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

Fernandez, Teresa de Souza; Souza, Jorge Moreira de; Silva, Maria Luiza Macedo; Tabak, Daniel; Abdelhay, Eliana

doi:10.1016/s0145-2126(97)00112-4

Cited by 33 publications

(17 citation statements)

References 23 publications

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“…Side 61 In contrast to these reports, we found no assocation between NRAS mutations or FLT3-LM and chromosome 7 abnormalities in MDS in our study. Therefore, a co-operation of -7 with these molecular markers can be discussed in single cases, but general conclusions should not be drawn at this time due to the low number of reported cases.…”

Section: Discussioncontrasting

confidence: 99%

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A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia

Bacher¹,

Haferlach²,

Kern³

et al. 2007

Haematologica

140

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Section: Discussioncontrasting

confidence: 99%

“…The high rates of normal karyotype in NRASmutated cases (79% of all NRAS-mutated MDS patients in this study, 57% in the study by De Souza et al) 61 support the hypothesis that NRAS mutations might represent the initial event in a proportion of MDS cases while additional aberrations induce leukemic transformation.…”

Section: Discussionsupporting

confidence: 87%

A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia

Bacher¹,

Haferlach²,

Kern³

et al. 2007

Haematologica

140

View full text Add to dashboard Cite

“…Thus, several AMLs and MDS with +8 as the sole cytogenetic aberration have been reported to harbor, e.g., CEBPA, FLT3, KRAS, NRAS, and RUNX1 mutations [162][163][164][165][166]. However, none of these mutated genes have proved to be specifically associated with AMLs and MDS with +8.…”

Section: Trisomy Is Not Sufficient For Leukemogenesismentioning

confidence: 99%

Trisomy 8 as the sole chromosomal aberration in acute myeloid leukemia and myelodysplastic syndromes

Paulsson

Johansson

2007

Pathologie Biologie

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“…The reaction mixtures contained 10 L of 10 ϫ buffer (Gene Amp PCR Core Reagent; PerkinElmer, Norwalk, CT) containing 100 mM Tris-HCl, pH 8.3; 500 mM KCl; 2.5 mM MgCl 2 ; 250 M deoxynucleotide triphosphate; 0.125 g of each primer; and 2.5 U of AmpliTaq for a total volume of 100 L. The PCR conditions and primers were described previously. 23 Also, the 5Ј end in each reaction was labeled with 32 P. The end labeling was carried out using 5000 Ci/ mmol/L adenosine triphosphate (Amersham, Arlington Heights, IL), as described by Albitar et al, 24 and the PCR products were used to probe dot blots containing all mutations. Filters were hybridized at room temperature and washed at 4°C with 6 ϫ standard saline citrate for 20 minutes; this was followed by 2 20-minute washes at 54°C in 3 M tetramethylammonium chloride; 50 mM Tris, pH 8.0; 2 mM ethylenediamine tetraacetic acid, pH 8.0; and 0.1% sodium dodecyl sulphate.…”

Section: Pcr and Rdbmentioning

confidence: 99%

The prognostic significance of bone marrow levels of neurofibromatosis‐1 protein and ras oncogene mutations in patients with acute myeloid leukemia and myelodysplastic syndrome

Lü

Nounou

Beran

et al. 2003

Cancer

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BACKGROUNDIt has been reported that point mutations of the ras gene occur frequently in acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS). However, the prognostic significance of ras gene mutations in patients with these disorders has been a controversial issue. Although abnormalities in the neurofibromatosis 1 (NF1) gene, which is a gene involved in the ras pathway, have been observed frequently in patients with juvenile chronic myelogenous leukemia, the role of these abnormalities in adult patients with AML or MDS is not clear.METHODSIn this study, bone marrow specimens that were obtained from previously untreated patients with AML and MDS were examined for ras mutations, and the levels of NF1 protein expression were measured.RESULTSRas point mutations were detected in 16 of 83 patients with AML (19%) and in 21 of 90 patients with MDS (23%). Fourteen of 28 patients with chronic myelomonocytic leukemia (50%) had ras gene mutations. Decreased bone marrow levels of NF1 protein (< 70% of the median level detected in control bone marrow specimens) were observed in 20 of 66 patients with AML (30.3%) and in 8 of 29 patients with MDS (27.6%); none of the patients with ras gene mutations had decreased bone marrow levels of NF1 protein. The presence of a mutant ras gene was associated with a shorter complete remission duration (CRD) in patients with MDS (P = 0.05) but had no effect on survival in patients with AML or MDS. Patients with AML who had decreased NF1 protein levels had a slightly longer CRD compared with patients who had normal NF1 levels (P = 0.07). However, the NF1 level had no significant impact on survival among patients with AML or MDS. When patients with low NF1 levels were grouped with patients who had ras mutations, the patients who had AML had a significantly longer CRD compared with the patients who had MDS (P = 0.02).CONCLUSIONSThe current results suggest that a reduction in NF1 protein expression and the presence of ras point mutations may complement each other and that they both play a complex role in the biology of AML and MDS. Cancer 2003;97:441–9. © 2003 American Cancer Society.DOI 10.1002/cncr.11036

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

Cited by 33 publications

References 23 publications

A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia

A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia

Trisomy 8 as the sole chromosomal aberration in acute myeloid leukemia and myelodysplastic syndromes

The prognostic significance of bone marrow levels of neurofibromatosis‐1 protein and ras oncogene mutations in patients with acute myeloid leukemia and myelodysplastic syndrome

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