":"10.1016/j.biopha.2024.117495","DOIUrl":"10.1016/j.biopha.2024.117495","url":null,"abstract":"<div><div>Postoperative adhesion is a common clinical disease caused by surgical trauma, accompanying serious subsequent complications. Current non-surgical drug therapy and biomaterial barrier administration have limited therapeutic effects due to their inherent deficiencies. Therefore, developing a simple, effective, and feasible method to effectively prevent postoperative adhesions after surgical procedures remains a challenge. An injectable chondroitin sulfate complex hydrogel was prepared based on aldehyde-modified chondroitin sulfate (ChS-CHO) and hydrazine-modified chondroitin sulfate (ChS-ADH). The hydrogel showed enhanced strength and good self-healing ability. By using the Schiff base reaction principle that aldehyde group reacts with hydrazide to form hydrazone bond, C-A hydrogel physical barrier is formed at the wound site to reduce the occurrence of postoperative adhesion. There is no use of chemical crosslinkers in the whole reaction system to prepare C-A hydrogel, which has excellent biocompatibility and is safe and non-toxic. The results showed that C-A hydrogel showed excellent mechanical properties, good self-healing, and biocompatibility. The cecal-abdominal wall adhesion model and hepatic adhesion model of rats were constructed respectively to evaluate its preventive effect on postoperative adhesion. The results showed that C-A hydrogel had a more significant preventive effect on postoperative adhesion, and appears to be a promising candidate for postoperative adhesion.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Design, synthesis and biological evaluation of dual inhibitors targeting AR/AR-Vs and PARP1 in castration resistant prostate cancer therapy 设计、合成靶向 AR/AR-Vs 和 PARP1 的双重抑制剂并对其进行生物学评估，用于治疗对阉割有抵抗力的前列腺癌

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117485

{"title":"Design, synthesis and biological evaluation of dual inhibitors targeting AR/AR-Vs and PARP1 in castration resistant prostate cancer therapy","authors":"","doi":"10.1016/j.biopha.2024.117485","DOIUrl":"10.1016/j.biopha.2024.117485","url":null,"abstract":"<div><div>The combination of androgen signaling inhibitors and PARP inhibitors has shown promising results in clinical trials for the treatment of castration-resistant prostate cancer (CRPC). Multi-target inhibitors can inhibit tumors through different pathways, addressing the limitations of traditional single target inhibitors. We designed and synthesized dual inhibitors targeting AR/AR-Vs and PARP1 using a pharmacophore hybridization strategy. The most potent compound, II-3, inhibits AR/AR-Vs signaling and induces DNA damage by inhibiting PARP1. The IC<sub>50</sub> values of II-3 in the castration-resistant prostate cancer cell lines 22RV1 and C4–2 are 4.38 ± 0.56 µM, and 3.44 ± 0.63 µM, respectively. II-3 not only suppresses the proliferation and migration of 22RV1 and C4–2 cells, but also promotes their apoptosis. Intraperitoneal injection of II-3 effectively inhibits tumor growth in 22RV1 xenograft nude mice without evident drug-induced toxicity. Overall, a series of novel dual inhibitors targeting AR/AR-Vs and PARP1 were designed and synthesized, and meanwhile the in vivo and in vitro effects were comprehensively explored, which provided a potential new therapeutic strategy for CRPC.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Investigation of the molecular mechanisms underlying the anti-inflammatory and antitumour effects of isorhapontigenin: Insights from in vitro and in vivo studies 异芹菜甙元抗炎和抗肿瘤作用的分子机制研究：体外和体内研究的启示

