التفاصيل البيبلوغرافية
| العنوان: |
Hoxa9 collaborates with E2A-PBX1 in mouse B cell leukemia in association with Flt3 activation and decrease of B cell gene expression |
| المؤلفون: |
Alexander Thompson, Mona Hassawi, Héloïse Frison, Marilaine Fournier, Daniel Sinnett, Gratianne Vaisson, Ramon Vidal, Elena A. Shestakova, Charles-Étienne Lebert-Ghali, Janet J. Bijl |
| المصدر: |
Developmental Dynamics. 243:145-158 |
| بيانات النشر: |
Wiley, 2013. |
| سنة النشر: |
2013 |
| مصطلحات موضوعية: |
fungi, T-cell leukemia, chemical and pharmacologic phenomena, hemic and immune systems, Biology, medicine.disease, Fusion protein, Molecular biology, Insertional mutagenesis, Transplantation, medicine.anatomical_structure, hemic and lymphatic diseases, B-cell leukemia, Gene expression, Cancer research, medicine, tissues, Transcription factor, B cell, Developmental Biology |
| الوصف: |
Background: The fusion protein E2A-PBX1 induces pediatric B cell leukemia in human. Previously, we reported oncogenic interactions between homeobox (Hox) genes and E2A-PBX1 in murine T cell leukemia. A proviral insertional mutagenesis screen with our E2A-PBX1 B cell leukemia mouse model identified Hoxa genes as potential collaborators to E2A-PBX1. Here we studied whether Hoxa9 could enhance E2A-PBX1 leukemogenesis. Results: We show that Hoxa9 confers a proliferative advantage to E2A-PBX1 B cells. Transplantation experiments with E2A-PBX1 transgenic B cells overexpressing Hoxa9 isolated from bone marrow chimeras showed that Hoxa9 accelerates the generation of E2A-PBX1 B cell leukemia, but Hoxa9 is unable to transform B cells alone. Quantitative-reverse transcriptase polymerase chain reaction analysis demonstrated a strong repression of B cell specific genes in these E2A-PBX1/Hoxa9 leukemias in addition to Flt3 activation, indicating inhibition of B cell differentiation in combination with enhanced proliferation. Overexpression of Hoxa9 in established E2A-PBX1 mouse leukemic B cells resulted in a growth advantage in vitro, which was also characterized by an enhanced expression of Flt3. Conclusions: we show for the first time that Hoxa9 collaborates with E2A-PBX1 in the oncogenic transformation of B cells in a mouse model that involves Flt3 signaling, which is potentially relevant to human disease. Developmental Dynamics 243:145–158, 2014. © 2013 Wiley Periodicals, Inc. |
| تدمد: |
1058-8388 |
| URL الوصول: |
https://explore.openaire.eu/search/publication?articleId=doi_________::75d28c92fc7b09fd7e3ba5496e3b6e04
https://doi.org/10.1002/dvdy.24056 |
| حقوق: |
CLOSED |
| رقم الأكسشن: |
edsair.doi...........75d28c92fc7b09fd7e3ba5496e3b6e04 |
| قاعدة البيانات: |
OpenAIRE |
