Oncology Research最新文献

筛选
英文 中文
Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers. 口腔鳞状细胞癌中PI3K/AKT信号失调:肿瘤微环境和表观遗传修饰因子是关键驱动因素。
IF 4.1 4区 医学
Oncology Research Pub Date : 2025-07-18 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.064010
Vinothkumar Veerasamy, Veeravarmal Veeran, Siddavaram Nagini
{"title":"Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.","authors":"Vinothkumar Veerasamy, Veeravarmal Veeran, Siddavaram Nagini","doi":"10.32604/or.2025.064010","DOIUrl":"10.32604/or.2025.064010","url":null,"abstract":"<p><p>The phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway is one of the most frequently dysregulated signaling networks in oral squamous cell carcinoma (OSCC). Although the tumor microenvironment (TME) and epigenetic modifiers are recognized to play a pivotal role in aberrant activation of the PI3K/AKT pathway in OSCC, the available evidence is fragmentary and a comprehensive analysis is warranted. This review evaluates the intricate mechanisms by which various components of the TME facilitate proliferation, apoptosis evasion, invasion, migration, angiogenesis, metastasis, as well as therapy resistance in OSCC through activation of PI3K/AKT signalling. The review has also analysed how epigenetic modifiers such as DNA methylation, histone modifications, and noncoding RNAs that have emerged as key players in orchestrating OSCC development and progression influence the PI3K/AKT pathway. Preclinical studies and clinical trials on the efficacy of PI3K/AKT inhibitors as viable options for OSCC treatment are discussed. Overall, this review supports the tenet that the PI3K/AKT pathway, which functions as a central hub through crosstalk with several oncogenic signaling pathways and overarching impact on all the hallmark traits of cancer, offers immense potential as a biomarker and oncotherapeutic target for OSCC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 8","pages":"1835-1860"},"PeriodicalIF":4.1,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760685","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
GPX4 predicts poor prognosis and regulates tumor proliferation and senescence in colorectal adenocarcinoma. GPX4在结直肠腺癌中预测预后不良,调节肿瘤增殖和衰老。
IF 4.1 4区 医学
Oncology Research Pub Date : 2025-07-18 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.063395
Y U Zhang, Qingkun Wang, Yue Han, Junjie Piao, Xiuying Jin
{"title":"GPX4 predicts poor prognosis and regulates tumor proliferation and senescence in colorectal adenocarcinoma.","authors":"Y U Zhang, Qingkun Wang, Yue Han, Junjie Piao, Xiuying Jin","doi":"10.32604/or.2025.063395","DOIUrl":"10.32604/or.2025.063395","url":null,"abstract":"<p><strong>Background: </strong>Colorectal adenocarcinoma (COAD) is one of the most common gastrointestinal malignancies. There is a pressing need to recognize reliable biomarkers that can improve diagnostic accuracy, predict prognosis, and serve as effective molecular targets. Glutathione peroxidase 4 (GPX4) is an important antioxidant protein. Evidence demonstrates that abnormal expression of GPX4 is related to cancer initiation and progression. However, the role of GPX4 in COAD remains unclear.</p><p><strong>Methods: </strong>We employed bioinformatics analysis and conducted subsequent validation of biological processes, including cell counting kit-8 assay (CCK-8), colony formation assay, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), 5-ethynyl-2'-deoxyuridine assay (EdU), western blot, immunohistochemistry, senescence associated β-galactosidase (SA-β-gal) staining and immunofluorescence to explore the expression status, prognostic value and biological function of GPX4 in COAD.</p><p><strong>Results: </strong>Our data revealed that GPX4 mRNA expression was upregulated in COAD tissues and could predict the prognosis in patients with COAD. High GPX4 expression was associated with increased infiltration of malignant cells. We also performed a series of cell experiments confirming that GPX4 knockdown inhibited proliferation and induced cellular senescence, as determined by using CCK-8, colony formation, and EdU assay. In addition, SA-β-gal staining and senescence-associated secretory phenotype (SASP) components, such as P21 and Interleukin-6 (IL-6), were increased in GPX4 knockdown cells, while Lamin B1 was decreased. Moreover, we predicted that high expression of GPX4 was related to low immune cell infiltration.</p><p><strong>Conclusion: </strong>This study demonstrates that GPX4 is a potential prognostic biomarker and target gene for COAD.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 8","pages":"1933-1945"},"PeriodicalIF":4.1,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760687","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
