Oncoscience最新文献

{"title":"Re-enforcing the strategy of targeting MEK/ERK signaling to overcome acquired resistance to third generation EGFR inhibitors.","authors":"Wen Zhao, Shi-Yong Sun","doi":"10.18632/oncoscience.539","DOIUrl":"https://doi.org/10.18632/oncoscience.539","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8336935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39301446","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}

{"title":"A precision approach to breast cancer treatment based on cell lineage-specific vulnerabilities.","authors":"Jay S Desgrosellier","doi":"10.18632/oncoscience.538","DOIUrl":"https://doi.org/10.18632/oncoscience.538","url":null,"abstract":"Breast cancers display significant intra-tumoral heterogeneity posing a major barrier to effective breast cancer treatments [1, 2]. This heterogeneity can be manifested in terms of genetic abnormalities or the presence of distinct cell types bearing similarities to the different epithelial lineages in the normal adult mammary gland including: luminal cells, basal cells, their respective progenitors, and stem cells [3]. The cell lineages present within a given tumor may determine the likelihood of progression. This is best exemplified by sub-populations of tumor-initiating cells present in aggressive breast cancers, some of which resemble adult mammary stem cells [4-9] and thus are termed stem-like. These stem-like cells are enriched in residual tumors after chemotherapy [10] as well as early metastatic lesions [11], suggesting they play a critical role in breast cancer progression. While attempts to treat breast cancers based on genetic mutations have largely been unsuccessful, therapies targeting particular cell lineages, including stem-like cells, are gaining renewed appreciation. Toward this goal, studies have uncovered distinct dependencies among different breast cancer cell types for particular cell death/survival pathways. These recent advances may open the door for new highly personalized approaches to breast cancer therapy. Our previous studies found that stem-like cells were highly sensitive to cell death induced by p53-upregulated mediator of apoptosis (PUMA) [12], a pro-apoptotic BH3-only member of the Bcl-2 family. These effects were specific to PUMA [12] as the related family member NOXA had no effect on stem-like cells consistent with its role in targeting basal-like breast cancer cells [13]. We further found that driving PUMA expression was sufficient to deplete stem-like cells and reduce metastasis in vivo, revealing its role as an important metastasis suppressor. Our results are consistent with published findings that PUMA-mediated cell death is the preferred response in some normal adult stem cell populations [14]. In an effort Research Perspective","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8192127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39092409","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}

{"title":"SCIRT lncRNA slows the formation of tumour initiating cells in breast cancer.","authors":"Alex de Giorgio, Leandro Castellano","doi":"10.18632/oncoscience.537","DOIUrl":"https://doi.org/10.18632/oncoscience.537","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8175088/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39068362","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}

{"title":"Radiomic-based diagnostics in oncology: challenges toward clinical practice.","authors":"Emanuele Barabino, Giovanni Rossi, Alessandro Fedeli, Giuseppe Cittadini, Carlo Genova","doi":"10.18632/oncoscience.536","DOIUrl":"https://doi.org/10.18632/oncoscience.536","url":null,"abstract":"Emanuele Barabino1, Giovanni Rossi2,3, Alessandro Fedeli4, Giuseppe Cittadini5 and Carlo Genova6,7 1Interventional Angiography, Ospedale Santa Corona ASL 2 Savonese, Pietra Ligure, Italy 2Medical Oncology Department, Ospedale Padre Antero Micone, Genova, Italy 3Department of Medical, Surgical and Experimental Sciences, University of Sassari, Sassari, Italy 4Department of Electrical, Electronic, Telecommunications Engineering, and Naval Architecture, University of Genoa, Genova, Italy 5UO Radiologia Generale, IRCCS Ospedale Policlinico San Martino, Genova, Italy 6UOC Clinica di Oncologia Medica, IRCCS Ospedale Policlinico San Martino, Genova, Italy 7Dipartimento di Medicina Interna e Specialità Mediche (DiMI), Facoltà di Medicina e Chirurgia, Università degli Studi di Genova, Genova, Italy","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8174115/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39068361","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}

{"title":"Constitutive activation of MEK5 promotes a mesenchymal and migratory cell phenotype in triple negative breast cancer.","authors":"Margarite D Matossian, Van T Hoang, Hope E Burks, Jacqueline La, Steven Elliott, Courtney Brock, Douglas B Rusch, Aaron Buechlein, Kenneth P Nephew, Akshita Bhatt, Jane E Cavanaugh, Patrick T Flaherty, Bridgette M Collins-Burow, Matthew E Burow","doi":"10.18632/oncoscience.535","DOIUrl":"10.18632/oncoscience.535","url":null,"abstract":"<p><p>Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited targeted therapeutic options. A defining feature of TNBC is the propensity to metastasize and acquire resistance to cytotoxic agents. Mitogen activated protein kinase (MAPK) and extracellular regulated kinase (ERK) signaling pathways have integral roles in cancer development and progression. While MEK5/ERK5 signaling drives mesenchymal and migratory cell phenotypes in breast cancer, the specific mechanisms underlying these actions remain under-characterized. To elucidate the mechanisms through which MEK5 regulates the mesenchymal and migratory phenotype, we generated stably transfected constitutively active MEK5 (MEK5-ca) TNBC cells. Downstream signaling pathways and candidate targets of MEK5-ca cells were based on RNA sequencing and confirmed using qPCR and Western blot analyses. MEK5 activation drove a mesenchymal cell phenotype independent of cell proliferation effects. Transwell migration assays demonstrated MEK5 activation significantly increased breast cancer cell migration. In this study, we provide supporting evidence that MEK5 functions through FRA-1 to regulate the mesenchymal and migratory phenotype in TNBC.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8131078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39010120","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}

