TY - JOUR AU - Campilan, B. AU - Schroeder, C. AU - Sagaityte, E. AU - Arditi, J. AU - Leary, O.P. AU - Gokaslan, Z.L. AU - Sullivan, P.L.Z. AU - Martinez-Moreno, M. TI - Animal model considerations for chordoma research: reproducing the tumor microenvironment in vivo with humanized mice JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1330254 UR - https://m2.mtmt.hu/api/publication/34807106 ID - 34807106 N1 - Export Date: 22 April 2024 LA - English DB - MTMT ER - TY - JOUR AU - Pöhlmann, J. AU - Weller, M. AU - Marcellusi, A. AU - Grabe-Heyne, K. AU - Krott-Coi, L. AU - Rabar, S. AU - Pollock, R.F. TI - High costs, low quality of life, reduced survival, and room for improving treatment: an analysis of burden and unmet needs in glioma JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1368606 UR - https://m2.mtmt.hu/api/publication/34804484 ID - 34804484 N1 - Covalence Research Ltd, Harpenden, United Kingdom Department of Neurology, University Hospital and University of Zurich, Zurich, Switzerland Economic Evaluation and HTA (EEHTA)-Centre for Economic and International Studies (CEIS), Faculty of Economics, University of Rome “Tor Vergata”, Rome, Italy Medac GmbH, Wedel, Germany Export Date: 22 April 2024 Correspondence Address: Pöhlmann, J.; Covalence Research LtdUnited Kingdom; email: poehlmann@covalence-research.com LA - English DB - MTMT ER - TY - JOUR AU - Qin, P. AU - Li, Q. AU - Zu, Q. AU - Dong, R. AU - Qi, Y. TI - Natural products targeting autophagy and apoptosis in NSCLC: a novel therapeutic strategy JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1379698 UR - https://m2.mtmt.hu/api/publication/34804096 ID - 34804096 N1 - First Clinical Medical College, Shandong University of Traditional Chinese Medicine, Jinan, China Shandong College of Traditional Chinese Medicine, Shandong, Yantai, China Department of Orthopedics, First Affiliated Hospital of Dalian Medical University, Dalian, China Department of Oncology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan, China Export Date: 22 April 2024 Correspondence Address: Qi, Y.; Department of Oncology, China; email: m13793132317@163.com LA - English DB - MTMT ER - TY - JOUR AU - Sriramareddy, S.N. AU - Jamakhani, M. AU - Vilanova, L. AU - Brossel, H. AU - Staumont, B. AU - Hamaidia, M. TI - Selective inhibition of DNA ligase IV provides additional efficacy to the treatment of anaplastic thyroid cancer JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1323313 UR - https://m2.mtmt.hu/api/publication/34798590 ID - 34798590 N1 - Molecular and Cellular Epigenetics, Interdisciplinary Cluster for Applied Genoproteomics (GIGA), University of Liège, Liège, Belgium Molecular Biology (TERRA), University of Liege, Gembloux, Belgium Export Date: 18 April 2024 Correspondence Address: Hamaidia, M.; Molecular and Cellular Epigenetics, Belgium; email: mhamaidia@uliege.be Chemicals/CAS: DNA ligase, 9015-85-4; doublecortin like kinase 1; doxorubicin, 23214-92-8, 25316-40-9; germinal center kinase; mammalian target of rapamycin complex 1; mammalian target of rapamycin complex 2; NIMA related kinase 1; oncogene protein v akt; oncogene protein v raf; polo like kinase 1; serine threonine protein kinase 3; serine threonine protein kinase ULK1; serine/threonine protein kinase WNK1 Tradenames: CellQuest Pro, Becton Dickinson Biosciences; FACSCalibur, Becton Dickinson Biosciences; FACScanto II, Becton Dickinson Biosciences; ImageJ, GE Healthcare; ImageQuant LAS4000, GE Healthcare Manufacturers: Becton Dickinson Biosciences; GE Healthcare Funding details: Foundation Fighting Blindness, FFB Funding details: Fonds De La Recherche Scientifique - FNRS, FNRS Funding details: Université de Liège, ULg Funding details: Fonds Léon Fredericq Funding text 1: The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work received financial support from the “Fonds National de la Recherche Scientifique” (FNRS), the Télévie, the Belgian Foundation against Cancer (FBC), and the “Fondation Léon Fredericq” (FLF). SS, MJ, LV, HB, BS, and MH are supported by grants from FNRS and the FBC. