Medical Oncology最新文献_第10页

Identification of Isovitexin as a novel CYP17A1 inhibitor through virtual screening and evaluation of its anti-cancer effects in MCF-7 breast cancer cells. 通过虚拟筛选和MCF-7乳腺癌细胞的抗癌作用评价，鉴定异牡荆素为一种新型CYP17A1抑制剂。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-26 DOI: 10.1007/s12032-025-02637-0

Lathika Shanmugam, Priyadharshini Kaliyamoorthy, Vivia Yazhini Sashikumar, Sowmya Ravichandran, Kanishka Padmanaban, Nithya Elango

{"title":"Identification of Isovitexin as a novel CYP17A1 inhibitor through virtual screening and evaluation of its anti-cancer effects in MCF-7 breast cancer cells.","authors":"Lathika Shanmugam, Priyadharshini Kaliyamoorthy, Vivia Yazhini Sashikumar, Sowmya Ravichandran, Kanishka Padmanaban, Nithya Elango","doi":"10.1007/s12032-025-02637-0","DOIUrl":"10.1007/s12032-025-02637-0","url":null,"abstract":"Over 75% of breast cancers are hormone receptor positive and are associated with better prognosis after treatment, when compared to other types of breast cancer. However, discontinuation of treatment due to side effects is common among one-third of the patients, leading to poor outcomes. On long-term treatment, development of resistance to the current therapeutics is common. CYP17A1, a key enzyme in androgen and estrogen synthesis, is associated in the development and progression of breast cancers. Phytochemicals, which are abundant in three traditional medicinal plants, Fenugreek, Ginger, and Basil, generally used in regulating hormonal disorders were screened for potential inhibition of CYP17A1, by molecular docking (Autodock Vina). The binding affinities were compared with standard CYP17A1 inhibitors Abiraterone and Ketoconazole. Docking analysis revealed that Isovitexin (- 9.5 kcal/mol) and Orientin (- 9.4 kcal/mol) showed comparable binding affinities to Abiraterone and Ketoconazole. Molecular Simulations and MM-GBSA were employed to explore the stability of ligand-protein complexes. Isovitexin had stable interactions with the CYP17A1 than Orientin evident from the RMSD, RMSF, Protein-Ligand contacts and MM-GBSA values. In silico ADMET profiles of the phytochemicals and standard breast cancer drugs (Letrozole, Tamoxifen, Paclitaxel, and Docetaxel) were evaluated using Swiss ADME and pkCSM and found to be similar. In in vitro assays, Isovitexin was found to be cytotoxic to MCF-7 cells, causing 46% apoptosis at < 10 nM levels. The study reveals that Isovitexin, with high cytotoxicity, may be effective in the treatment of both ER- and PR-positive (MCF-7) cancers. Overall, the findings have implications for the therapeutic development of hormone receptor-positive breast cancers.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 5","pages":"137"},"PeriodicalIF":2.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Effect of PRKD3 on cell cycle in gastric cancer progression and downstream regulatory networks. PRKD3对胃癌进展过程中细胞周期及下游调控网络的影响。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-25 DOI: 10.1007/s12032-025-02663-y

Shuaiyang Wang, Bei Xie, Haohua Deng, Xingyuan Ma, Baoyuan Tang, Lei Ma, Jinmei Zhu, Jing Li, Linjing Li

{"title":"Effect of PRKD3 on cell cycle in gastric cancer progression and downstream regulatory networks.","authors":"Shuaiyang Wang, Bei Xie, Haohua Deng, Xingyuan Ma, Baoyuan Tang, Lei Ma, Jinmei Zhu, Jing Li, Linjing Li","doi":"10.1007/s12032-025-02663-y","DOIUrl":"10.1007/s12032-025-02663-y","url":null,"abstract":"Protein kinase D3 (PRKD3), belonging to the protein kinase D family, significantly influences tumor development and progression. The role of PRKD3 in advancing gastric cancer (GC) and its effects on the cell cycle are not well understood, necessitating detailed investigation. Assessment of PRKD3 expression in both malignant and normal gastric tissues was performed using bioinformatics databases. The influence of PRKD3 on GC's malignant characteristics was evaluated through in vitro experiments utilizing cell line models of GC. Additionally, proteomic analyses were conducted to investigate the potential mechanisms of PRKD3 in GC progression. PRKD3 was notably overexpressed in GC tissues, correlating with adverse outcomes for patients. PRKD3 knockdown impaired GC cell malignancy, manifesting as a 2.12-fold decline in proliferation(p < 0.01), 2.64-fold suppression of migration(p < 0.01), 2.16-fold inhibition of invasion(p < 0.01), and G2/M phase arrest. Proteomic and Western blot analyses had revealed a substantial enrichment in differentially expressed proteins (DEPs) associated with tumor-related signaling pathways, including FoxO and p53, which was paralleled by significant alterations in the levels of key cell cycle proteins such as CDK1, CyclinB1, CHK1 and PLK1, with a 6.8-fold elevation in CHK1 levels(p < 0.05). The overexpression of PRKD3 was intricately linked with the aggressive behaviors of GC. Targeting PRKD3 activity offers potential for effective treatments of GC.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 5","pages":"135"},"PeriodicalIF":2.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gastrointestinal perforation in general oncology, metastatic colorectal cancer, and metastatic melanoma population. 胃肠道穿孔在一般肿瘤，转移性结直肠癌和转移性黑色素瘤人群。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-25 DOI: 10.1007/s12032-025-02691-8