OTUD7B Stabilization by METTL14-Mediated m6A Methylation Drives HIF-1α Expression in Esophageal Squamous Cell Carcinoma. mettl14介导的m6A甲基化稳定OTUD7B驱动食管鳞状细胞癌中HIF-1α的表达。
IF 4.1 4区 医学
Oncology Research Pub Date : 2025-07-18 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.061301
Fei Ren, Yansen Cai, Yang Song
{"title":"OTUD7B Stabilization by METTL14-Mediated m6A Methylation Drives HIF-1<b>α</b> Expression in Esophageal Squamous Cell Carcinoma.","authors":"Fei Ren, Yansen Cai, Yang Song","doi":"10.32604/or.2025.061301","DOIUrl":"10.32604/or.2025.061301","url":null,"abstract":"<p><strong>Objectives: </strong>Epigenetic changes, particularly N6-methyladenosine (m6A) modifications, play a pivotal role in cancer development. This study explored the role of ovarian tumor deubiquitinase 7B (OTUD7B) in esophageal squamous cell carcinoma (ESCC) in the context of m6A methylation and the hypoxia-inducible factor-1α (HIF-1α) pathway.</p><p><strong>Methods: </strong>The GSE179267 dataset was used to conduct differential gene expression analysis to identify key m6A-enriched genes. The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), and Sequence-based RNA Adenosine Methylation Site Predictor (SRAMP) databases were used to evaluate the expression of OTUD7B in ESCC and its correlation with methyltransferase-like 14 (METTL14) and HIF-1α. The m6A content in total RNA extracted from ESCC cells was assessed using a dot blot assay. Gene-specific m6A-PCR was used to quantify m6A modifications in OTUD7B mRNA. The functional role of OTUD7B was explored using clonogenic and Transwell assays. The effect of OTUD7B on HIF-1α ubiquitination was detected using a co-immunoprecipitation assay.</p><p><strong>Results: </strong>OTUD7B was identified as a pivotal m6A-driven oncogene correlated with METTL14 and HIF-1α. METTL14 enhanced the mRNA stability and expression of OTUD7B through m6A methylation. OTUD7B overexpression counteracted the inhibitory effects of METTL14 knockdown on cell proliferation and invasion and stabilized HIF-1α by promoting deubiquitination.</p><p><strong>Conclusion: </strong>METTL14 plays a crucial role in the stabilization of OTUD7B through m6A methylation, thereby inhibiting the ubiquitin-proteasomal degradation of HIF-1α in ESCC. These findings highlight the potential of targeting the METTL14-OTUD7B axis as a therapeutic strategy for ESCC.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 8","pages":"2055-2074"},"PeriodicalIF":4.1,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308248/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760696","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
Correlation of senescence-related gene FEN1 on neuroblastoma progression and cisplatin chemotherapy sensitivity. 衰老相关基因FEN1与神经母细胞瘤进展和顺铂化疗敏感性的相关性
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.060021
Youyang Hu, Yishu Luo, Tianyue Xie, Yuehua Chen, Jun Zhao, Weichao Ji, Zhiwei Yan, Sitong Qiu, Kexin Gao, Haixia Zhu, Limin Ma, Qiyou Yin
{"title":"Correlation of senescence-related gene FEN1 on neuroblastoma progression and cisplatin chemotherapy sensitivity.","authors":"Youyang Hu, Yishu Luo, Tianyue Xie, Yuehua Chen, Jun Zhao, Weichao Ji, Zhiwei Yan, Sitong Qiu, Kexin Gao, Haixia Zhu, Limin Ma, Qiyou Yin","doi":"10.32604/or.2025.060021","DOIUrl":"10.32604/or.2025.060021","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;Neuroblastoma (NB) is frequently associated with high-risk pediatric cases that demonstrate limited response to cisplatin, contributing to a poor prognosis. Recent studies have explored the role of tumor cell senescence in increasing sensitivity to this chemotherapy agent. This study aims to identify genes related to cell senescence in children diagnosed with NB, evaluate their influence on cisplatin sensitivity, and investigate potential strategies to enhance the efficacy of chemotherapy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Gene expression profiles and clinical data were obtained for 498 NB patients from the GEO database (GSE49710). The study focused on identifying genes that were differentially expressed between stage IV and other stages, particularly those linked to cell