[Immunohistochemical characterization of acute leukemia. Study of 31 bone marrow biopsies]. / Caractérisation immunohistochimique des leucémies aiguës. Etude de 31 biopsies ostéo-médullaires.

An immunohistochemical study by avidin-biotin-peroxidase was performed on paraffin-embedded and decalcified bone marrow biopsies in 31 acute leukemias (19 myeloid and 12 lymphoblastic). The Ulex Europaeus lectin and 14 antibodies (anti-CD45, -CD34, -myeloperoxidase, -lysozyme, -CD15, -CD68, -carcinoembryonic antigen, -factor VIII-related antigen, BNH9, anti-CD45RO, -CD3, -CD20, DBB42 and DBA44) were tested. All acute myeloid leukemias from M0 to M5 type were stained by either the anti-myeloperoxidase or anti-lysozyme antibodies. CD68, CD15 and the carcinoembryonic antigen were respectively expressed in 80%, 40% and 20% of myeloid leukemias from M1 to M5 type. The Ulex Europaeus lectin and the anti-factor VIII-related antigen antibody stained only the M7 leukemia and the anti-CD3 antibody stained only the T acute lymphoblastic leukemia. DBB42 was expressed by 63% of B-lineage lymphoblastic leukemias and CD20 by 36%. No leukemia was stained by DBA44. Immunohistochemistry on bone marrow biopsy can assess the lineage of most acute leukemias with the use of a panel of antibodies such as the anti-myeloperoxidase, -lysozyme, -CD68, -CD20, DBB42, -CD3, BNH9, anti-factor VIII-related antigen antibodies and the Ulex Europaeus lectin.

[Iron deficiency anemia]. / Anémies par carence en fer.

Iron deficiency anaemia is characterized by the conjunction of a microcytic, typically are generative anaemia and a biochemical syndrome in which sideropoenia is associated with transferrin increase. It is usually due to a chronic exsudative gastrointestinal or gynaecological bleeding. Diagnosing the mechanism of anaemia is easy in most cases, but difficulties arise from association with a pathology, such as chronic inflammatory syndrome, disturbing the haematological or biochemical data. The prognosis of iron deficiency anaemia depends on its cause. Treatment is aetiological (the cause of chronic bleeding is suppressed) and symptomatic (the body's iron reserves are quickly restored).

[Chelation]. / La chélation.

The use of chelation in endodontics demands a knowledge of the workings of its physico-chemical process. To explain this, we must define unsaturated salts and contrast them with the complexes to which the chelates belong. A few examples of application illustrate these different properties especially the action of E.D.T.A. on the calcified tissues of the endodontium. The mode of action of liquid E.D.T.A. or chelating gels in calcified root canals, poses several questions. The varied studies realized in this domaine allow us to affirm the usefulness of E.D.T.A. in root canal disinfection and in opening up lateral and accessory canals. Also, we must consider the possible influence of chelating agents on the apical seal when the permanent root filling is post poned, and their role in changing the permeability of dentine.

Successive transformation of chronic myelomonocytic leukaemia into acute myeloblastic then lymphoblastic leukaemia, both with minor-bcr rearrangement.

We report a case of chronic myelomonocytic leukaemia (CMML), which transformed first into acute myeloblastic leukaemia (AML) and then into acute lymphoblastic leukaemia (ALL). In the AML and ALL phases, chromosome analysis showed a classic Philadelphia chromosome (Ph) t(9:22)(q34:q11). Molecular studies showed breakpoint cluster region rearrangement between exons e1 and a2 compatible with a p190(bcr/abl) breakpoint as observed in Ph-positive lymphoblastic acute leukaemia. The minor (m-bcr) rearrangement was also detected during complete remission. This observation supports a multistep pathogenesis of leukaemias, and that the p190(bcr/abl) breakpoint may influence the course of the disease.

Use of collagen for standardization of PBSC graft quality evaluation: a multicenter comparative analysis of commercial collagen-based and methylcellulose-based colony-forming unit (CFU) assay kits.

The colony-forming unit-granulocyte-macrophage (CFU-GM) assay, an essential test in evaluation of the quality of autologous grafts of hematopoietic stem cells, has yet to be standardized. With this aim in view, we carried out a multicenter study of five commercially available culture kits for CFU-GM evaluation. Four kits were methylcellulose-based (H4431, H4434, H4435, StemBio1d) and one was collagen-based (EasyClone-Multi). Using fresh and frozen samples of PBSC grafts, we compared CFU-GM and burst-forming unit-erythrocytes (BFU-E) growth using the EasyClone kit to each of the methylcellulose kits. BFU-E and CFU-GM clonogenicity of both fresh and frozen PBSC was clearly inferior with the H4431 kit, which provides conditioned medium only. CFU-GM numbers obtained with fresh and frozen PBSC samples were significantly higher with the EasyClone kit than with the H4434 and StemBio kits. BFU-E numbers were also higher with the EasyClone kit, but only when colonies were scored after May-Grünwald-Giemsa (MGG) staining. Finally, although the H4435 kit provides higher doses of recombinant cytokines than the EasyClone kit, CFU-GM and BFU-E numbers obtained for fresh or frozen PBSC with both kits were similar. In addition, CFU-GM and BFU-E numbers correlated well with CD34+ cell numbers for all five kits for both fresh and frozen PBSC. In summary, our study shows that the EasyClone-Multi and H4435 kits provide the best CFU-GM growth. The collagen-based EasyClone kit has the additional advantage of allowing gel staining and storage, which facilitates colony identification and, more importantly, makes gel exchange possible for standardization of the CFU-GM assay.

Deregulated expression of the TAL1 gene by t(1;5)(p32;31) in patient with T-cell acute lymphoblastic leukemia.

TAL1 gene deregulation is frequent in T-cell acute lymphoblastic leukemia (T-ALL) and can result from translocations involving 1p32 or, more frequently, from a cytogenetically undetectable interstitial deletion of chromosome 1. This study presents a case of T-ALL with a t(1;5)(p32;q31) involving TAL1, in which the breakpoint occurs approximately 10kbp 5' to the gene and leads to transcriptional activation and synthesis of a TAL1 protein, and extends the spectrum of recognized TAL1 gene translocations associated with T-ALL.