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Dive into the research topics where Maria Luiza Macedo Silva is active.

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Featured researches published by Maria Luiza Macedo Silva.


Leukemia & Lymphoma | 1993

Acute Megakaryoblastic Leukemia in Children and Adolescents: A Retrospective Analysis of 24 Cases

Raul C. Ribeiro; Maria S. Pombo de Oliveira; Diane L. Fairclough; Craig A. Hurwitz; Joseph Mirro; Frederick G. Behm; David R. Head; Maria Luiza Macedo Silva; Susana C. Raimondi; William M. Crist; Robert A. Krance

In order to characterize the clinical, cytogenetic, and outcome features of childhood acute megakaryoblastic leukemia (AMKL), we reviewed 24 cases; 14 were identified among 150 consecutive newly diagnosed acute myelogenous leukemia (AML) patients at St. Jude Childrens Research Hospital, and 10 were cases referred to the National Institute of Cancer in Rio de Janeiro, Brazil. There were 5 Down syndrome patients and one patient with chronic myeloid leukemia (Ph+) in blastic crisis. Twelve patients had significant hepatosplenomegaly. Leukemic cell morphology and cytochemistry were consistent with the M7 classification in 17 cases, and all cases tested expressed megakaryocytic surface antigens. AMKL patients were significantly younger than other AML patients (P = 0.0001) and had poorer responses to therapy (P = 0.03, univariate analysis only). Ten of 24 failed induction, and only 5 are disease-free at 6 months to 4.5+ years. We conclude that AMKL usually affects young children, frequently producing marked organomegaly. It comprises approximately 10% of pediatric AML cases, and responds poorly to intensive AML therapies.


Pediatric Blood & Cancer | 2006

Molecular Cytogenetic Findings of Acute Leukemia Included in the Brazilian Collaborative Study Group of Infant Acute Leukemia

Mariana Emerenciano; Diana Patricia Agudelo Arias; Virginia Maria Coser; Gilena Dantas de Brito; Maria Luiza Macedo Silva; Maria S. Pombo-de-Oliveira

Chromosome abnormalities often occur prenatally in childhood leukemia, characterizing an early event in leukemogenesis. The majority of the abnormalities occurring in infants involve the MLL gene on chromosome band 11q23. We describe the molecular cytogenetic findings of 207 infant acute leukemia (IAL) cases included in the Brazilian Collaborative Study Group of Infant acute leukemia.


Leukemia Research | 1998

Correlation of N-ras point mutations with specific chromosomal abnormalities in primary myelodysplastic syndrome

Teresa de Souza Fernandez; Jamison M. de Souza; Maria Luiza Macedo Silva; Daniel Tabak; Eliana Abdelhay

A cytogenetic and N-ras point mutation study was done in patients with primary myelodysplastic syndrome (MDS) from Rio de Janeiro, Brazil, in order to evaluate the progression of preleukemic states to overt leukemia. Cytogenetic analysis was performed in 50 patients with MDS and clonal chromosomal abnormalities were detected in 19 (38%) of them. Patients with refractory anemia (RA) or with ringed sideroblasts (RARS) presented normal karyotypes or single abnormalities as del(5q) or -Y, while patients in more advanced states as RA with excess of blasts (RAEB), RAEB in transformation (RAEB-t) and chronic myelomonocytic leukemia (CMML) showed complex karyotypes and single abnormalities involving chromosomes 7 or 8, which were related to poor prognosis and elevated risk of transformation to acute myeloid leukemia (AML). The frequency of ras activation was studied in these 50 patients with MDS. Samples of bone marrow were screened for oncogenic point mutations by DNA amplification followed by oligonucleotide hybridization analysis (PCR-ASO) at codon 12 of N-ras proto-oncogene. We detected N-ras point mutations in 21 patients (42%). Progression from MDS to AML was observed in 9 patients (18%). The correlation analysis between N-ras point mutations and specific chromosomal abnormalities indicated that although mutated N-ras was found in cells with del(5q) and monosomy 7, cells with those abnormalities and normal N-ras were also identified. Otherwise trisomy of chromosome 8 showed a correlation with N-ras point mutations and in all cases, patients showed progression of MDS to AML during the follow-up study. MDS comprises a heterogeneous group of hematopoietic disorders and probably several steps are implicated in the evolution to AML. In this work we suggest that one possible pathway of leukemogenesis in MDS includes N-ras point mutations in association with trisomy of chromosome 8.


Cancer Genetics and Cytogenetics | 2002

Cytogenetic analysis of 100 consecutive newly diagnosed cases of acute lymphoblastic leukemia in Rio de Janeiro.

