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Squamous cell carcinoma of the oral cavity - follow up treatment and distant metastatic behavior. 口腔鳞状细胞癌的随访治疗和远处转移行为。
Oncoscience Pub Date : 2023-01-01 DOI: 10.18632/oncoscience.582
Florian Dudde, Ina Giersdorf, Filip Barbarewicz, Kai-Olaf Henkel
{"title":"Squamous cell carcinoma of the oral cavity - follow up treatment and distant metastatic behavior.","authors":"Florian Dudde, Ina Giersdorf, Filip Barbarewicz, Kai-Olaf Henkel","doi":"10.18632/oncoscience.582","DOIUrl":"https://doi.org/10.18632/oncoscience.582","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10424877/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10012658","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
Think outside the box - atypical infections in chronic sinusitis. 跳出常规思维——慢性鼻窦炎中的非典型感染。
Oncoscience Pub Date : 2023-01-01 DOI: 10.18632/oncoscience.576
Florian Dudde, Kai-Olaf Henkel, Filip Barbarewicz
{"title":"Think outside the box - atypical infections in chronic sinusitis.","authors":"Florian Dudde, Kai-Olaf Henkel, Filip Barbarewicz","doi":"10.18632/oncoscience.576","DOIUrl":"https://doi.org/10.18632/oncoscience.576","url":null,"abstract":"Inflammations of the paranasal sinuses represent a common clinical picture. The annual prevalence of chronic sinusitis in Europe is up to 10% [1]. Sinusitis can be divided into acute and chronic forms. In particular, the chronic forms (>12 weeks duration) are often challenging in the context of therapy. In general, all ventilation disorders of the paranasal sinuses (concha bullosa, nasal septal deviations, etc.,) represent risk factors for the development of any form of sinusitis [2]. In addition, an immune deficiency or systemic diseases relevant to the immune system predispose to infections with atypical pathogens. Most sinusitis are caused by viruses, sometimes bacteria and, in rare cases, fungal infections [3]. Furthermore, sinusitis can be differentiated with regard to the affected paranasal sinuses. Unilateral sinusitis can often result from a dental focus and/or a fungal infection such as aspergillosis [4, 5]. However, pathophysiologically, active and chronic sinusitis differ in terms of the sometimes irreversible remodeling processes in the mucosa [6].","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10228541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9922649","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
Mitochondrial regulator ATAD3A: a molecular determinant favoring head and neck cancer development. 线粒体调节因子ATAD3A:促进头颈癌发展的分子决定因素
Oncoscience Pub Date : 2023-01-01 DOI: 10.18632/oncoscience.574
Yong Teng
{"title":"Mitochondrial regulator ATAD3A: a molecular determinant favoring head and neck cancer development.","authors":"Yong Teng","doi":"10.18632/oncoscience.574","DOIUrl":"https://doi.org/10.18632/oncoscience.574","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10109270/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9385171","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
Cancer cell repopulation after therapy: which is the mechanism? 治疗后癌细胞再生:机制是什么?