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. Acknowledgments Funding text 2: We thank Pr. Karin Forsberg Nilsson (Uppsala University, Sweden) for cell lines and Vera Gorbunova (University of Rochester, USA) for reporter plasmids. We thank Pr. Luc Willems (University of Liege and FNRS) for scientific input and financial support. We thank Jean-Rock Jacques for his technical expertise. We thank the GIGA Imaging technology platforms for their advice and support. AB - Background: Although the incidence of anaplastic thyroid carcinoma (ATC) is low (2.5% of thyroid cancer cases), this cancer has a very poor prognosis (survival rates < 5 months) and accounts for 14–39% of deaths. Conventional therapies based on surgery in combination with radiotherapy or chemotherapy showed limited effectiveness primarily due to the robust and protective DNA damage response in thyroid cancer cells. Methods: We used single-cell transcriptomic data from patients with different subtypes of thyroid cancer to study expression of genes involved in homologous recombination (HR) and non-homologous end joining (NHEJ) pathways. Then, we investigated the mechanisms of DNA damage and repair in anaplastic (C643 and Hth74) and papillary (TPC-1) thyroid cancer cell lines. The effect of caffeine (inhibitor of ATM and ATR) and UCN-01 (CHK1 inhibitor) was evaluated in cell cycle progression of thyroid cancer cells after γ‐radiation or doxorubicin treatment. The DNA damage response was monitored after staining of phosphorylated γ-H2AX and 53BP1. Reporter plasmids were used to determine the efficacy of double-strand DNA breaks (DSBs) repair by HR and NHEJ in thyroid cancer cells. We evaluated the combination of selective inhibition of the DNA ligase IV by SCR7 and doxorubicin on cellular apoptosis and tumor growth in xenograft murine models of anaplastic thyroid cancer. Results: Single-cell RNA-Seq showed that NHEJ- and HR-related genes are expressed in ATC and PTC patients. We showed that ATC cells undergo mitosis in the presence of unrepaired DNA damage caused by γ‐radiation and doxorubicin treatment. To proliferate and survive, these cells efficiently repair DNA lesions using homologous recombination (HR) and non-homologous end joining (NHEJ). The combination of SCR7 with doxorubicin, significantly increased apoptosis and impaired ATC tumor growth in a xenograft mouse model compared to doxorubicin monotherapy. Conclusion: This study shows the therapeutic value of the combination of a DNA ligase IV inhibitor and DNA-damaging agents (doxorubicin and/or γ-radiation) for the treatment of anaplastic thyroid cancer. Copyright © 2024 Sriramareddy, Jamakhani, Vilanova, Brossel, Staumont and Hamaidia. LA - English DB - MTMT ER - TY - JOUR AU - Morozas, A. AU - Malyško-Ptašinskė, V. AU - Kulbacka, J. AU - Ivaška, J. AU - Ivaškienė, T. AU - Novickij, V. TI - Electrochemotherapy for head and neck cancers: possibilities and limitations JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1353800 UR - https://m2.mtmt.hu/api/publication/34798586 ID - 34798586 N1 - Department of Immunology and Bioelectrochemistry, State Research Institute Centre of Innovative Medicine, Vilnius, Lithuania Faculty of Electronics, Vilnius Gediminas Technical University, Vilnius, Lithuania Department of Molecular and Cellular Biology, Wroclaw Medical University, Wroclaw, Poland Faculty of Medicine, Vilnius University, Vilnius, Lithuania Export Date: 18 April 2024 Correspondence Address: Novickij, V.; Department of Immunology and Bioelectrochemistry, Lithuania; email: vitalij.novickij@vilniustech.lt Funding text 1: The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article. AB - Head and neck cancer continues to be among the most prevalent types of cancer globally, yet it can be managed with appropriate treatment approaches. Presently, chemotherapy and radiotherapy stand as the primary treatment modalities for various groups and regions affected by head and neck cancer. Nonetheless, these treatments are linked to adverse side effects in patients. Moreover, due to tumor resistance to multiple drugs (both intrinsic and extrinsic) and radiotherapy, along with numerous other factors, recurrences or metastases often occur. Electrochemotherapy (ECT) emerges as a clinically proven alternative that offers high efficacy, localized effect, and diminished negative factors. Electrochemotherapy involves the treatment of solid tumors by combining a non-permeable cytotoxic drug, such as bleomycin, with a locally administered pulsed electric field (PEF). It is crucial to employ this method effectively by utilizing optimal PEF protocols and drugs at concentrations that do not possess inherent cytotoxic properties. This review emphasizes an examination of diverse clinical practices of ECT concerning head and neck cancer. It specifically delves into the treatment procedure, the choice of anti-cancer drugs, pre-treatment planning, PEF protocols, and electroporation electrodes as well as the efficacy of tumor response to the treatment and encountered obstacles. We have also highlighted the significance of assessing the spatial electric field distribution in both tumor and adjacent tissues prior to treatment as it plays a pivotal role in determining treatment success. Finally, we compare the ECT methodology to conventional treatments to highlight the potential for improvement and to facilitate popularization of the technique in the area of head and neck cancers where it is not widespread yet while it is not the case with other cancer types. Copyright © 2024 Morozas, Malyško-Ptašinskė, Kulbacka, Ivaška, Ivaškienė and Novickij. LA - English DB - MTMT ER - TY - JOUR AU - Zhang, Y. AU - Zhou, B.