Medical Oncology最新文献

{"title":"Investigation of anticancer potential of a novel bioactive molecule from Trichosporon asahii VITSTB1 in breast cancer cell lines: an in vitro study.","authors":"B Stany, Shatakshi Mishra, P V Tharani, Anwesha Sarkar, Abul Kalam Azad Mandal, K V Bhaskara Rao","doi":"10.1007/s12032-024-02569-1","DOIUrl":"https://doi.org/10.1007/s12032-024-02569-1","url":null,"abstract":"<p><p>The current study investigates the anticancer activity of protein derived from yeast against breast cancer. Yeast-derived proteins illustrate potential as an anticancer agent through mechanisms, such as immune system stimulation via beta-glucans, cytotoxic effects, and modulation of gut microbiota by probiotic strains. The antioxidant activity of yeast-derived proteins can aid in anticancer activity by neutralizing free radicals, thereby reducing oxidative stress and preventing damage to cellular DNA. Employing a comprehensive methodology encompassing yeast isolation, antioxidant screening, molecular characterization, bioactive protein purification, and MTT assay, the research provides crucial insights into the anticancer attributes of the protein extracted from the yeast. The findings reveal significant antioxidant activity that reduces reactive oxygen species (ROS) levels, which are implicated in cancer development. The MTT assay on MCF-7 breast cancer cell lines, characterized by estrogen receptor and progesterone receptor positivity and HER-2 negativity, determined an IC₅₀ value of 54.89 µg/ml, indicating a dose-dependent decrease in cytotoxic effects. These results suggest that the protein derived from Trichosporon asahii VITSTB1 exhibits promising anti-breast cancer properties. Further research is necessary to elucidate the underlying mechanisms, assess efficacy and safety profiles, explore synergies with existing therapies, and conduct animal model studies. Advancing this line of inquiry will significantly contribute to biomedical research and industrial innovation.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"19"},"PeriodicalIF":2.8,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751170","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}

{"title":"Exosomes in esophageal cancer: function and therapeutic prospects.","authors":"Chong Wang, Zhi-Zhou Shi","doi":"10.1007/s12032-024-02543-x","DOIUrl":"10.1007/s12032-024-02543-x","url":null,"abstract":"<p><p>Esophageal cancer (EC) is one of the most common malignant tumors worldwide. Exosomes are a type of extracellular vesicles produced by eukaryotic cells and present in all body fluids. Recent studies have revealed that exosomes can be used as a tool for cell signaling and have great potential in cancer diagnosis and treatment strategies. This article reviews the research progress of exosomes in EC in recent years, mainly including the mechanism of action, diagnostic markers, therapeutic targets, and drug carriers. The challenges faced are discussed to provide guidelines for further research in future.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"18"},"PeriodicalIF":2.8,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142730240","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}

{"title":"The AXL-mediated modulation of myeloid-derived suppressor cells (MDSC) in nasopharyngeal carcinoma.","authors":"Yu Lv, Jiahui Zhu, Sichen Ge, Tao Jiang, Yajia Xu, Weige Yao, Chengyi Jiang","doi":"10.1007/s12032-024-02561-9","DOIUrl":"https://doi.org/10.1007/s12032-024-02561-9","url":null,"abstract":"<p><p>AXL has ubiquitous expression in multiple cancers, and is strongly linked to both tumor progression, metastasis, and poor prognosis, as well as anti-tumor immune response suppression and induction of tumor resistance to immunotherapy. Therefore, it is a strong target for cancer intervention. Despite the wide application of AXL inhibitors in clinical trials, the role of AXL in the tumor immune microenvironment (TIME) remains undetermined. Herein, we established cell lines with stable AXL knockdown or overexpression using lentiviral infection. Subsequently, we co-cultured the cells with healthy human blood-derived CD33 + PBMCs. After two days of culture, we evaluated the differentiation of PBMCs into MDSCs. Additionally, the culture supernatants were collected from both the co-culture system and the individual cultures of each cell group to measure the concentrations of IL-6 and GM-CSF. Additionally, we subcutaneously administered nasopharyngeal carcinoma (NPC) cells into mice, and evaluated the association between AXL content and MDSC recruitment in the resulting tumors. We demonstrated that AXL is a critical modulator of MDSC differentiation and accumulation in NPC. It modulates IL-6, GM-CSF, and Toll-like receptor contents to achieve the aforementioned actions. Herein, we revealed a strong and direct link between AXL, cytokines in TIME, and MDSC differentiation and accumulation. Our work highlights novel approaches to optimizing existing immunotherapeutic interventions.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"17"},"PeriodicalIF":2.8,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142730242","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}