Arun Parashar, Vineet Mehta, Varsha Sharma, Muskan Thakur

{"title":"Gastrointestinal perforation in general oncology, metastatic colorectal cancer, and metastatic melanoma population.","authors":"Arun Parashar, Vineet Mehta, Varsha Sharma, Muskan Thakur","doi":"10.1007/s12032-025-02691-8","DOIUrl":"10.1007/s12032-025-02691-8","url":null,"abstract":"Gastrointestinal perforation (GIP) is a rare and potentially fatal adverse event of antineoplastic therapy. GIP is a rare but serious complication in oncology patients, often leading to significant morbidity and mortality. In general oncology patients, the incidence of GIP ranged from 0.5 to 1.9%. A meta-analysis of six clinical trials with 4579 patients reported an incidence of 1.0%. Among mCRC patients, the incidence varied between 0.5 and 2.4%, with geographic differences-1.5% in the USA and 2.4% in Australia. For metastatic melanoma patients, the incidence of GIP ranged from 0.4 to 0.67%, with U.S. rates of 0.57% and 0.67% and a lower rate of 0.40% reported in Germany. The findings suggest that the risk of GIP varies significantly across oncology populations and treatment regimens, with higher risks noted in metastatic cancer patients undergoing therapies such as VEGF inhibitors or immune checkpoint inhibitors. These data highlight the need for careful monitoring and early intervention in high-risk populations to reduce the impact of GIP on patient outcomes. This systematic review aims to summarize the incidence of GIP in general oncology, metastatic colorectal cancer (mCRC), and metastatic melanoma (MM) populations. A literature search was conducted in Embase and Medline databases from January 1, 2011 to August 30, 2017, identifying relevant studies on GIP incidence.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 5","pages":"133"},"PeriodicalIF":2.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fatty acid synthase inhibitor cerulenin attenuates glioblastoma progression by reducing EMT and stemness phenotypes, inducing oxidative and ER stress response, and targeting PI3K/AKT/NF-κB axis. 脂肪酸合成酶抑制剂cerulenin通过降低EMT和干性表型，诱导氧化和内质网应激反应，以及靶向PI3K/AKT/NF-κB轴，减缓胶质母细胞瘤的进展。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-25 DOI: 10.1007/s12032-025-02697-2

Murat Pekmez, Şefika Beyza Mete, Yunus Aksüt, İrem Öğütcü, Fatma Nur Baştürk, Yusuf Can Gerçek, Aslıhan Şengelen

