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Biomedical subjects

L Degos

Publications and source records attributed to L Degos.

At least 325 records · Page 18Linked to original sources
PubMedDate not supplied

CT and MR patterns of spinal involvement in Richter syndrome.

Richter syndrome is the transformation of chronic lymphocytic leukemia (CLL) into large cell lymphoma. Besides the involvement of lymph nodes, liver, and spleen, bone lesions occur infrequently. We report one case of a patient with a paraspinous mass and destruction of the vertebra by large cell transformation of CLL seen on CT and MRI. There was nothing specific about the clinical presentation, imaging characteristics, and histopathological pattern of bone biopsy that would allow for confident differentiation from infectious spondylitis.

Diagnosis, Differential↗
PubMedDate not supplied

H-2 influence on the production of real but not of apparent H-2-specific antibodies induced by the association of syngeneic class I heavy chains with bovine beta 2-microglobulin.

Immunogenic properties of class I molecules resulting from the association of mouse class I heavy chains with a xenogeneic beta 2-microglobulin (beta 2-m) were investigated by studying the antibody response of mice of injections to syngeneic Con A lymphoblasts, induced in conditions allowing the replacement of endogenous beta 2-m by exogenously added bovine beta 2-m provided by fetal calf serum (FCS-Con A blasts). Lymphocytotoxic antibodies were regularly produced and according to their specificities they could be divided into two types: antibodies whose reactivity was (1) dependent on and (2) independent of the presence of bovine beta 2-m on target cells. Although both types displayed an H-2 dependent polymorphic reaction pattern, only antibodies recognizing class I molecules without bovine beta 2-m can be considered as real H-2-specific antibodies. The others are only apparent H-2-specific antibodies: their polymorphic reaction pattern is dependent both on the presence of bovine beta 2-m on the surface of target cells and on their H-2 haplotype. A comparison of the antibody response of mice with various H-2 haplotypes to injections of syngeneic FCS-Con A blasts showed no significant difference in the induction of bovine beta 2-m-dependent antibodies (apparent H-2-specific) among the mice from all strains tested (H-2b, H-2p, H-2q, and H-2s). Unexpectedly, for most strains more than 60% of the immunized mice produced also beta 2-m-independent antibodies (real H-2-specific), with the exception of H-2q mice, in which only 30% of sera were positive. The real H-2-specific antibody response is of two types: some mice (H-2p and H-2s) produced antibodies only reactive with allogeneic target cells whereas others (H-2b and H-2q) produced in addition antibodies that were reactive with syngeneic cells. Thus H-2 appears to play an important role in the induction and specificity of the lymphocytotoxic H-2-specific antibodies induced upon immunization with cells expressing syngeneic class I heavy chains associated with bovine beta 2-m.

Animals↗
PubMedDate not supplied

Retinoic acid modulates RAR alpha and RAR beta receptors in human glioma cell lines.

To identify retinoic acid (RA) signalling pathways involved in growth and differentiation in cells of the glial lineage, two human glioma ceh lines were studied. The three RA receptors (RARs) mRNAs were constitutively expressed, and of the three RXRs, RXR beta appeared predominant. Western blotting analysis confirmed the constitutive expression of RAR alpha and RAR beta. Treatment with all-trans-RA induced morphological changes in the two cell lines, which progressed from their normal pattern of randomly oriented spindle-shaped cells to fibroblast-like glial cells. RA up-regulated RAR alpha and RAR beta mRNAs in both cell lines. Interestingly, RA treatment up-regulated RAR beta proteins but not RAR alpha proteins, suggesting post-transcriptional regulations of RAR transcripts in glioma cells.

Brain Neoplasms↗
PubMedDate not supplied

Differential expression of c-myc and c-fos oncogenes during the differentiation of human leukemic cells by Ara-C.

1-B-D-arabinofuranosyl cytosine (Ara-C) is, at very low concentrations, an inducer of monocytic differentiation of human leukemic cells. By what mechanisms this differentiation is obtained and how the monocytic pathway is determined, is not yet understood. We studied the effect of Ara-C on the RNA transcript levels of two c-oncogenes often associated to cell proliferation and differentiation. In the monoblastic U-937 cell line, where Ara-C has a maximum (100%) monocytic differentiation, RNA transcript level of c-myc is not detectable, whereas c-fos levels are rapidly increased. On the other hand, in the bipotential promyelocytic HL-60 cells, Ara-C induces only 40% monocytic differentiation after 7 days; this is associated to a weaker decrement of c-myc expression; c-fos is however greatly induced 3 log after 2 days treatment, but before monocytic phenotype is observed. Ara-C, at low concentrations, may, by arresting cell proliferation, restore the leukemic's cell proliferation/differentiation equilibrium. The rapid inducement of c-fos expression may allow to foresee a rapid prescreening of Ara-C sensitive-blasts.

Cell Division↗
PubMedDate not supplied

Discrepancy between in vitro and in vivo passaged U-937 human leukemic cells: tumorigenicity and sensitivity to differentiating drugs.

The treatment of nude mice bearing tumors of transplanted human leukemic cells with drugs known to induce differentiation of the same leukemic cells in vitro does not always affect tumor yield, tumor cell differentiation or nude mice survival. We have transplanted human monoblastic leukemic cells of the U-937 cell line into newborn Swiss nu/nu mice. Priming with cyclophosphamide, followed by subcutaneous injections of at least 10 x 10(6) cells allowed us to obtain solid tumors. The cytology, HLA phenotype and in vitro proliferation characteristics of the U-937 tumor cells were conserved. However, these tumor cells were more tumorigenic when reinjected into nude mice and showed a modified response to differentiation induction. A decreased capacity to differentiate with retinoic acid (RA) and a resistance to 1-beta-D arabinofuranosyl cytosine (Ara-C) and 1-25 dihydroxy vitamin D3 (1-25 (OH)2 D3) were noted in three tumor cell lines tested. With regard to the latter, the resistance was not due to a modification of the number of cell receptors. The study shows that though in vivo transplantation of human leukemic cells in nude mice may lead to a selection of resistant cells, systematic checking of in vitro differentiation characteristics of the tumor cells permits the nude mouse model to be maintained for the in vivo screening of new differentiating agents.

Animals↗