{"title":"Associations between the life's essential 8, genetic risk and breast cancer incidence in premenopausal and postmenopausal women: a prospective study in UK Biobank.","authors":"Zengle Zhao, Tongmin Chang, Xinjie Liu, Hao Bai, Zhen Li, Yuan Zhang, Hao Chen, Tongchao Zhang, Yuan Zhang, Ming Lu","doi":"10.1007/s12032-024-02570-8","DOIUrl":"https://doi.org/10.1007/s12032-024-02570-8","url":null,"abstract":"<p><p>The combined effect of cardiovascular risk factors on breast cancer in women is unknown. The relationship between genetic risk combined with cardiovascular health (CVH) levels and breast cancer has not been confirmed. This study aims to explore the relationship between CVH level based on life's essential 8 (LE8) score and breast cancer risk in women with different menopausal statuses and to estimate further the effect of CVH level combined with genetic susceptibility on breast cancer risk. A total of 118,911 women from UK Biobank were included in the study, including 22,676 premenopausal women and 96,235 postmenopausal women. The association between the CVH level and the risk of breast cancer in women with different menopausal statuses was assessed using the Cox proportional hazards regression models, with the healthiest CVH group as the reference. In addition, risk ratios (HRs) and 95% confidence intervals (95% CIs) for the joint effect of the CVH level and polygenic risk score (PRS) were calculated using the PRS from the UK Biobank. During a mean follow-up period of 13.8 years, we observed 733 cases and 3,645 cases of breast cancer in premenopausal and postmenopausal women, respectively. In premenopausal women, the risk of breast cancer was significantly increased in the intermediate CVH group (HR, 1.28; 95%CI 1.08-1.52) and the low CVH group (HR, 1.44; 95%CI 1.13-1.85). In postmenopausal women, the risk of incidence was also significantly increased in the intermediate CVH group (HR, 1.20; 95%CI 1.07-1.32) and the low CVH group (HR, 1.34; 95%CI 1.17-1.54). In the joint effect analysis, the risk of breast cancer for women in the low CVH group and the high genetic risk group was highest in both premenopausal (HR, 8.26; 95%CI 4.44-15.35) and postmenopausal (HR, 8.10; 95%CI 5.50-11.93) women. Women with lower LE8 scores and higher genetic susceptibility have the higher risk of breast cancer. This suggests that women with lower levels of CVH and higher genetic susceptibility have an increased risk of breast cancer under different menopausal statuses.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"16"},"PeriodicalIF":2.8,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142730237","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}

{"title":"Telomerase inhibition in breast cancer and breast cancer stem cells: a brief review.","authors":"İrem Yildirim, Çığır Biray Avci","doi":"10.1007/s12032-024-02562-8","DOIUrl":"10.1007/s12032-024-02562-8","url":null,"abstract":"<p><p>Breast cancer is a major health problem, accounting for one third of all cancers in women. There is no definitive treatment for breast cancer and its incidence is increasing worldwide every year. Furthermore, breast cancer stem cells cause resistance to radiation and chemotherapy. Telomerase is an enzyme that protects telomeres and is activated in 90% of cancer cells, and telomerase activation is a hallmark of cancer. In this review, we examine telomerase activation in breast cancer and breast cancer stem cells and the therapeutic effects of telomerase inhibition in these cells. In this review, we aim to highlight the importance and impact of telomerase inhibition in the treatment of breast cancer and the lack of studies specifically in breast cancer stem cells.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"14"},"PeriodicalIF":2.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710578","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}