{"title":"Fatty acid synthase inhibitor cerulenin attenuates glioblastoma progression by reducing EMT and stemness phenotypes, inducing oxidative and ER stress response, and targeting PI3K/AKT/NF-κB axis.","authors":"Murat Pekmez, Şefika Beyza Mete, Yunus Aksüt, İrem Öğütcü, Fatma Nur Baştürk, Yusuf Can Gerçek, Aslıhan Şengelen","doi":"10.1007/s12032-025-02697-2","DOIUrl":"10.1007/s12032-025-02697-2","url":null,"abstract":"Targeting cellular metabolism is becoming a critical approach for stopping cancer progression. Limited information is available regarding the effects of inhibiting the lipogenic enzyme fatty acid synthase (FASN) in glioblastoma (GB) cells (grade-IV-astrocytoma), which have high invasion and low response to standard treatments. Herein, we used cerulenin (CER) to inhibit FASN. CER treatments (3.6 μg/mL/48 h and 5.55 μg/mL/48 h indicate IC20 and IC50 values, respectively) led to a dose- and time-dependent decrease in the viability of the U-87MG human GB cells. A significant decrease was detected in the levels of fatty acids, including palmitic acid, determined by GS-MS analysis. FASN inhibition attenuated cell motility, 2D and 3D-clonogenic survival, and cell differentiation characteristics (related markers of epithelial-mesenchymal transition/EMT and stemness). Moreover, treatments caused mitochondrial membrane potential (MMP) collapse and increased intracellular reactive oxygen species (ROS) levels. Protein aggregates and ER stress in the cells also increased. Remarkably, despite increased Hsp70 and p-HSF1 levels against induced cellular stress, CER promoted markedly autophagy and apoptosis. The network pharmacology approach revealed that protein and lipid kinases are crucial targets in cell signaling, and PI3K, AKT, and NF-κB levels were confirmed by immunoblotting. The results demonstrated for the first time that inhibiting FA production and FASN function induces cell death through ROS generation and ER stress while simultaneously reducing the motility and aggressiveness of U-87MG human glioblastoma cells by attenuating EMT and stemness phenotypes. Therefore, blocking lipid metabolism using CER may be considered as a good candidate for GB therapeutic option.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 5","pages":"136"},"PeriodicalIF":2.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11937156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710550","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

Smart nanomedicines powered by artificial intelligence: a breakthrough in lung cancer diagnosis and treatment. 人工智能驱动的智能纳米药物：肺癌诊断和治疗的突破。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-25 DOI: 10.1007/s12032-025-02680-x

Moloudosadat Alavinejad, Maryam Shirzad, Mohammad Javad Javid-Naderi, Abbas Rahdar, Sonia Fathi-Karkan, Sadanand Pandey

{"title":"Smart nanomedicines powered by artificial intelligence: a breakthrough in lung cancer diagnosis and treatment.","authors":"Moloudosadat Alavinejad, Maryam Shirzad, Mohammad Javad Javid-Naderi, Abbas Rahdar, Sonia Fathi-Karkan, Sadanand Pandey","doi":"10.1007/s12032-025-02680-x","DOIUrl":"10.1007/s12032-025-02680-x","url":null,"abstract":"Lung cancer remains one of the leading causes of cancer-related mortality worldwide, primarily due to challenges in early detection, suboptimal therapeutic efficacy, and severe adverse effects associated with conventional treatments. The convergence of nanotechnology and artificial intelligence (AI) offers transformative potential in precision oncology, enabling innovative solutions for lung cancer diagnosis and therapy. Intelligent nanomedicines facilitate targeted drug delivery, enhanced imaging, and theranostic applications, while AI-driven models harness big biomedical data to optimize nanomedicine design, functionality, and clinical application. This review explores the synergistic integration of AI and nanotechnology in lung cancer care, highlighting recent advancements, key challenges, and future directions for clinical translation. Ethical considerations, including data standardization and privacy concerns, are also addressed, providing a comprehensive roadmap to overcome current barriers and advance the adoption of AI-driven intelligent nanomedicines in precision oncology. This synthesis underscores the critical role of emerging technologies in revolutionizing lung cancer management.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 5","pages":"134"},"PeriodicalIF":2.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Note: Molecular and therapeutic effect of CRISPR in treating cancer. 注：CRISPR在治疗癌症中的分子和治疗作用。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-24 DOI: 10.1007/s12032-025-02692-7

Sawani Rodrigo, Kaveesha Senasinghe, Sameer Quazi

引用次数: 0

Molecular crosstalk between GPCR and receptor tyrosine-protein kinase in neuroblastoma: molecular mechanism and therapeutic implications. 神经母细胞瘤中GPCR与酪氨酸蛋白激酶受体之间的分子串扰：分子机制及其治疗意义。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-23 DOI: 10.1007/s12032-025-02685-6

Kousik Maparu, Dhrita Chatterjee, Romanpreet Kaur, Nileshwar Kalia, Omkar Kumar Kuwar, Mayank Attri, Shamsher Singh