senescence and cisplatin resistance. To analyze the prognostic significance of these differentially expressed genes, we employed LASSO regression and multivariate Cox proportional hazards models. Transcriptomic and proteomic analyses of 15 NB specimens revealed a significant correlation between Flap endonuclease-1 (FEN1) expression levels and both cellular senescence and sensitivity to cisplatin. We quantified FEN1 expression and cisplatin IC50 values in four different NB cell lines. The influence of FEN1 knockdown and overexpression on NB cell proliferation, invasion, and migration was evaluated using cloning assays, transwell assays, and scratch assays. Furthermore, we utilized Western blotting to analyze senescence-associated proteins p21 and proliferating cell nuclear antigen (PCNA), thereby evaluating the role of FEN1 in cellular senescence. The impact of FEN1 on cisplatin sensitivity was investigated via the CCK-8 cell counting assay. Additionally, we investigated how FEN1 inhibitors might impact NB cell proliferation and enhance the therapeutic efficacy of cisplatin treatment.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;FEN1 was found to be highly expressed in stage IV NB and showed a strong association with cisplatin sensitivity, establishing it as a critical molecular marker linked to poor patient prognosis. Notably, elevated FEN1 expression correlated with reduced sensitivity to cisplatin, as evidenced by higher IC50 values. In the SH-SY5Y cell line, FEN1 knockdown led to significant reductions in cell proliferation, invasion, and migration, along with an increase in β-galactosidase staining-indicative of senescence. This knockdown also resulted in elevated levels of the p21 protein and decreased expression of PCNA, concurrently lowering cisplatin IC50 values. Conversely, FEN1 overexpression in the SK-N-SH cell line resulted in enhanced cell proliferation, invasion, and migration. This overexpression was associated with reduced β-galactosidase staining, decreased levels of p21, and increased expression of PCNA, ultimately resulting in higher cisplatin IC50 values. Importantly, FEN1 inhibitors alone significantly impeded NB cell proliferation, and their","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1695-1708"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560719","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
Retraction: Inhibition of Proliferation, Migration, and Invasion by Knockdown of Pyruvate Kinase-M2 (PKM2) in Ovarian Cancer SKOV3 and OVCAR3 Cells. 收缩:通过敲低丙酮酸激酶- m2 (PKM2)抑制卵巢癌SKOV3和OVCAR3细胞的增殖、迁移和侵袭。
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.068988
{"title":"Retraction: Inhibition of Proliferation, Migration, and Invasion by Knockdown of Pyruvate Kinase-M2 (PKM2) in Ovarian Cancer SKOV3 and OVCAR3 Cells.","authors":"","doi":"10.32604/or.2025.068988","DOIUrl":"https://doi.org/10.32604/or.2025.068988","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3727/096504016X14685034103671.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1801-1802"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560653","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
Correction: MicroRNA-101 Targets CXCL12-Mediated Akt and Snail Signaling Pathways to Inhibit Cellular Proliferation and Invasion in Papillary Thyroid Carcinoma. 更正:MicroRNA-101靶向cxcl12介导的Akt和蜗牛信号通路,抑制甲状腺乳头状癌的细胞增殖和侵袭。
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.064363
Fang Chen, Dongqiang Yang, Yuhua Ru, Shan Cao, Aishe Gao
{"title":"Correction: MicroRNA-101 Targets CXCL12-Mediated Akt and Snail Signaling Pathways to Inhibit Cellular Proliferation and Invasion in Papillary Thyroid Carcinoma.","authors":"Fang Chen, Dongqiang Yang, Yuhua Ru, Shan Cao, Aishe Gao","doi":"10.32604/or.2025.064363","DOIUrl":"https://doi.org/10.32604/or.2025.064363","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3727/096504018X15426763753594.].</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1799-1800"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560717","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
SIK2 inhibitor SIC-19 enhances the sensitivity of PARP inhibitors in triple-negative breast cancers and pancreatic cancers. SIK2抑制剂SIC-19增强PARP抑制剂在三阴性乳腺癌和胰腺癌中的敏感性。
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.062539
Qian Li, Shunpeng Zhu, Mingxian Zhu, Fang Wang, Jinhua Zhou
