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1.  Acute lymphoblastic leukemia and developmental biology 
Cell Cycle  2011;10(20):3473-3486.
The latest scientific findings in the field of cancer research are redefining our understanding of the molecular and cellular basis of the disease, moving the emphasis toward the study of the mechanisms underlying the alteration of the normal processes of cellular differentiation. The concepts best exemplifying this new vision are those of cancer stem cells and tumoral reprogramming. The study of the biology of acute lymphoblastic leukemias (ALLs) has provided seminal experimental evidence supporting these new points of view. Furthermore, in the case of B cells, it has been shown that all the stages of their normal development show a tremendous degree of plasticity, allowing them to be reprogrammed to other cellular types, either normal or leukemic. Here we revise the most recent discoveries in the fields of B-cell developmental plasticity and B-ALL research and discuss their interrelationships and their implications for our understanding of the biology of the disease.
doi:10.4161/cc.10.20.17779
PMCID: PMC3266177  PMID: 22031225
leukemia; hematopoietic development; leukemic stem cells; lymphopoiesis; developmental plasticity; B cells; stem cells; cancer; B-ALL
2.  Essential role for telomerase in chronic myeloid leukemia induced by BCR-ABL in mice 
Oncotarget  2012;3(3):261-266.
The telomerase protein is constitutively activated in malignant cells from many patients with cancer, including the chronic myeloid leukemia (CML), but whether telomerase is essential for the pathogenesis of this disease is not known. Here, we used telomerase deficient mice to determine the requirement for telomerase in CML induced by BCR-ABL in mouse models of CML. Loss of one telomerase allele or complete deletion of telomerase prevented the development of leukemia induced by BCR-ABL. However, BCR-ABL was expressed and active in telomerase heterozygous and null leukemic hematopoietic stem cells. These results demonstrate that telomerase is essential for oncogene-induced reprogramming of hematopoietic stem cells in CML development and validate telomerase and the genes it regulates as targets for therapy in CML.
PMCID: PMC3359883  PMID: 22408137
cancer; cancer stem cells (CSC); stem cells; mouse models; Telomerase inhibitors; drug discovery

Results 1-2 (2)