{"title":"An overview on the interaction between non-coding RNAs and CTLA-4 gene in human diseases.","authors":"Amir Ebrahimi, Tahereh Barati, Zohreh Mirzaei, Fatemeh Fattahi, Sima Mansoori Derakhshan, Mahmoud Shekari Khaniani","doi":"10.1007/s12032-024-02552-w","DOIUrl":"10.1007/s12032-024-02552-w","url":null,"abstract":"<p><p>Cytotoxic T lymphocyte antigen 4 (CTLA-4), in conjunction with PD-1 and CD28, plays a pivotal role in the modulation of T-cell activation. Specifically, CTLA-4 exerts its influence by impeding the generation of IL-2 and the proliferation of T cells. CTLA-4, being a receptor with a high affinity, engages in competitive binding with CD28 for the interaction with primary T-cell activator molecules, specifically CD80 and CD86. The appropriate functioning of T-cell activation is contingent upon maintaining a precise equilibrium between CTLA-4 and CD28. Consequently, any disruption in the expression of CTLA-4 significantly enhances the risk for a range of severe ailments, such as cancer, infectious diseases, allergies, and notably autoimmune diseases. The significance of epigenetic regulation of CTLA-4, particularly through non-coding RNAs (ncRNAs) such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), has considerable weight within this particular framework. To date, there have been associations shown between various abnormalities in the expression of ncRNAs that regulate CTLA-4 and clinicopathological characteristics. Nevertheless, it is evident that there is a lack of a comprehensive investigation. Hence, the present work was undertaken to summarize the existing research on the epigenetic control of CTLA-4, with a primary emphasis on elucidating the regulatory procedures, biological processes, and clinical applications in human diseases. The objective of this review is to acquire a thorough comprehension of the relationship between RNA/lncRNA/miRNA/mRNA (CTLA-4) and its role in the progression of diverse human disorders.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"13"},"PeriodicalIF":2.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710556","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}

{"title":"Exploring the role of antigen-presenting cancer-associated fibroblasts and CD74 on the pancreatic ductal adenocarcinoma tumor microenvironment.","authors":"Michael E Thomas, Emily Jie, Austin M Kim, Trenton G Mayberry, Braydon C Cowan, Harrison D Luechtefeld, Mark R Wakefield, Yujiang Fang","doi":"10.1007/s12032-024-02564-6","DOIUrl":"10.1007/s12032-024-02564-6","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC) has proven to be a formidable cancer primarily due to its tumor microenvironment (TME). This highly desmoplastic, hypoxic, and pro-inflammatory environment has not only been shown to facilitate the growth and metastasis of PDAC but has also displayed powerful immunosuppressive capabilities. A critical cell involved in the development of the PDAC TME is the fibroblast, specifically the antigen-presenting cancer-associated fibroblast (apCAF). The pro-inflammatory environment of PDAC induces the proliferation of apCAFs, promoting immunosuppression through immune cell inactivation, immune response regulation, and expression of CD74. In conjunction with apCAFs and tumor cells, CD74 serves as a versatile promoter of PDAC by preventing tumor antigen-expression on tumor cells, upregulating the expression of immunosuppressive chemical mediators, and activating proliferative pathways to induce PDAC malignancy. This review will highlight critical mediators and pathways that promote the PDAC stroma and TME with its hypoxic and immunosuppressive properties. Further, we will highlight the nature of apCAFs and CD74, their specific roles in the PDAC TME, and their potential as targets for immunotherapy.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"15"},"PeriodicalIF":2.8,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710557","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}

{"title":"N6-methyladenosine RNA modification in head and neck squamous cell carcinoma (HNSCC): current status and future insights.","authors":"Pramodha Janakiraman, Jayasree Peroth Jayaprakash, Sridhanya Velayudham Muralidharan, Kumar Pranav Narayan, Piyush Khandelia","doi":"10.1007/s12032-024-02566-4","DOIUrl":"10.1007/s12032-024-02566-4","url":null,"abstract":"<p><p>N6-methyladenosine (m6A) plays a pivotal role in regulating epitranscriptomic mechanisms and is closely linked to the normal functioning of diverse classes of RNAs, both coding as well as noncoding. Recent research highlights the role of m6A RNA methylation in the onset and progression of several cancers, including head and neck squamous cell carcinoma (HNSCC). HNSCC ranks as the seventh most common cancer globally, with a five-year patient survival rate of just 50%. Elevated m6A RNA methylation levels and deregulated expression of various m6A modifiers, i.e. writers, readers, and erasers, have been reported across nearly all HNSCC subtypes. Numerous studies have demonstrated that m6A modifications significantly impact key hallmarks of HNSCC, such as proliferation, apoptosis, migration, and invasion. Furthermore, m6A impacts epithelial-mesenchymal transition (EMT), drug resistance, and aerobic glycolysis, and disrupts the tumor microenvironment. Additionally, transcripts regulated by m6A in HNSCC present themselves as potential diagnostic and prognostic biomarkers. This review attempts to comprehensively summarize the role of m6A RNA methylation and its modifiers in regulating various facets of HNSCC pathogenesis.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"12"},"PeriodicalIF":2.8,"publicationDate":"2024-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142710559","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}