{"title":"SIK2 inhibitor SIC-19 enhances the sensitivity of PARP inhibitors in triple-negative breast cancers and pancreatic cancers.","authors":"Qian Li, Shunpeng Zhu, Mingxian Zhu, Fang Wang, Jinhua Zhou","doi":"10.32604/or.2025.062539","DOIUrl":"10.32604/or.2025.062539","url":null,"abstract":"<p><strong>Objectives: </strong>Our previous research demonstrated that SIC-19, an innovative inhibitor of salt-inducible kinase 2 (SIK2), effectively reduces SIK2 protein levels through the ubiquitin-proteasome pathway and exhibits synthetic lethal effects with poly ADP-ribose polymerase (PARP) inhibitors in ovarian cancer. However, the role of SIC-19 in triple-negative breast cancer (TNBC) and pancreatic cancer (PC) remains poorly defined. This study aims to investigate whether SIC-19 combined with PARP inhibitors can induce synthetic lethal effects in TNBC and PC.</p><p><strong>Methods: </strong>Cell lines with high SIK2 expression were identified through Western blot analysis. The combination's impact was evaluated using Cell Counting Kit-8 (CCK8), clone formation, and apoptosis assays, as well as <i>in vivo</i> xenograft models.</p><p><strong>Results: </strong>Our findings indicated that the IC50 of SIC-19 was inversely correlated with endogenous SIK2 expression in TNBC and PC cell lines. SIC-19 modulates the homologous recombination repair pathway by suppressing levels of RAD50-pS635, thereby enhancing the sensitivity of TNBC and PC cells, as well as xenografts, to PARP inhibitors.</p><p><strong>Conclusion: </strong>These results underscore the potential of combining PARP inhibitors in combination with SIK2 inhibitors as a novel therapeutic approach to increase PARP inhibition's effectiveness in treating TNBC and PC. This innovative combination therapy represents a promising approach for overcoming resistance mechanisms and improving the outcomes for patients with these challenging malignancies.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1757-1767"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215576/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560654","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
Clinically proven natural products against breast cancer, with mechanistic insights. 临床证明的天然产品抗乳腺癌,与机制的见解。
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.062778
Md Mahmudul Hasan, Shah Md Wasin, Mishu Rahman, Eva Azme, Md Saqline Mostaq, Md Mahedi Hasan Nahid, Nor Mohammad, Farjana Afrin Tanjum, Md Anamul Haque, Md Ashiq Mahmud, Mohammad Nurul Amin
{"title":"Clinically proven natural products against breast cancer, with mechanistic insights.","authors":"Md Mahmudul Hasan, Shah Md Wasin, Mishu Rahman, Eva Azme, Md Saqline Mostaq, Md Mahedi Hasan Nahid, Nor Mohammad, Farjana Afrin Tanjum, Md Anamul Haque, Md Ashiq Mahmud, Mohammad Nurul Amin","doi":"10.32604/or.2025.062778","DOIUrl":"10.32604/or.2025.062778","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer still stands to be the foremost contributor to cancer-related incidence and mortality in women globally accounting for about 14% of all female cancer-related deaths worldwide. This research seeks to illustrate the mechanisms and clinical findings of natural products against breast cancer treatment.</p><p><strong>Methodology: </strong>Required data for this review article was retrieved employing several readily obtainable search databases, including Web of Science<sup>®</sup> (Thomson Reuters, USA), PubMed<sup>®</sup> (U.S. National Library of Medicine, USA), and SciVerse Scopus<sup>®</sup> (Elsevier Properties S.A., USA), taking into consideration certain search terms like \"breast cancer,\" \"natural products against breast cancer,\" and \"Clinically proven natural products in the treatment of breast cancer\" and so on.</p><p><strong>Results: </strong>Several natural products, namely Omega-3 fatty acids, dietary isothiocyanates, curcumin, green tea, flaxseed, limonene, and others, were found to modulate crucial pathways in breast cancer cells. These substances suppressed angiogenesis by downregulating the vascular endothelial growth factor (VEGF), promoted apoptosis by activating caspase enzymes, and prevented cell proliferation by controlling cyclin-dependent kinases. Clinical studies demonstrated improved outcomes in patients receiving these natural products with standard treatment procedures.</p><p><strong>Discussion: </strong>The findings underscore the multifaceted functions of natural products in breast cancer therapy, highlighting their potential to increase the efficacy of conventional treatments while reducing adverse effects. Further exploration of synergistic actions and optimal dosages is needed.