Rita Fragoso

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Oncogenes, which are essential for tumor initiation, development, and maintenance, are valuable targets for cancer therapy. However, it remains a challenge to effectively inhibit oncogene activity by targeting their downstream pathways without causing significant toxicity to normal tissues. Here we show that deletion of mir-181a-1/b-1 expression inhibits(More)
OBJECTIVE Given their involvement in pathological and physiological angiogenesis, there has been growing interest in understanding and manipulating endothelial progenitor cells (EPC) for therapeutic purposes. However, detailed molecular analysis of EPC before and during endothelial differentiation is lacking and is the subject of the present study. (More)
The presence of persistent circulating leukemia cells, or engrafted into extramedullary tissues, is a bad prognostic factor for patients with acute leukemia. However, little is known about the mechanisms that regulate the exit of leukemia cells from the bone marrow (BM) microenvironment. We reveal that vascular endothelial growth factor receptor 1 (FLT-1)(More)
Data obtained from animal models, and partially confirmed in pre-clinical studies, have provided clear evidence of the importance of angiogenesis for the growth of solid tumors. Similarly, in hematological cancers such as leukemias and lymphomas, the role of angiogenesis has been under intense scrutiny. However, the molecular singularities of leukemia,(More)
Much has been learned about the molecular and cellular components critical for the control of immune responses and tolerance. It remains a challenge, however, to control the immune response and tolerance at the system level without causing significant toxicity to normal tissues. Recent studies suggest that microRNA (miRNA) genes, an abundant class of(More)
BACKGROUND Secondary bone marrow (BM) myelodysplastic syndromes (MDS) are increasingly common, as a result of radio or chemotherapy administered to a majority of cancer patients. Patients with secondary MDS have increased BM cell apoptosis, which results in BM dysfunction (cytopenias), and an increased risk of developing fatal acute leukemias. In the(More)
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological cancer that arises from clonal expansion of transformed T-cell precursors. In this review we summarize the current knowledge on the external stimuli and cell-intrinsic lesions that drive aberrant activation of pivotal, pro-tumoral intracellular signaling pathways in T-cell(More)
Leukemia stem cells (LSCs) are considered responsible for leukemia initiation, relapse and resistance to chemotherapy. These cells have self-renewal capacity and originate the other cells in the leukemia pool. Therefore, in order to completely eradicate leukemia cells and consequently cure the disease, therapies should in principle necessarily target LSCs.(More)
Imatinib has revolutionized the treatment of Bcr-Abl1(+) chronic myeloid leukemia (CML), but, in most patients, some leukemia cells persist despite continued therapy, while others become resistant. Here, we report that PlGF levels are elevated in CML and that PlGF produced by bone marrow stromal cells (BMSCs) aggravates disease severity. CML cells foster a(More)
Vascular endothelial growth factor (VEGF) signals on vascular and hematopoietic cells via its receptors, VEGFR-2 (KDR) and VEGFR-1 (FLT-1). Elevated levels of VEGF, such as during tumor growth or inflammation, have been suggested to suppress hematopoiesis; most studies refer to KDR as the main receptor involved in this inhibitory effect. In the present(More)