Oncoscience Pub Date : 2023-01-01 DOI: 10.18632/oncoscience.577
Rewati Prakash, Carlos M Telleria
{"title":"Cancer cell repopulation after therapy: which is the mechanism?","authors":"Rewati Prakash,&nbsp;Carlos M Telleria","doi":"10.18632/oncoscience.577","DOIUrl":"https://doi.org/10.18632/oncoscience.577","url":null,"abstract":"<p><p>Cancer cell repopulation after therapy is a phenomenon that leads to therapeutic failure with the consequent relapse of the disease. The process is understudied and mechanisms need to be uncovered. Here we discuss the issue of cancer cell repopulation after chemo- and radio-therapies. We compile evidence alleging that the repopulation of cancer cells can be originated from either cancer stem cells resistant to therapy, cancer cells that in response to therapy become polyploid and thereafter germinate into near-diploid rapid proliferating cells, and/or cells that respond to treatment undergoing senescence as a transient mechanism to survive, followed by the reinitiation of the cell cycle. Approaches targeted to prevent this post-therapy cancer cell repopulation should be uncovered to prevent tumor relapse and thus increase overall survival from this devastating disease.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10234569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9578364","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: 1
Lipiodol: from intrusion until exile from the tumor microenvironment. 脂碘醇:从侵入到被肿瘤微环境驱逐。
Oncoscience Pub Date : 2023-01-01 DOI: 10.18632/oncoscience.584
Sheena Anand, Jean-François Geschwind, Vahid Etezadi, Nariman Nezami
{"title":"Lipiodol: from intrusion until exile from the tumor microenvironment.","authors":"Sheena Anand,&nbsp;Jean-François Geschwind,&nbsp;Vahid Etezadi,&nbsp;Nariman Nezami","doi":"10.18632/oncoscience.584","DOIUrl":"https://doi.org/10.18632/oncoscience.584","url":null,"abstract":"Lipiodol or ethiodized oil, which is extracted from poppyseed oil, is a transparent straw-colored oil which sinks when combined with water [1]. Lipiodol does not dissolve when combined with aqueous solutions and can be iodinated with I 131 , thus making the compound both imageable and therapeutic. The radiopacity of lipiodol originates from its iodine content.","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10434996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10050585","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
Exiting the pandemic together: achieving global immunity and equity. 共同退出大流行:实现全球免疫和公平。
Oncoscience Pub Date : 2023-01-01 DOI: 10.18632/oncoscience.585
Yuxin Ying, Jola Bytyci, Lennard Yw Lee
{"title":"Exiting the pandemic together: achieving global immunity and equity.","authors":"Yuxin Ying,&nbsp;Jola Bytyci,&nbsp;Lennard Yw Lee","doi":"10.18632/oncoscience.585","DOIUrl":"https://doi.org/10.18632/oncoscience.585","url":null,"abstract":"","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10473133/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10208225","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
Modulation of heme and tumor vascular oxygenation- a novel strategy for lung cancer therapy. 调节血红素和肿瘤血管氧合-肺癌治疗的新策略。
Oncoscience Pub Date : 2022-12-02 eCollection Date: 2022-01-01 DOI: 10.18632/oncoscience.569
Poorva Ghosh, Ralph P Mason, Li Liu, Li Zhang
{"title":"Modulation of heme and tumor vascular oxygenation- a novel strategy for lung cancer therapy.","authors":"Poorva Ghosh,&nbsp;Ralph P Mason,&nbsp;Li Liu,&nbsp;Li Zhang","doi":"10.18632/oncoscience.569","DOIUrl":"https://doi.org/10.18632/oncoscience.569","url":null,"abstract":"<p><p>Hypoxia and faulty vasculature are well-known hallmarks of cancer and in addition to being associated with poor prognosis in patients, these hallmarks are also known to contribute to therapy resistance. In recent years, therapeutics that alleviate hypoxia and promote normalization of vasculature are being explored for cancer therapy. In addition to being hypoxic, cancers such as non-small cell lung cancers exhibit elevated oxidative phosphorylation. Therapeutic strategies that can normalize vasculature and reduce oxidative phosphorylation could greatly benefit the landscape of cancer therapeutics. Here, we highlight a heme-targeting therapeutic strategy that demonstrates significant tumor growth inhibition in non-small cell lung cancer mouse models using multi-spectral optoacoustic tomography.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9718586/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"35210835","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: 1
Ikaros as a downstream mediator of BCR blockade therapy in B-cell non-Hodgkin lymphoma. Ikaros作为b细胞非霍奇金淋巴瘤BCR阻断治疗的下游介质。
