Academic Journal
Different niches for stem cells carrying the same oncogenic driver affect pathogenesis and therapy response in myeloproliferative neoplasms
العنوان: | Different niches for stem cells carrying the same oncogenic driver affect pathogenesis and therapy response in myeloproliferative neoplasms |
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المؤلفون: | Grockowiak, Elodie, Korn, Claudia, Rak, Justyna, Lysenko, Veronika, Hallou, Adrien, Panvini, Francesca M, Williams, Matthew, Fielding, Claire, Fang, Zijian, Khatib-Massalha, Eman, García-García, Andrés, Li, Juan, Khorshed, Reema A, González-Antón, Sara, Baxter, E Joanna, Kusumbe, Anjali, Wilkins, Bridget S, Green, Anna, Simons, Benjamin D, Harrison, Claire N, Green, Anthony R, Lo Celso, Cristina, Theocharides, Alexandre P A, Méndez-Ferrer, Simón |
المصدر: | Grockowiak, Elodie; Korn, Claudia; Rak, Justyna; Lysenko, Veronika; Hallou, Adrien; Panvini, Francesca M; Williams, Matthew; Fielding, Claire; Fang, Zijian; Khatib-Massalha, Eman; García-García, Andrés; Li, Juan; Khorshed, Reema A; González-Antón, Sara; Baxter, E Joanna; Kusumbe, Anjali; Wilkins, Bridget S; Green, Anna; Simons, Benjamin D; Harrison, Claire N; Green, Anthony R; Lo Celso, Cristina; Theocharides, Alexandre P A; Méndez-Ferrer, Simón (2023). Different niches for stem cells carrying the same oncogenic driver affect pathogenesis and therapy response in myeloproliferative neoplasms. Nature Cancer, 4(8):1193-1209. |
بيانات النشر: | Nature Publishing Group |
سنة النشر: | 2023 |
المجموعة: | University of Zurich (UZH): ZORA (Zurich Open Repository and Archive |
مصطلحات موضوعية: | Clinic for Oncology and Hematology, 610 Medicine & health |
الوصف: | Aging facilitates the expansion of hematopoietic stem cells (HSCs) carrying clonal hematopoiesis-related somatic mutations and the development of myeloid malignancies, such as myeloproliferative neoplasms (MPNs). While cooperating mutations can cause transformation, it is unclear whether distinct bone marrow (BM) HSC-niches can influence the growth and therapy response of HSCs carrying the same oncogenic driver. Here we found different BM niches for HSCs in MPN subtypes. JAK-STAT signaling differentially regulates CDC42-dependent HSC polarity, niche interaction and mutant cell expansion. Asymmetric HSC distribution causes differential BM niche remodeling: sinusoidal dilation in polycythemia vera and endosteal niche expansion in essential thrombocythemia. MPN development accelerates in a prematurely aged BM microenvironment, suggesting that the specialized niche can modulate mutant cell expansion. Finally, dissimilar HSC-niche interactions underpin variable clinical response to JAK inhibitor. Therefore, HSC-niche interactions influence the expansion rate and therapy response of cells carrying the same clonal hematopoiesis oncogenic driver. |
نوع الوثيقة: | article in journal/newspaper |
وصف الملف: | application/pdf |
اللغة: | English |
تدمد: | 2662-1347 |
Relation: | https://www.zora.uzh.ch/id/eprint/239035/1/s43018_023_00607_x.pdf; info:pmid/37550517; urn:issn:2662-1347 |
الاتاحة: | https://www.zora.uzh.ch/id/eprint/239035/ https://www.zora.uzh.ch/id/eprint/239035/1/s43018_023_00607_x.pdf |
Rights: | info:eu-repo/semantics/openAccess ; Creative Commons: Attribution 4.0 International (CC BY 4.0) ; http://creativecommons.org/licenses/by/4.0/ |
رقم الانضمام: | edsbas.1DA254AC |
قاعدة البيانات: | BASE |
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