Genetic background affects susceptibility to tumoral stem cell reprogramming

The latest studies of the interactions between oncogenes and its target cell have shown that certain oncogenes may act as passengers to reprogram tissue-specific stem/progenitor cell into a malignant cancer stem cell state. In this study, we show that the genetic background influences this tumoral s...

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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Tex.), 2013-08, Vol.12 (15), p.2505-2509
Main Authors: García-Ramírez, Idoia, Ruiz-Roca, Lucía, Martín-Lorenzo, Alberto, Blanco, Óscar, García-Cenador, María Begoña, García-Criado, Francisco Javier, Vicente-Dueñas, Carolina, Sánchez-García, Isidro
Format: Article
Language:English
Subjects:
Animals
cancer
cancer stem cell
cancer therapy
Cell Transformation, Neoplastic - genetics
Fusion Proteins, bcr-abl - genetics
Genetic Predisposition to Disease
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics
Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology
Mice
Mice, Inbred C57BL
Mice, Transgenic
mouse model
Neoplastic Stem Cells - physiology
oncogenes
stem cells
Thymus Neoplasms - genetics
Thymus Neoplasms - pathology
Tumor Burden
tumoral reprogramming
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Summary:The latest studies of the interactions between oncogenes and its target cell have shown that certain oncogenes may act as passengers to reprogram tissue-specific stem/progenitor cell into a malignant cancer stem cell state. In this study, we show that the genetic background influences this tumoral stem cell reprogramming capacity of the oncogenes using as a model the Sca1-BCRABLp210 mice, where the type of tumor they develop, chronic myeloid leukemia (CML), is a function of tumoral stem cell reprogramming. Sca1-BCRABLp210 mice containing FVB genetic components were significantly more resistant to CML. However, pure Sca1-BCRABLp210 FVB mice developed thymomas that were not seen in the Sca1-BCRABLp210 mice into the B6 background. Collectively, our results demonstrate for the first time that tumoral stem cell reprogramming fate is subject to polymorphic genetic control.
ISSN:1538-4101
1551-4005
DOI:10.4161/cc.25544