Maria Luiza Macedo Silva; Maria Helena Ornellas de Souza; Raul C. Ribeiro; Marcelo Gerardin Poirot Land; Alice Maria Boulhosa de Azevedo; Felippe Vasconcelos; Luize Otero; Zilton Vasconcelos; Luiz Fernando Bouzas; Eliane Abdelhay

We report the cytogenetic analysis of newly diagnosed Brazilian children with acute lymphocytic leukemia (ALL). We investigated 100 ALL cases from four different institutions in Rio de Janeiro. The frequency of chromosomal abnormalities was 92.3%. The karyotype profile and recurrent abnormalities found in this study do not differ essentially from those described by other groups. Although the Brazilian population is usually the product of different ethnic groups, our results show that the frequency of each recurrent abnormality is similar to that found in populations without our degree of diverse ethnic composition. Hence, our results suggest that childhood ALL in Brazil has the same biological features as that in developed countries, supporting the use of similar treatment protocols. We can therefore expect to reach the same survival rates in the coming years, depending possibly on the efficacy of the support therapy and extent of social assistance.


Cancer Genetics and Cytogenetics | 1991

CD7+, CD4−/CD8− acute leukemia with t(11;14)(p15;q11) in a child☆

Maria Luiza Macedo Silva; Maria S. Pombo de Oliveira; Aloisio N. Valente; Eliana F. Ss Abdelhay; Luis Fernando Bouzas; Lisselot Laun; Raul C. Ribeiro

A t(11;14)(p15;q11) was the sole chromosome abnormality observed in the malignant cells of a 10-year-old boy with acute leukemia. Morphologically, these cells were classified as L1 by the criteria of the French-American-British Working Group. Cytochemical analysis revealed that the leukemic cells were negative for Sudan Black B, periodic acid Schiff, and esterases, and positive for acid phosphatase. Immunophenotyping disclosed that the cells expressed a very immature antigenic profile [CD34+, CD7+, cytoplasmic CD3+, membrane CD3-, CD4-, and CD8-]. In spite of very intensive chemotherapy, complete remission was never induced, and the child died of progressive disease. The relationship of this case to other reported cases of acute leukemia arising from immature pluripotent hematopoietic cells is discussed.


Cancer Genetics and Cytogenetics | 2008

Banding and molecular cytogenetic studies detected a CBFB-MYH11 fusion gene that appeared as abnormal chromosomes 1 and 16 in a baby with acute myeloid leukemia FAB M4-Eo.

Maria Luiza Macedo Silva; Susana C. Raimondi; Eliana Abdelhay; Madeleine Gross; Hasmik Mkrtchyan; Amanda Faria de Figueiredo; Raul C. Ribeiro; Terezinha de Jesus Marques-Salles; Elaine S. Sobral; Marcelo Land; Thomas Liehr

The acute myeloid leukemia (AML) subtype M4Eo occurs in 5% of all AML cases and is usually associated with either an inv(16)(p13.1q22) or a t(16;16)(p13.1;q22) chromosomal abnormality. At the molecular level, these abnormalities generate a CBFB-MYH11 fusion gene. Patients with this genetic alteration are usually assigned to a low-risk group and thus receive standard chemotherapy. AML-M4Eo is rarely found in infants. We describe clinical, conventional banding, and molecular cytogenetic data for a 12-month-old baby with AML-M4Eo and a chimeric CBFB-MYH11 fusion gene masked by a novel rearrangement between chromosomes 1 and 16. This rearrangement characterizes a new type of inv(16)(p13.1q22) masked by a chromosome translocation.


Cancer Genetics and Cytogenetics | 1995

Translocation 11;14 in three children with acute lymphoblastic leukemia of T-cell origin

Ilana Zalcberg; Maria Luiza Macedo Silva; Eliana Abdelhay; Daniel Tabak; Maria Helena Ornellas; Felippe V. Simões; W. Pucheri; R. Ribeiro; Héctor N. Seuánez

Clinical, karyotypic, immunophenotypic, and molecular profiles of three TALL cases carrying a t(11;14) are discussed and compared with data in the literature. As previously reported, t(11;14)(p13;q11) was associated in one patient with a TALL profile of intermediate stage of maturation (CD7+, CD4+, CD8+). However, the same translocation was found to be present in another patient with a more immature, pro-TALL profile (CD7+, CD4-, CD8-). Both patients showed molecular rearrangements of the TCR beta chain gene. A third patient, with a very immature pro-TALL profile (CD34+, CD7+, CD4-, CD8-), carrying a t(11;14)(p15;q11), showed molecular rearrangements of the TCR beta and gamma chain genes, while the IgH chain genes were in germline configuration. Our data indicate that t(11;14) can also be present in TALLs of more immature stages of intrathymic development; the significant factor determining the clinical behavior of TALLs is apparently related more to cell differentiation than to the presence of this chromosome rearrangement.