{"title":"Molecular crosstalk between GPCR and receptor tyrosine-protein kinase in neuroblastoma: molecular mechanism and therapeutic implications.","authors":"Kousik Maparu, Dhrita Chatterjee, Romanpreet Kaur, Nileshwar Kalia, Omkar Kumar Kuwar, Mayank Attri, Shamsher Singh","doi":"10.1007/s12032-025-02685-6","DOIUrl":"10.1007/s12032-025-02685-6","url":null,"abstract":"Neuroblastoma is an aggressive pediatric tumor condition derived from neural crest cells that typically affect infants and children under the age of five. It can often originate in the adrenal glands but can also develop in the sympathetic nervous system. G-protein-coupled receptors (GPCRs) and receptor tyrosine kinases have been shown in recent research to have a vital role in the progression of neuroblastoma. GPCR-RTK crosstalk stimulates signaling pathways such as MAP kinase, and the activation of the GPCR-AKT signaling pathway plays a critical role in neuroblastoma progression by promoting cell growth, survival, and resistance to apoptosis through complex interactions with insulin signaling pathways. ALK (Anaplastic lymphoma kinase), a member of the RTK family, and any mutations can lead to oncogenic signaling and resistance to targeted therapy in neuroblastoma. By interfering with cellular signaling via novel therapeutic strategies by selective RET inhibitors, ALK inhibitors, and Trk-specific inhibitors may be able to reduce the prevalence of neuroblastoma. Understanding the complicated signaling relationships between GPCRs, RTKs, and the insulin pathway is critical when developing new cancer treatments. The integration of these signaling networks offers promising avenues for enhancing the effectiveness of existing treatments and improving patient outcomes in neuroblastoma.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 5","pages":"131"},"PeriodicalIF":2.8,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Note: Niosomes: a novel targeted drug delivery system for cancer. 撤稿说明：Niosomes：一种新型癌症靶向给药系统。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-22 DOI: 10.1007/s12032-025-02693-6

Maryam Moghtaderi, Kamand Sedaghatnia, Mahsa Bourbour, Mahdi Fatemizadeh, Zahra Salehi Moghaddam, Faranak Hejabi, Fatemeh Heidari, Sameer Quazi, Bahareh Farasati Far

引用次数: 0

Retraction Note: In vitro cytotoxicity and anti-cancer drug release behavior of methionine-coated magnetite nanoparticles as carriers. 撤回注：甲硫氨酸包被的磁性纳米颗粒作为载体的体外细胞毒性和抗癌药物释放行为。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-22 DOI: 10.1007/s12032-025-02688-3

Faten Eshrati Yeganeh, Amir Eshrati Yeganeh, Mahdi Fatemizadeh, Bahareh Farasati Far, Sameer Quazi, Muhammad Safdar

引用次数: 0

The prevalence of post-therapy epilepsy in patients treated for high-grade glial tumors: a systematic review and meta-analysis. 高级别神经胶质肿瘤患者治疗后癫痫的患病率：一项系统回顾和荟萃分析。

IF 2.8 4区医学

Medical Oncology Pub Date : 2025-03-21 DOI: 10.1007/s12032-025-02677-6

Marta Pereira Ferreira, Ruben Lopes Carvalho, Daniel Filipe Borges, Joana Isabel Soares, João Casalta-Lopes

{"title":"The prevalence of post-therapy epilepsy in patients treated for high-grade glial tumors: a systematic review and meta-analysis.","authors":"Marta Pereira Ferreira, Ruben Lopes Carvalho, Daniel Filipe Borges, Joana Isabel Soares, João Casalta-Lopes","doi":"10.1007/s12032-025-02677-6","DOIUrl":"10.1007/s12032-025-02677-6","url":null,"abstract":"Gliomas are the most prevalent type of primary brain tumor of the adult central nervous system. High-grade gliomas (HGG) are the most common type of glioma. Epilepsy is often the first clinical manifestation of HGG. Since epilepsy leads to increased morbidity and mortality rates, seizure control is one of the main therapeutic goals for patients with glioma-related epilepsy. Post-therapy epilepsy is observed in a significant percentage of patients, hence, this work aimed to quantify the prevalence of post-therapy epilepsy after HGG treatment. Our search was conducted across PubMed®, EMBASE®, Web of Science™, Cochrane Library, Sicelo and Scopus, adhering to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. This review included articles published in Portuguese or English that evaluate adult patients with newly diagnosed HGG, who were treated with at least surgery or radiation. Thirty-six studies reporting on 4036 HGG patients were included in our meta-analysis. The mean age ranged from 44 to 73 years. Glioblastoma was the most commonly observed HGG, representing 77,8% of all glioma patients. The pre-treatment seizure frequency was observed in 21,2%. All patients underwent surgery as the main therapy, and 1842 patients received standard adjuvant therapy. We also observed a pooled prevalence of post-therapy seizures of 25.5% (95% confidence interval of [19.9%; 31.1%]). Substantial heterogeneity in all assessed variables was observed. Conducting larger prospective studies with suitable epilepsy diagnostic methods would help provide a more precise estimate of the number of HGG patients who develop post-therapy epilepsy.","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 4","pages":"128"},"PeriodicalIF":2.8,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0