</p><p><strong>Conclusion: </strong>Clinically proven natural products represent a potential avenue for breast cancer treatment with their mechanistic insights that facilitate their incorporation into treatment regimens. To maximize clinical applications, future inquiries should center on elucidating the full spectrum of these anticancer functions.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1611-1632"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215606/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560716","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
Plasticity of myeloid-derived suppressor cells in cancer and cancer therapy. 髓源性抑制细胞在癌症和癌症治疗中的可塑性。
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.060063
Jiajia Lv, Xiaoyou Zhong, Lin Wang, Weifei Fan
{"title":"Plasticity of myeloid-derived suppressor cells in cancer and cancer therapy.","authors":"Jiajia Lv, Xiaoyou Zhong, Lin Wang, Weifei Fan","doi":"10.32604/or.2025.060063","DOIUrl":"10.32604/or.2025.060063","url":null,"abstract":"<p><p>The tumor microenvironment (TME) is a complex and dynamic network comprised of tumor cells, surrounding cellular components, various signaling molecules, and the stroma. Myeloid-derived suppressor cells (MDSCs) are pivotal players in the immunosuppressive landscape of the TME, effectively hindering antitumor immune responses and facilitating tumor progression. Originating from pathologically activated myeloid precursors and relatively immature myeloid cells, MDSCs retain plasticity to further differentiate into other myeloid cells, such as macrophages or dendritic cells, which underpins their heterogeneity and adaptability in response to the TME. In this review, we delve into the plasticity of MDSCs in the tumor microenvironment and illuminate the underlying mechanisms that enable them to modulate immune responses. Furthermore, we explore the implications of MDSCs plasticity for cancer therapy, particularly its role in enhancing the efficiency of combination treatments.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1581-1592"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215559/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560651","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
Research review of the mechanism and clinical application prospects of tertiary lymphoid structures in the immune micro-environment of gastrointestinal tumors. 胃肠道肿瘤免疫微环境中三级淋巴结构的机制及临床应用前景研究综述。
IF 2 4区 医学
Oncology Research Pub Date : 2025-06-26 eCollection Date: 2025-01-01 DOI: 10.32604/or.2025.058957
Jiang Zhu
{"title":"Research review of the mechanism and clinical application prospects of tertiary lymphoid structures in the immune micro-environment of gastrointestinal tumors.","authors":"Jiang Zhu","doi":"10.32604/or.2025.058957","DOIUrl":"10.32604/or.2025.058957","url":null,"abstract":"<p><p>Changes in the intestinal immune micro-environment of the gastrointestinal tract are indispensable in the occurrence and development of gastrointestinal cancer. Tertiary lymphoid structure (TLS) is an immune cell aggregation structure found around gastrointestinal cancer in recent years. More and more research proves that tertiary lymphoid structure plays a key biological role and clinical value in disease progression, patient prognosis, and adjuvant treatment. This review aims to explore the research progress, biological significance, and potential clinical applications of TLSs in gastrointestinal tumors. The formation, development, and interaction of TLSs with tumor microenvironment have been reviewed and analyzed in recent years. Meanwhile, this review not only evaluates the clinical value of TLSs as prognostic biomarkers and predictors of treatment response but also explores their role in guiding the formulation of immunotherapy strategies for gastrointestinal tumors. In addition, this review points out the main problems in the current research of TLSs and looks forward to their future development, especially their broad application prospects in the diagnosis, treatment, and prognostic evaluation of gastrointestinal tumors.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"33 7","pages":"1571-1580"},"PeriodicalIF":2.0,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560652","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
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信