التفاصيل البيبلوغرافية
| العنوان: |
Tumor-derived interleukin-1α and leukemia inhibitory factor promote extramedullary hematopoiesis |
| المؤلفون: |
Barisas, Derek A. G., Kabir, Ashraf Ul, Wu, Jun, Krchma, Karen, Kim, Minseo, Subramanian, Madhav, Zinselmeyer, Bernd H., Stewart, Colin L., Choi, Kyunghee |
| المساهمون: |
Bhandoola, Avinash, National Institutes of Health, Foundation for Barnes-Jewish Hospital |
| المصدر: |
PLOS Biology ; volume 21, issue 5, page e3001746 ; ISSN 1545-7885 |
| بيانات النشر: |
Public Library of Science (PLoS) |
| سنة النشر: |
2023 |
| المجموعة: |
PLOS Publications (via CrossRef) |
| الوصف: |
Extramedullary hematopoiesis (EMH) expands hematopoietic capacity outside of the bone marrow in response to inflammatory conditions, including infections and cancer. Because of its inducible nature, EMH offers a unique opportunity to study the interaction between hematopoietic stem and progenitor cells (HSPCs) and their niche. In cancer patients, the spleen frequently serves as an EMH organ and provides myeloid cells that may worsen pathology. Here, we examined the relationship between HSPCs and their splenic niche in EMH in a mouse breast cancer model. We identify tumor produced IL-1α and leukemia inhibitory factor (LIF) acting on splenic HSPCs and splenic niche cells, respectively. IL-1α induced TNFα expression in splenic HSPCs, which then activated splenic niche activity, while LIF induced proliferation of splenic niche cells. IL-1α and LIF display cooperative effects in activating EMH and are both up-regulated in some human cancers. Together, these data expand avenues for developing niche-directed therapies and further exploring EMH accompanying inflammatory pathologies like cancer. |
| نوع الوثيقة: |
article in journal/newspaper |
| اللغة: |
English |
| DOI: |
10.1371/journal.pbio.3001746 |
| الإتاحة: |
https://doi.org/10.1371/journal.pbio.3001746Test |
| حقوق: |
http://creativecommons.org/licenses/by/4.0Test/ |
| رقم الانضمام: |
edsbas.FF6AC088 |
| قاعدة البيانات: |
BASE |