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117479

{"title":"Investigation of the molecular mechanisms underlying the anti-inflammatory and antitumour effects of isorhapontigenin: Insights from in vitro and in vivo studies","authors":"","doi":"10.1016/j.biopha.2024.117479","DOIUrl":"10.1016/j.biopha.2024.117479","url":null,"abstract":"<div><div>Isorhapontigenin (ISO), a naturally-occurring stilbene derivative, has garnered significant attention due to its potent anticancer and anti-inflammatory properties. This review synthesizes current knowledge regarding the mechanisms of action, efficacy, and potential therapeutic applications of Isorhapontigenin acquired <em>in vitro</em> and <em>in vivo</em>. It systematically analyzes its effects on various cancer cell lines, tumor models, and inflammatory conditions, examining its impact on cell proliferation, apoptosis, metastasis, and inflammatory mediators. <em>In vitro</em> studies reveal that Isorhapontigenin induces cell cycle arrest, promotes apoptosis, and inhibits cancer cell migration through modulation of key signaling pathways, including EGFR-PI3K-Akt and NF-κB. It also demonstrates potent antioxidant and anti-inflammatory effects by enhancing Nrf2 signaling and suppressing pro-inflammatory cytokine production. These findings are corroborated by <em>in vivo</em> studies confirming its ability to inhibit tumor growth in xenograft models and attenuate inflammatory responses in various disease models. Notably, Isorhapontigenin exhibits superior pharmacokinetic profiles then resveratrol, with higher oral bioavailability. Isorhapontigenin demonstrates multi-target actions, including epigenetic modulation through microRNA regulation, which highlight its potential as a versatile therapeutic agent. This review also identifies current limitations in Isorhapontigenin research that require further investigation. Overall, Isorhapontigenin offers promise as a multi-faceted compound for the treatment of cancer, inflammatory diseases, and metabolic disorders, providing a solid foundation for future research and potential clinical applications.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

DPP-IV as a potential candidate in anti-obesity and obesity-related diseases treatment DPP-IV 作为抗肥胖和肥胖相关疾病治疗的潜在候选药物

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117464

引用次数: 0

Soybean Extract Ameliorates Lung Injury induced by Uranium Inhalation: An integrated strategy of network pharmacology, metabolomics, and transcriptomics 大豆提取物可改善铀吸入引起的肺损伤：网络药理学、代谢组学和转录组学的综合策略

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117451

{"title":"Soybean Extract Ameliorates Lung Injury induced by Uranium Inhalation: An integrated strategy of network pharmacology, metabolomics, and transcriptomics","authors":"","doi":"10.1016/j.biopha.2024.117451","DOIUrl":"10.1016/j.biopha.2024.117451","url":null,"abstract":"<div><h3>Aim</h3><div>This study aimed to evaluate the protective effect of soybean extract (SE) against uranium-induced lung injury in rats.</div></div><div><h3>Materials and methods</h3><div>A rat lung injury model was established through nebulized inhalation of uranyl nitrate. Pretreatment with SE or sterile water (control group) by gavage for seven days before uranium exposure and until the experiment endpoints. The levels of uranium in lung tissues were detected by ICP-MS. Paraffin embedding-based hematoxylin & eosin staining and Masson’s staining for the lung tissue were performed to observe the histopathological imaging features. A public database was utilized to analyze the network pharmacological association between SE and lung injury. The expression levels of proteins indicating fibrosis were measured by enzyme-linked immunosorbent assay. RNA-seq transcriptomic and LC-MS/MS targeted metabolomics were conducted in lung tissues.</div></div><div><h3>Results</h3><div>Uranium levels in the lung tissues were lower in SE-pretreated rats than in the uranium-treated group. Inflammatory cell infiltration and the deposition of extracellular matrix were attenuated, and the levels of alpha-smooth muscle actin, transforming growth factor beta1, and hydroxyproline decreased in SE-pretreated rats compared to the uranium-treated group. Active ingredients of SE were related to inflammation, oxidative stress, and drug metabolism. A total of 67 differentially expressed genes and 39 differential metabolites were identified in the SE-pretreated group compared to the uranium-treated group, focusing on the drug metabolism-cytochrome P450, glutathione metabolism, IL-17 signaling pathway, complement, and coagulation cascades.</div></div><div><h3>Conclusions</h3><div>These findings suggest that SE may ameliorate uranium-induced pulmonary inflammation and fibrosis by regulating glutathione metabolism, chronic inflammation, and immune regulation.</div></div>","PeriodicalId":8966,"journal":{"name":"Biomedicine & Pharmacotherapy","volume":null,"pages":null},"PeriodicalIF":6.9,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142320234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Therapeutic prospects of sex hormone receptor signaling in hormone-responsive cancers 性激素受体信号在激素反应性癌症中的治疗前景

IF 6.9 2区医学

Biomedicine & Pharmacotherapy Pub Date : 2024-09-25 DOI: 10.1016/j.biopha.2024.117473

引用次数: 0