{"title":"Dual roles of extracellular vesicles in acute lymphoblastic leukemia: implications for disease progression and theranostic strategies.","authors":"Mahya Sadat Lajevardi, Mahshad Ashrafpour, Shaden M H Mubarak, Behnoosh Rafieyan, Arash Kiani, Effat Noori, Marzieh Roayaei Ardakani, Maryam Montazeri, Niloofar Kouhi Esfahani, Naghmeh Asadimanesh, Saeed Khalili, Zahra Payandeh","doi":"10.1007/s12032-024-02547-7","DOIUrl":"10.1007/s12032-024-02547-7","url":null,"abstract":"<p><p>Acute Lymphoblastic Leukemia (ALL) is a heterogeneous blood cancer characterized by the uncontrolled growth of immature lymphoid cells due to dysregulated signaling pathways. It is the most common pediatric cancer, with high cure rates in children, but significantly lower survival rates in adults. Current theranostic strategies, including chemotherapy, immunotherapy, and nanomedicine, aim to improve detection and treatment precision but are limited by side effects, drug resistance, high costs, and stability issues. Notably, extracellular vesicles (EVs) offer a promising alternative, addressing these limitations through their natural biocompatibility and targeted delivery capabilities. EVs play a dual role in ALL: they contribute to leukemia progression by promoting tumor growth, immune suppression, and drug resistance via the transfer of oncogenic molecules, while also serving as valuable non-invasive biomarkers due to their specific miRNA and protein content. Their ability to deliver therapeutic agents directly to leukemic cells, combined with their stability and low immunogenicity, makes EVs a compelling tool for improving ALL treatments. Indeed, by targeting the molecular pathways influenced by EVs or leveraging them for drug delivery, innovative therapeutic strategies can be developed to enhance treatment outcomes and reduce side effects. Thus, EVs represent a promising frontier for advancing theranostic strategies in ALL, offering new opportunities to improve diagnosis and treatment while overcoming the limitations of traditional therapies. This review will explore the dual roles of EVs in ALL, addressing their contributions to disease progression and their potential as therapeutic agents and biomarkers for early diagnosis and targeted therapies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"11"},"PeriodicalIF":2.8,"publicationDate":"2024-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11582151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142687365","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}

{"title":"Letter to the editor: the potential value of NDUFA4L2 in colon adenocarcinoma remains to be fully evaluated.","authors":"Ziye Zhuang, Qiang Cao, Hao Chi","doi":"10.1007/s12032-024-02571-7","DOIUrl":"https://doi.org/10.1007/s12032-024-02571-7","url":null,"abstract":"<p><p>This letter addresses the recent study by Zhou et al. on NDUFA4L2's role in colon adenocarcinoma (COAD), highlighting its potential as a therapeutic target. While the research is laudable, we identify areas for further refinement. Firstly, we suggest employing Weighted Gene Co-expression Network Analysis (WGCNA) to better understand NDUFA4L2's functional role in COAD by examining gene modules that co-vary with its expression. Secondly, we recommend expanding the analysis to include potential drugs targeting NDUFA4L2 using the Comparative Toxicogenomics Database (CTD) and molecular simulations to validate these interactions. Lastly, we propose Mendelian randomization analysis to establish a causal link between NDUFA4L2 expression and COAD risk. By implementing these suggestions, the study could be significantly enhanced, offering deeper insights into COAD's molecular mechanisms and more precise therapeutic strategies. Our commentary aims to enrich the genomic findings and contribute to the advancement of COAD research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 1","pages":"10"},"PeriodicalIF":2.8,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142682237","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}