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F Brizard

Publications and source records attributed to F Brizard.

24 records · Page 2Linked to original sources

Unclassifiable high grade malignant T-cell lymphoma with clonal evolution.

We report a case of leukemic malignant T-cell lymphoma with mixed small and large cells. The small cells displayed a mature CD8-positive phenotype, a diploid DNA distribution by cell cycle analysis, and structural karyotypic abnormalities. Large cells were near triploid, showed additional structural cytogenetic abnormalities and a more immature membrane phenotype without CD8 expression. Altogether, these data provide suggestive evidence for a clonal evolution from a mature small cell T-cell lymphoma to a more immature large cell proliferation.

Aged↗

Detection of monosomy 7 and trisomies 8 and 11 in myelodysplastic disorders by interphase fluorescent in situ hybridization. Comparison with acute non-lymphocytic leukemias.

Cells from 50 patients with myelodysplastic syndrome (MDS) and 20 patients with acute non-lymphoblastic leukemia (ANLL) were studied by fluorescent in situ hybridization (FISH) using alphoid biotinylated probes to detect numerical chromosome 7, 8 and 11 aberrations in interphase nuclei. FISH data were compared with cytogenetic results. Both methods were in agreement in 25/50 MDS and 20/20 ANLL cases. Trisomy 11 was found neither by cytogenetic study nor by FISH. In 11 MDS patients the percentage of abnormal cells was higher by FISH than by classical cytogenetic analysis. FISH revealed monosomy 7 which was undetectable by karyotypic study in 5-22% cells from 15 MDS patients. It also allowed the identification of two small markers and a ring chromosome in two MDS cases. FISH hence appears to be useful for the detection of minor abnormal clones and is a convenient complement to conventional cytogenetic analysis in the study of MDS.

Aged↗

Chromosomal analysis of purified B-chronic lymphocytic leukemia lymphocyte cultures: comparison with whole blood cultures and in situ hybridization.

Chromosomal analysis of stimulated whole blood cells and purified B lymphocytes was performed in 13 stage A(0) and 1 stage C(IV) chronic lymphocytic leukemia (B-CLL) patients. Abnormal clones were found in 6 cases in purified B lymphocytes cultures and in a single one in whole blood cultures. In situ hybridization with a chromosome 12 probe was in accordance with the chromosomal analysis of purified B-CLL lymphocytes and not with the results obtained using whole blood culture. Cytogenetic analysis of isolated B cells is simple and sensitive. It enhances the detection of abnormal clones in B-CLL and applied to larger series of patients, it should allow a precise evaluation of the incidence of chromosomal abnormalities in CLL and of their clinical (prognostic) significance.

Aged↗

Improvement of cytogenetic results in B-cell chronic lymphocytic leukemia using immuno-purified leukemic cells.

Cytogenetics of purified B lymphocytes and whole blood cultures were studied in 14 patients with B-CLL and fluorescence in situ hybridization (FISH) was performed on interphase cells in 12 of these cases in order to detect trisomy 12. Only one minor abnormal clone was found on whole blood cell cultures, clonal anomalies were found in a large proportion of mitoses of 6/14 cultures of purified B cells. FISH detected a trisomy 12 in a case, not found in whole blood cultures but found in 78% metaphases of cultures of purified B lymphocyte. This method may be as sensitive as FISH for the detection of trisomy 12 and improves the detection of clonal abnormalities in CLL.

Adult↗

Recurrence of childhood acute lymphoblastic leukemia presenting as a tumor of the middle ear: a case report.

PURPOSE: Extramedullary relapse of childhood acute lymphoblastic leukemia most commonly occurs in the central nervous system or in the testes. Otologic involvement is very rare and has only been reported as an autopsy finding. PATIENT AND METHODS: We describe the case of a 5-year-old girl with CD10 positive acute lymphoblastic leukemia (ALL) who developed an isolated otologic relapse 18 months after the initial diagnosis of ALL. RESULTS: This otologic relapse presented as an atypical otitis media related to a mass of the middle ear. The leukemic infiltration of the middle ear was demonstrated by histologic examination. A cytogenetic change characterized by the occurrence of t(1;19)(q23;p13) was observed in the leukemic cells from the middle ear, and the t(1;19) molecular fusion transcript E2A-PBX1 was detected in the bone marrow by polymerase chain reaction. CONCLUSION: The ear is an exceedingly rare site of relapse in children with acute lymphoblastic leukemia. Molecular analysis demonstrates that such an extramedullary relapse can represent an early manifestation of systemic relapse.

Child, Preschool↗

Persistence of transcriptionally silent BCR-ABL rearrangements in chronic myeloid leukemia patients in sustained complete cytogenetic remission.

Persistence of BCR-ABL rearrangements was demonstrated by D-FISH technique in chronic myeloid leukemia (CML) patients in complete cytogenetic response (CCR) after allogeneic bone marrow transplantation (BMT) or interferon-alpha therapy (IFN-alpha). Samples from bone marrow aspirate or peripheral blood or both were analyzed by conventional cytogenetics, Southern blot, fluorescent interphase in situ hybridization (FISH), and quantitative reverse transcription polymerase chain reaction (Q-RT-PCR). In all patients, FISH detected 1% to 12% nuclei with a BCR-ABL fusion gene, whereas Q-RT-PCR were negative or weakly positive. Based on these results, we hypothesize that the BCR-ABL genomic rearrangement remains unexpressed in a small percentage of cells whatever the treatment (IFN-alpha or BMT), and this in spite of the negativity of the RT-PCR-based classical molecular remission criterion. These data corroborate those obtained by other investigators and point to the need for follow-up of CML patients in CCR over an extensive period, at the DNA level to evaluate the residual disease and at the RNA level (Q-RT-PCR) to estimate the risk of relapse and guide the therapeutic decision. Experimental models suggesting the persistence of positive BCR-ABL cells are discussed and tentative explanations of tumor "dormancy" are proposed.

Chromosomes, Human, Pair 22↗