-G. AU - Zhan, J.-D. AU - Du, B.-B. TI - Association between metabolic dysfunction-associated steatotic liver disease and risk of incident pancreatic cancer: a systematic review and meta-analysis of cohort studies JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1366195 UR - https://m2.mtmt.hu/api/publication/34797318 ID - 34797318 N1 - Department of General Medicine, The Hospital of Huazhong University of Science and Technology, Hubei, Wuhan, China Dalian Medical University, Liaoning, Dalian, China Export Date: 18 April 2024 Correspondence Address: Du, B.-B.; Department of General Medicine, Hubei, China; email: dbinbin811@163.com LA - English DB - MTMT ER - TY - JOUR AU - Zhang, H. AU - Song, J. AU - Ward, R. AU - Han, Y. AU - Hunt, A. AU - Shriwas, P. AU - Steed, A. AU - Edwards, C. AU - Cao, Y. AU - Co, M. AU - Chen, X. TI - Diverse temporal and spatial mechanisms work, partially through Stanniocalcin-1, V-ATPase and senescence, to activate the extracellular ATP-mediated drug resistance in human cancer cells JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1276092 UR - https://m2.mtmt.hu/api/publication/34794878 ID - 34794878 N1 - Department of Biological Science, Ohio University, Athens, OH, United States The Edison Biotechnology Institute, Ohio University, Athens, OH, United States The Program of Molecular and Cellular Biology, Ohio University, Athens, OH, United States The Honor Tutorial College, Ohio University, Athens, OH, United States Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, United States Department of Biomedical Science, Heritage College of Osteopathic Medicine, Ohio University, Athens, OH, United States Export Date: 17 April 2024 Correspondence Address: Chen, X.; Department of Biological Science, United States; email: chenx@ohio.edu Chemicals/CAS: adenosine triphosphatase, 37289-25-1, 9000-83-3; adenosine triphosphate, 15237-44-2, 56-65-5, 987-65-5; gefitinib, 184475-35-2, 184475-55-6, 184475-56-7; glutathione, 70-18-8; glutathione disulfide, 27025-41-8; hypocalcin, 76687-96-2; multidrug resistance associated protein 1; paclitaxel, 33069-62-4; sunitinib, 341031-54-7, 557795-19-4, 1327155-72-5 Tradenames: AXIO Observer, Carl Zeiss; CFX Connect Real-Time PCR Detection System, Biorad, United States; Cytation 3 imaging reader, Biotek; liquid LS 6500 Scintillation Counter, Beckman Coulter, United States; Odyssey Fc imaging system, LI COR; SYBR Green qPCR Master Mix, Thermo, United States Manufacturers: Beckman Coulter, United States; Biorad, United States; Biotek; Carl Zeiss; LI COR; Thermo, United States Funding details: National Institutes of Health, NIH, R15CA242177 Funding details: Ohio University, OU Funding text 1: The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study is supported by an NIH grant R15CA242177 to XC and an Ohio University Student Enhancement Award to HZ, and John Kopchick MCB/TBS Undergraduate Student Research Fund, and Provost Undergraduate Research Fund to RW. Acknowledgments AB - Introduction: Resistance to drug therapies is associated with a large majority of cancer-related deaths. ATP-binding cassette (ABC) transporter-mediated drug efflux, epithelial-mesenchymal transition (EMT), cancer stem cells (CSCs), glutathione (GSH), senescence, and vacuole-type ATPase (V-ATPase) all contribute to the resistance. We recently showed that extracellular ATP (eATP) induces and regulates EMT, CSC formation, and ABC transporters in human cancer cells and tumors. eATP also consistently upregulates Stanniocalcin-1 (STC1), a gene that significantly contributes to EMT, CSC formation, and tumor growth. We also found that eATP enhances drug resistance in cancer cells through eATP internalization mediated by macropinocytosis, leading to an elevation of intracellular ATP (iATP) levels, induction of EMT, and CSC formation. However, these factors have never been systematically investigated in the context of eATP-induced drug resistance. Methods: In this study, we hypothesized that eATP increases drug resistance via inducing ABC efflux, EMT, CSCs, STC1, and their accompanied processes such as GSH reducing activity, senescence, and V-ATPase. RNA sequencing, metabolomics, gene knockdown and knockout, and functional assays were performed to investigate these pathways and processes. Results and discussion: Our study results showed that, in multiple human cancer lines, eATP induced genes involved in drug resistance, elevated ABC transporters’ efflux activity of anticancer drugs; generated transcriptomic and metabolic profiles representing a drug