{"title":"p53 activation vs. stabilization: an acetylation tale from the C-terminal tail.","authors":"Ning Kon,&nbsp;Wei Gu","doi":"10.18632/oncoscience.534","DOIUrl":"https://doi.org/10.18632/oncoscience.534","url":null,"abstract":"Ning Kon1, and Wei Gu1,2,3 1 Institute for Cancer Genetics, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA 2 Department of Pathology and Cell Biology, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA 3 Herbert Irving Comprehensive Cancer Center, Vagelos College of Physicians & Surgeons, Columbia University Irving Medical Center, New York, NY 10032, USA","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8115982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39000587","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}

{"title":"A \"two-hit\" (chemo)therapy to improve checkpoint inhibition in cancer.","authors":"Paolo Falvo, Stefania Orecchioni, Alessandro Raveane, Giulia Mitola, Francesco Bertolini","doi":"10.18632/oncoscience.533","DOIUrl":"10.18632/oncoscience.533","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8115984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39000586","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}

{"title":"A novel RNA-based approach to counteract EMT.","authors":"Sabrina Garbo,&nbsp;Marco Tripodi,&nbsp;Cecilia Battistelli","doi":"10.18632/oncoscience.532","DOIUrl":"https://doi.org/10.18632/oncoscience.532","url":null,"abstract":"Epithelial to mesenchymal transition (EMT) is a key signature in both physiological processes (i.e. development, regeneration, wound healing) and in tumor metastasis [1]. While the involvement of transcription factors (e.g. SNAIL, SLUG, ZEB1/2, TWIST1/2) has been extensively explored, the contribution of epigenetic mechanisms has emerged only in the last decades [2]; furthermore, interest is growing in the role of ncRNAs (e.g. miRNAs and lncRNAs) in modulating cell plasticity. In particular, it was reported that HOTAIR, a well-established predictor of metastasis in different solid tumors, is involved in chromatin modification, acting as a scaffold for the general chromatin modifier PRC2 complex in tumorigenesis [3, 4]; however, the mechanisms conferring specificity to the PRC2 recruitment to genomic loci during EMT was not disclosed. In the last years, we focused on the role of the lncRNA HOTAIR in relation to the EMT master transcriptional factor SNAIL. We reported that SNAIL directly interacts with HOTAIR, thus conferring the site-specificity to the recruitment of PRC2 complex on promoters of epithelial genes upon EMT induction [5]. The central mechanistic role of HOTAIR is represented by its bridging activity that allows the interaction between SNAIL and the catalytic subunit of the PRC2 complex, EZH2. Functionally, HOTAIR depletion was shown to inhibit the SNAIL repressive capacity. Building on this evidence, we designed an RNAbased dominant negative molecular approach to counteract HOTAIR function in hepatocellular carcinoma (HCC) cells. RNA therapeutics represent a growing field of investigation and application. The use of RNA molecules shows several advantages since they show a very low immunogenicity, are able to penetrate the cell/nuclear membrane, and to target the desired gene even if highly expressed, they are cheap and easy to synthesize, and can be chemically modified, in order to increase their stability or to stabilize secondary structures. Moreover, concerning the delivery of these molecules, in recent years, many strategies have been developed for increasing the efficient delivery of RNA therapeutic molecules to specific target cells. Some of these strategies are represented by the use Research Perspective","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8115983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39000585","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}

{"title":"Alternative splicing of CERS2 promotes cell proliferation and migration in luminal B subtype breast cancer cells.","authors":"Trishna Pani,&nbsp;Kajal Rajput,&nbsp;Animesh Kar,&nbsp;Ujjaini Dasgupta","doi":"10.18632/oncoscience.531","DOIUrl":"https://doi.org/10.18632/oncoscience.531","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8057095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38897116","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}

{"title":"Importance of amino acids in brain parenchyma invasion by cancer cells.","authors":"Alessio Paone,&nbsp;Amani Bouzidi,&nbsp;Serena Rinaldo,&nbsp;Giorgio Giardina,&nbsp;Francesca Cutruzzolà","doi":"10.18632/oncoscience.530","DOIUrl":"https://doi.org/10.18632/oncoscience.530","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8045980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38897115","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}