Oncoscience Pub Date : 2022-11-28 eCollection Date: 2022-01-01 DOI: 10.18632/oncoscience.568
Marcelo Lima Ribeiro, Emmanuel Normant, Gaël Roué
{"title":"Ikaros as a downstream mediator of BCR blockade therapy in B-cell non-Hodgkin lymphoma.","authors":"Marcelo Lima Ribeiro,&nbsp;Emmanuel Normant,&nbsp;Gaël Roué","doi":"10.18632/oncoscience.568","DOIUrl":"https://doi.org/10.18632/oncoscience.568","url":null,"abstract":"B cell receptor (BCR) complex is essential for B cell development and function, being its downstream effectors involved in the regulation of several biological process such as immune response, cell growth, adhesion, differentiation, survival, cytoskeletal remodeling, and apoptosis [1]. Genetic events leading to BCR constitutive activation and consequent enhancement of tumor cell proliferation and survival, are frequently observed in B-cell non-Hodgkin lymphoma (B-NHL) patients [2]. In the last decade, numerous studies have highlighted that pharmacological targeting of Bruton’s tyrosine kinase (BTK), an apical component of the BCR axis, represents an excellent anti-tumor strategy in chronic lymphocytic leukemia (CLL) and in determined subtype of B-NHL including mantle cell lymphoma (MCL) and follicular lymphoma (FL). Most BTK inhibitors bind irreversibly to the ATP binding site of BTK at the Cys481 amino acid residue, forming a covalent bond that impairs the Editorial","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9708099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40456982","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: 1
A murine model for human early/immature T-cell precursor acute lymphoblastic leukemia (EITP ALL). 人早期/未成熟t细胞前体急性淋巴细胞白血病(EITP ALL)小鼠模型的建立。
Oncoscience Pub Date : 2022-10-24 eCollection Date: 2022-01-01 DOI: 10.18632/oncoscience.567
Vijay Negi, Peter D Aplan
{"title":"A murine model for human early/immature T-cell precursor acute lymphoblastic leukemia (EITP ALL).","authors":"Vijay Negi,&nbsp;Peter D Aplan","doi":"10.18632/oncoscience.567","DOIUrl":"https://doi.org/10.18632/oncoscience.567","url":null,"abstract":"<p><p>Early/immature T cell precursor acute lymphoblastic leukemia (EITP ALL) represents a subset of human leukemias distinct from other T-ALL, and associated with poor prognosis. Clinical studies have identified chromosomal translocations involving the <i>NUP98</i> gene and point mutations of <i>IDH</i> genes as recurrent mutations in patients with EITP-ALL. In a recent study using genetically engineered mice, we demonstrated that cooperation of an <i>Idh2<sup>R140Q</sup></i> mutation with a <i>NUP98-HOXD13</i> (<i>NHD13</i>) fusion gene resulted in EITP-ALL. Highlights of this double transgenic mouse model included the similarity of the immunophenotypic, mutational and gene expression landscape with human EITP-ALL. Additional studies showed that the <i>Idh2<sup>R140Q</sup></i> /<i>NHD13 EITP-ALL</i> are sensitive to selective mutant <i>IDH2</i> inhibitors <i>in vitro</i>, leading to the possibility that these mice can serve as a useful model for the study of EITP ALL development and therapy.</p>","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9628740/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40443797","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
GM-CSF - an oncogenic driver of HER2+ breast leptomeningeal metastasis. GM-CSF - HER2阳性乳腺轻脑膜转移的致癌驱动因子
Oncoscience Pub Date : 2022-10-10 eCollection Date: 2022-01-01 DOI: 10.18632/oncoscience.566
Rachana Garg, Kai Jandial, Mike Chen
{"title":"GM-CSF - an oncogenic driver of HER2+ breast leptomeningeal metastasis.","authors":"Rachana Garg,&nbsp;Kai Jandial,&nbsp;Mike Chen","doi":"10.18632/oncoscience.566","DOIUrl":"https://doi.org/10.18632/oncoscience.566","url":null,"abstract":"and OPCs, cultured alone or with Lepto cells, revealed TPP1 as the regulator of GM-CSF; it mediates GM-CSF proteolytic degradation and suppresses signaling, thereby decreasing Lepto cell viability and tumor progression. Remarkably, combinatorial treatment of anti-GM-CSF antibody with a pan-Aurora kinase inhibitor (CCT137690) synergistically halts GM-CSF signaling and HER2+ LC growth in vitro and in vivo . Our work has demonstrated neural niche-specific crosstalk between HER2+ LC tumors and OPCs and established the efficacy of intrathecal administration of TPP1 protease, anti-GM-CSF antibodies, and pan-Aurora kinase inhibitors in combating HER2+ LC (Figure 1). This may offer a targetable axis to treat HER2+ LC in the clinics.","PeriodicalId":19508,"journal":{"name":"Oncoscience","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9549905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33502640","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: 1
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