Oncotarget最新文献_第2页

Retraction: Ftx non coding RNA-derived miR-545 promotes cell proliferation by targeting RIG-I in hepatocellular carcinoma.

Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28695

Zhikui Liu, Changwei Dou, Bowen Yao, Meng Xu, Linglong Ding, Yufeng Wang, Yuli Jia, Qing Li, Hongyong Zhang, Kangsheng Tu, Tao Song, Qingguang Liu

引用次数: 0

Leukopenia, weight loss and oral mucositis induced by 5-Fluorouracil in hamsters' model: A regenerative approach using electrospun poly(Lactic-co-Glycolic Acid) membrane.

Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28685

Ana Chor, Hélio Dos Santos Dutra, Marcos Lopes Dias, Raquel Pires Gonçalves, Christina Maeda Takiya, Alexandre Malta Rossi, Marcos Farina

{"title":"Leukopenia, weight loss and oral mucositis induced by 5-Fluorouracil in hamsters' model: A regenerative approach using electrospun poly(Lactic-co-Glycolic Acid) membrane.","authors":"Ana Chor, Hélio Dos Santos Dutra, Marcos Lopes Dias, Raquel Pires Gonçalves, Christina Maeda Takiya, Alexandre Malta Rossi, Marcos Farina","doi":"10.18632/oncotarget.28685","DOIUrl":"10.18632/oncotarget.28685","url":null,"abstract":"Clinical parameters of leukogram and weight were analyzed in animal models before and after seven days of 5-FU infusions. A comparison of leukograms before and after 5-FU administrations was analyzed. The results showed a significant difference (p = 0,004), confirming immunosuppression. There was a decrease in the weight of the animals after 7 days of 5-FU infusions (p = 0.02). After immunosuppression occurred, oral mucositis (OM) ulcerative lesions were observed. Two of the animals were selected to receive PLGA dressings. Then, electrospun PLGA membranes, with or without autologous cells, were applied to the ulcerative lesions, aiming to accelerate the regeneration process. Although this therapeutic innovation for OM lesions was still not tested in the bioengineering area, morphological analysis presented promising results. Lesions covered by cell-free PLGA, exhibited areas of inflammation persistence and angiogenesis. The cell-seeded cell-seeded PLGA membrane exhibited complete reepithelialization after 6 days, with minor inflammatory infiltrate. Interestingly, the present work showed preclinical parameters of cachexia induced by chemotherapy for cancer treatment. Moreover, it showed an innovative approach by applying dressings consisting of electrospun PLGA with the addition of autologous mesenchymal cells for OM ulcerative lesions. This promising innovation will pave the way for future applications in oral mucosa lesions.","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"103-117"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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: Methylation-mediated repression of microRNA-129-2 suppresses cell aggressiveness by inhibiting high mobility group box 1 in human hepatocellular carcinoma.

Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28694

Zhikui Liu, Changwei Dou, Bowen Yao, Meng Xu, Linglong Ding, Yufeng Wang, Yuli Jia, Qing Li, Hongyong Zhang, Kangsheng Tu, Tao Song, Qingguang Liu

引用次数: 0

Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells.

Oncotarget Pub Date : 2025-02-18 DOI: 10.18632/oncotarget.28690

Jessica J Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J Munoz, Fred Bunz

{"title":"Robust p53 phenotypes and prospective downstream targets in telomerase-immortalized human cells.","authors":"Jessica J Miciak, Lucy Petrova, Rhythm Sajwan, Aditya Pandya, Mikayla Deckard, Andrew J Munoz, Fred Bunz","doi":"10.18632/oncotarget.28690","DOIUrl":"10.18632/oncotarget.28690","url":null,"abstract":"Cancers that retain wild type TP53 presumably harbor other clonal alterations that permitted their precursors to bypass p53-mediated growth suppression. Consequently, studies that employ TP53-wild type cancer cells and their isogenic derivatives may systematically fail to appreciate the full scope of p53 functionality. Several TP53 phenotypes are known to be absent in the widely used isogenic HCT116 colorectal cancer (CRC) model, which originated from a tumor that had retained wild type TP53. In contrast, we show that restoration of p53 in the TP53-mutant CRC cell line DLD-1 impeded cell proliferation, increased levels of senescence and sensitized cells to ionizing radiation (IR). To study p53 in a non-cancer context, we disrupted TP53 in hTERT-RPE1 cells. Derived from primary cells that were immortalized in vitro, hTERT-RPE1 expressed striking p53-dependent phenotypes and appeared to select for p53 loss during routine culture. hTERT-RPE1 expressed a p53-responsive transcriptome that was highly representative of diverse experimental systems. We discovered several novel downstream p53 targets of potential clinical relevance including ALDH3A1, which is involved in the detoxification of aldehydes and the metabolism of reactive oxygen species, and nectin cell adhesion molecule 4 (NECTIN4) which encodes a secreted surface protein that is overexpressed in many tumors.","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"79-100"},"PeriodicalIF":0.0,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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: Catalytic inhibitors of DNA topoisomerase II suppress the androgen receptor signaling and prostate cancer progression.

Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28692

Haolong Li, Ning Xie, Martin E Gleave, Xuesen Dong

引用次数: 0

Could Panitumumab with very low dose Capecitabine be an option as a maintenance regimen.

Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28687

Doaa A Gamal, Aiat Morsy, Mervat Omar

{"title":"Could Panitumumab with very low dose Capecitabine be an option as a maintenance regimen.","authors":"Doaa A Gamal, Aiat Morsy, Mervat Omar","doi":"10.18632/oncotarget.28687","DOIUrl":"10.18632/oncotarget.28687","url":null,"abstract":"Background: Anti-epidermal growth factor receptor therapy showed an overall median survival improvement in wild type Ras metastatic colorectal cancer. Maintenance with anti EGFR in metastatic colorectal cancer wild type Ras was studied in many trials with promising results and many of these trials gave combined chemo with the target therapy and this combination had shown benefit in the form of synergistic effect and in delaying the resistance to the anti EGFR.Method: In our study patients received 6 cycles of 5-FU based chemotherapy with Panitumumab and patients who had partial response, complete response or stationary disease received metronomic Capecitabine with Panitumumab every 2 weeks for one year. The primary end point was progression free survival (PFS) and the secondary end points were safety, toxicity and overall survival (OS).Results: The median PFS for all patients was 18 ± 1.4 months and the median OS was 45 months. Patients with synchronous metastasis and those who received Oxaliplatin based regimen with Panitumumab were found to have longer PFS compared to those with metachronous metastasis or those who received other chemotherapy regimen with accepted toxicity profile to the maintenance therapy.Conclusion: Using Panitumumab with metronomic Capecitabine is considered an accepted maintenance regimen in wild type Ras metastatic colorectal cancer regardless of the primary site.","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"67-78"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11823472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.

Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28688

Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, Antonin Marchais

{"title":"SETDB1 amplification in osteosarcomas: Insights from its role in healthy tissues and other cancer types.","authors":"Elodie Verdier, Nathalie Gaspar, Maria Eugenia Marques Da Costa, Antonin Marchais","doi":"10.18632/oncotarget.28688","DOIUrl":"10.18632/oncotarget.28688","url":null,"abstract":"Epigenetic modifications, which reversibly regulate gene expression without altering the DNA sequence, are increasingly described in the literature as essential elements in the processes leading to cancer development. SETDB1 regulates histone 3 (H3) K9 di- and trimethylation, promoting heterochromatin formation, and plays a key role in gene silencing. Epigenetic deregulation of SETDB1 expression appears to be involved in different cancers types, particularly in aggressive, relapsing or treatment-resistant subtypes. Despite advances in research, the full range of mechanisms through which this protein acts remains unclear; however, it is evident that SETDB1 has a pivotal role, particularly in the mesenchymal stem cells differentiation, tumor evasion and treatment resistance. Its role in genetically complex sarcomas, such as osteosarcoma, has not been fully explored, although recent Omics analyses suggest its presence and amplification in osteosarcoma. Given its involvement in osteoblastogenesis and adipogenesis, we discuss the potential of SETDB1 as a key target for new therapeutic strategies in osteosarcoma.","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"51-62"},"PeriodicalIF":0.0,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11823473/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143409755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","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: Downregulation of c-SRC kinase CSK promotes castration resistant prostate cancer and pinpoints a novel disease subclass.

Oncotarget Pub Date : 2025-02-12 DOI: 10.18632/oncotarget.28693

Chih-Cheng Yang, Ladan Fazli, Salvatore Loguercio, Irina Zharkikh, Pedro Aza-Blanc, Martin E Gleave, Dieter A Wolf

引用次数: 0

Retraction: MicroRNA-145 down-regulates mucin 5AC to alleviate airway remodeling and targets EGFR to inhibit cytokine expression.

Oncotarget Pub Date : 2025-02-05 DOI: 10.18632/oncotarget.28689

Zhe Cheng, Ling-Ling Dai, Xi Wang, Liu-Qun Jia, Xiao-Gang Jing, Peng-Fei Li, Meng Liu, Huan Wang, Lin An

引用次数: 0

Acquired RUFY1-RET rearrangement as a mechanism of resistance to lorlatinib in a patient with CD74-ROS1 rearranged non-small cell lung cancer: A case report.

Oncotarget Pub Date : 2025-02-05 DOI: 10.18632/oncotarget.28682

Jenny L Wu, Wade T Iams

{"title":"Acquired RUFY1-RET rearrangement as a mechanism of resistance to lorlatinib in a patient with CD74-ROS1 rearranged non-small cell lung cancer: A case report.","authors":"Jenny L Wu, Wade T Iams","doi":"10.18632/oncotarget.28682","DOIUrl":"10.18632/oncotarget.28682","url":null,"abstract":"ROS1 and RET fusions are targetable mutations that occur in a subset of patients with non-small cell lung cancer (NSCLC). ROS1 and RET have been understood to be independent oncogenic drivers which do not co-occur with other common tyrosine kinase receptor mutations except in the acquired resistance setting. Here we present a case of a patient with stage IV CD-74-ROS1 fusion NSCLC discovered initially with RNA next generation sequencing (NGS) who acquired resistance to lorlatinib after 6 months on therapy through a novel RUFY1-RET fusion, detected only through RNA NGS. Combination therapy targeting RET and ROS1 using pralsetinib and lorlatinib achieved a partial response with limited durability of only four months. This is the first reported case of a RET fusion as a potential mechanism of resistance to lorlatinib, it identifies a novel RET fusion partner, and it emphasizes the importance of testing for acquired resistance mutations with both DNA and RNA at the time of progression in patients with targetable oncogenic drivers.","PeriodicalId":19499,"journal":{"name":"Oncotarget","volume":"16 ","pages":"39-42"},"PeriodicalIF":0.0,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11798477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143190084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0