resistant state; upregulated activities of GSH, senescence, and V-ATPase to promote drug resistance. Collectively, these newly found players shed light on the mechanisms of eATP-induced as well as STC1- and V-ATPase-mediated drug resistance and offer potential novel targets for combating drug resistance in cancers. Copyright © 2024 Zhang, Song, Ward, Han, Hunt, Shriwas, Steed, Edwards, Cao, Co and Chen. LA - English DB - MTMT ER - TY - JOUR AU - Gulyás, Anita AU - Pinczés, László Imre AU - Mátyus, János AU - Végh, Edit AU - Bedekovics, Judit AU - Tóth, Judit AU - Barna, Sándor Kristóf AU - Hunya, Zsolt AU - Szabó, Imre Lőrinc AU - Gazdag, Annamária AU - Illés, Árpád AU - Magyari, Ferenc TI - Case report: Targeted treatment strategies for Erdheim-Chester disease JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1305518 UR - https://m2.mtmt.hu/api/publication/34794833 ID - 34794833 LA - English DB - MTMT ER - TY - JOUR AU - Zhu, Yingze AU - Zhou, Miao AU - Li, Congling AU - Kong, Wenyue AU - Hu, Yuning TI - Gastric cancer with brain metastasis: from molecular characteristics and treatment JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1310325 UR - https://m2.mtmt.hu/api/publication/34793601 ID - 34793601 AB - Gastric cancer is one of the cancers with increasing incidence and ranks fourth globally among the most frequent causes of cancer-related mortality. Early gastric cancer is often asymptomatic or presents with atypical symptoms, and the majority of patients present with advanced disease upon diagnosis. Brain metastases are present in approximately 1% of gastric cancer patients at the time of diagnosis, which significantly contributed to the overall mortality of the disease worldwide. Conventional therapies for patients with brain metastases remain limited and the median overall survival of patients is only 8 months in advanced cases. Recent studies have improved our understanding of the molecular mechanisms underlying gastric cancer brain metastases, and immunotherapy has become an important treatment option in combination with radiotherapy, chemotherapy, targeted therapy and surgery. This review aims to provide insight into the cellular processes involved in gastric cancer brain metastases, discuss diagnostic approaches, evaluate the integration of immune checkpoint inhibitors into treatment and prognosis, and explore the predictive value of biomarkers in immunotherapy. LA - English DB - MTMT ER - TY - JOUR AU - Abdalhadi, A. AU - Omar, N.E. AU - Kohla, S. AU - Aakel, H. AU - Ekeibed, Y. AU - Mohsen, R. TI - Aplastic anemia secondary to adjuvant Osimertinib therapy: a case report and a review of literature JF - FRONTIERS IN ONCOLOGY J2 - FRONT ONCOL VL - 14 PY - 2024 SN - 2234-943X DO - 10.3389/fonc.2024.1275275 UR - https://m2.mtmt.hu/api/publication/34791559 ID - 34791559 N1 - Export Date: 16 April 2024 Correspondence Address: Abdalhadi, A.; Medical Oncology, Qatar; email: AAbdalhadi@hamad.qa Chemicals/CAS: carboplatin, 41575-94-4; eltrombopag, 376591-99-0, 443130-00-5, 496775-61-2, 496775-62-3, 2336813-25-1; epidermal growth factor receptor, 79079-06-4; filgrastim, 121181-53-1; hemoglobin, 9008-02-0; osimertinib, 1421373-65-0, 1421373-66-1; pemetrexed, 137281-23-3, 150399-23-8, 357166-29-1, 357166-30-4 Funding details: Qatar National Library, QNL Funding text 1: This study received funding from the Qatar National Library. The funder was not involved in the study design, collection, analysis, interpretation of data, the writing of this article, or the decision to submit it for publication. All authors declare no other competing interests. AB - Aplastic anemia is a rare hematological disorder characterized by suppressed hematopoiesis and pancytopenia. Although several drugs have been associated with aplastic anemia, its occurrence in response to Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is extremely rare. We present a case report of a 63-year-old patient with locally advanced non-small cell lung cancer (NSCLC) who developed aplastic anemia following adjuvant treatment with Osimertinib. Extensive investigations ruled out infectious etiology, and the absence of bone marrow involvement or other identifiable causes suggested a drug-induced etiology, specifically Osimertinib. This case report emphasizes the importance of recognizing this adverse event and considering it as a potential complication of Osimertinib therapy. Vigilant monitoring and prompt management are essential for optimizing patient outcomes. Further studies are needed to better understand the risk factors, underlying mechanisms, and management strategies for Osimertinib-induced aplastic anemia in the adjuvant settings. Copyright © 2024 Abdalhadi, Omar, Kohla, Aakel, Ekeibed and Mohsen. LA - English DB - MTMT ER -