International Journal of Hematology | 2011

Secondary abnormalities involving 1q or 13q and poor outcome in high stage Burkitt leukemia/lymphoma cases with 8q24 rearrangement at diagnosis

Mariana Tavares de Souza; Hasmik Mkrtchyan; Rocio Hassan; Daniela Ribeiro Ney-Garcia; Alice Maria Boulhosa de Azevedo; Elaine Sobral da Costa; Amanda Faria de Figueiredo; Thomas Liehr; Eliana Abdelhay; Maria Luiza Macedo Silva

Classical Burkitt lymphoma/leukemia (BL/L) presenting L3 morphology is found in 1% of childhood ALL. Recently, it has been described that secondary abnormalities could influence the prognosis of these patients. However, little information is available on these cytogenetic abnormalities and their prognostic importance in BL/L. Here, we report four new childhood BL/L cases associated with duplication within 1q or 13q, which exhibited a very unfavorable therapeutic response. We performed both classical and molecular cytogenetic analysis by multicolor chromosome banding of the secondary abnormalities involving the long arms of chromosome 1 or 13. These patients were previously treated with BFM-90 protocol. All of them died during or after the initial treatment. Here, for the first time, the exact breakpoints of the derivative chromosomes involved were determined at the cytogenetic level as 1q21 and 13q33 each.


Research in Microbiology | 2010

β-Galactofuranose-containing structures present in the cell wall of the saprophytic fungus Cladosporium (Hormoconis) resinae.

Renata Oliveira da Rocha Calixto; Bianca Mattos; Vera Carolina B. Bittencourt; Lívia Lopes; Lauro Mera de Souza; Guilherme L. Sassaki; Thales R. Cipriani; Maria Luiza Macedo Silva; Eliana Barreto-Bergter

A peptidogalactomannan was isolated from mycelia of Cladosporium (Hormoconis) resinae and characterized using methylation-fragmentation analysis, partial acid hydrolysis and ¹H and ¹³C-NMR spectroscopy. The galactomannan component was a branched structure and consisted of a main chain containing (1→6)-linked α-d-Manp residues substituted at O-2 by side chains containing (1→2)-linked α-D-Manp residues. β-D-Galf residues were present as side chains of 3-4 units that are (1→5)-interlinked. This structure is very similar to a pGM isolated from Aspergillus fumigatus and differs from that of Cladosporium werneckii (currently named Hortaea werneckii), with this pGM and other fungal galactomannans having single terminal (1→6)-linked β-Galf residues. The importance of the carbohydrate moiety of Cladosporium resinae pGM in immunoassays was also demonstrated. On FACS examination, a decrease (60%) in rabbit serum anti- C. resinae binding to C. resinae conidia occurred when this serum had been previously incubated with pGMs from C. resinae and A. fumigatus or with mannoprotein from Candida parapsilosis, suggesting the presence of cross-reactive determinants in these fungi.


Cancer Genetics and Cytogenetics | 2002

Translocation (11;11)(p13- p15;q23) in a child with therapy-related acute myeloid leukemia following chemotherapy with DNA-topoisomerase II inhibitors for Langerhans cell histiocytosis.

Maria Luiza Macedo Silva; Marcelo Gerardin Poirot Land; Simone Maradei; Luize Otero; Melissa Veith; Gilena Dantas de Brito; Claudete Esteves Klumb; Teresa de Souza Fernandez; Maria S. Pombo-de-Oliveira

We report a new case of therapy-related acute myeloid leukemia in a child with Langerhans cell histiocytosis. This patient was previously treated with a protocol of multidrug chemotherapy, containing a relatively low dose of etoposide (total dose of 900/m(2)). Twenty-six months after the end of the therapy, the patient returned to the hospital with fever and anemia. The white blood cell count was 53 x 10(9)/L. The bone marrow examination showed massive infiltration with French-American-British acute myeloid leukemia classification M4 blast cells. The patient did not respond to an intensive treatment with high dose ARA-C and idarubicin. He died 6 months later. The cytogenetic abnormality of the blast cells was a t(11;11)(p13 -15;q23), that has not been described before in a secondary leukemia case.

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Eliana Abdelhay

Federal University of Rio de Janeiro

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Raul C. Ribeiro

St. Jude Children's Research Hospital

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Teresa de Souza Fernandez

Federal University of Rio de Janeiro

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Daniel Tabak

Rio de Janeiro State University

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Neide Santos

Federal University of Pernambuco

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