2 research outputs found
Positive response to imatinib mesylate therapy for childhood chronic myeloid leukemia
6 p. : il.Chronic myeloid leukemia (CML) is rare in the pediatric population, accounting for 2-3% of childhood leukemia cases, with
an annual incidence of one case per million children. The low toxicity profile of imatinib mesylate has led to its approval as a
front-line therapy in children for whom interferon treatment has failed or who have relapsed after allogeneic transplantation. We
describe the positive responses of 2 children (case 1 - from a 7-year-old male since May 2005; case 2 - from a 5-year-old female
since June 2006) with Philadelphia-positive chromosome CML treated with imatinib (300 mg/day, orally) for up to 28 months,
as evaluated by morphological, cytogenetic, and molecular approaches. Our patients are alive, are in the chronic phase, and
are in continuous morphological complete remission
The Wnt signaling pathway regulates Nalm-16 b-cell precursor acute lymphoblastic leukemic cell line survival and etoposide resistance
10 p. : il.B-cell precursor acute lymphoblastic leukemia (BCP-ALL) is the most common malignancy in children.
The Wnt signaling pathway has been found to be extensively involved in cancer onset and progression
but its role in BCP-ALL remains controversial.Weevaluate the role of the Wnt pathway in maintenance of
BCP-ALL cells and resistance to chemotherapy. Gene expression profile revealed that BCP-ALL cells are
potentially sensitive to modulation of Wnt pathway. Nalm-16 and Nalm-6 cell lines displayed low levels
of canonical activation, as reflected by the virtually complete absence of total b-catenin in Nalm-6 and
the b-catenin cell membrane distribution in Nalm-16 cell line. Canonical activation with Wnt3a induced
nuclear b-catenin translocation and led to BCP-ALL cell death. Lithium chloride (LiCl) also induced a
cytotoxic effect on leukemic cells. In contrast, both Wnt5a and Dkk-1 increased Nalm-16 cell survival.
Also, Wnt3a enhanced the in vitro sensitivity of Nalm-16 to etoposide (VP-16) while treatment with
canonical antagonists protected leukemic cells from chemotherapy-induced cell death. Overall, our
results suggest that canonical activation of the Wnt pathway may exerts a tumor suppressive effect, thus
its inhibition may support BCP-ALL cell survival