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G Delsol

Publications and source records attributed to G Delsol.

At least 217 records · Page 12Linked to original sources
PubMed1985

[Diagnosis of undifferentiated tumors by means of monoclonal antibodies on paraffin sections].

The diagnostic value of 3 monoclonal antibodies applied on to routinely processed surgical biopsies was assessed. These antibodies were directed against keratin polypeptide (KL1), epithelial membrane antigen (DAKO-EMA) and leucocyte common antigen (DAKO-LC). First, using a three-step immunoperoxidase procedure, we determined the phenotype of well differentiated carcinomas (21 cases), non-Hodgkin's malignant lymphomas (44 cases), malignant histiocytoses (3 cases), melanomas (5 cases), sarcomas (6 cases) and miscellaneous tumors (16 cases). Nineteen out of the 21 carcinomas reacted with KL1 and DAKO-EMA antibodies but not with DAKO-LC. Forty out of the 44 non-Hodgkin's malignant lymphomas reacted with DAKO-LC. All these tumors were negative with KL1 antibodies but three of them, as well as 3 cases of malignant histiocytosis, expressed the epithelial membrane antigen. The value of these 3 antibodies was then assessed in the differential diagnosis of 30 undifferentiated tumors. A definite diagnosis was made in 28 cases: there were 11 undifferentiated carcinomas and 11 large cell malignant lymphomas. The phenotype of 6 tumors was highly suggestive of malignant histiocytosis, the peculiarity of which is to express both leucocyte common (DAKO-LC+) and epithelial membrane antigens (DAKO-EMA+). Only two tumors did not react with these 3 antibodies. We conclude that it is now possible to determine the nature of nearly all undifferentiated tumors on paraffin-embedded biopsy specimens.

Antibodies, Monoclonal↗
PubMed1985

The expression of the Hodgkin's disease associated antigen Ki-1 in reactive and neoplastic lymphoid tissue: evidence that Reed-Sternberg cells and histiocytic malignancies are derived from activated lymphoid cells.

Ki-1 is a monoclonal antibody (raised against a Hodgkin's disease-derived cell line) that, in biopsy tissue affected by Hodgkin's disease, reacts selectively with Reed-Sternberg cells. The expression of Ki-1 antigen has been analyzed by immunocytochemical techniques in a wide range of human tissue and cell samples, including fetal tissue, malignant lymphomas (290 cases), and mitogen- and virus-transformed peripheral blood lymphocytes. The antigen was detectable on a variable proportion of cells in all cases of lymphomatoid papulosis and angio-immunoblastic lymphadenopathy and in 28% of the cases of peripheral T cell lymphomas (including lympho-epithelioid lymphomas). It was also expressed (more strongly) on tumor cells in 45 cases of diffuse large-cell lymphoma, most of which had originally been diagnosed as malignant histiocytosis or anaplastic carcinoma, because of their bizarre morphology. However, all of these cases lacked macrophage and epithelial antigens. Thirty-five cases expressed T cell-related antigens (associated in nine cases with the coexpression of B cell-related antigens), seven bore B cell-related antigens alone, and three were devoid of T and B cell markers. DNA hybridization with a JH specific probe showed a germline configuration in 11 cases of T cell phenotype, in two cases lacking T and B cell antigens, and in one case of mixed T/B phenotype, while rearrangement was found in two cases of clear B cell type and in one mixed T/B case. Expression of the Ki-1 antigen could be induced, together with interleukin 2 (IL 2) receptor, on normal lymphoid cells of both T and B cell type by exposure to phytohemagglutinin, human T leukemia viruses, Epstein-Barr virus, or Staphylococcus aureus. The results obtained indicate that Ki-1 antigen is an inducible lymphoid-associated molecule that identifies a group of hitherto poorly characterized normal and neoplastic large lymphoid cells. Tumors comprised solely of these cells show both morphological and immunological similarities to the neoplastic cells in Hodgkin's disease. This suggests that both disorders represent the neoplastic proliferation of activated lymphoid cells of either T cell or, less commonly, B cell origin. Disorders in which only a minority of cells express Ki-1 antigen (lymphomatoid papulosis, angio-immunoblastic lymphadenopathy, and certain T cell lymphomas) probably represent lesions in which only some of the abnormal cells have transformed into an "activation state." In direct support of this view is the finding that the Ki-1 expression in these lesions is accompanied by the expression of HLA-DR and IL 2 receptors.

Adolescent↗
PubMed1985

[Merkel cell carcinoma of the skin. Anatomoclinical, ultrastructural and immunohistochemical study of 14 cases].

The clinical and pathological features of 14 cases of Merkel cell carcinoma are reported. They commonly arise in the skin of elderly patients, particularly on the face and pelvis. They have a loco-regional aggressivity (nodal metastases in 4 cases) but some patients die with disseminated metastases (2 cases). These tumors are composed of round cells with scanty cytoplasm, arranged in solid or trabecular sheets. Mitotic figures are usually numerous. The ultrastructural study reveal secretory granules and paranuclear collection of intermediate filaments. Immunohistochemical phenotype is highly characteristic: cytoplasmic diffuse positivity with an anti-neuron-specific enolase polyclonal antibody; polar and/or diffuse positivity with anti-cytokeratin, anti-epithelial membrane antigen and anti-S100 protein monoclonal antibodies; polar positivity with an anti-neurofilament monoclonal antibody. The negativity with an anti-common leucocyte antigen monoclonal antibody is helpful to differentiate Merkel cell carcinoma from cutaneous malignant lymphoma.

Adult↗
PubMed1984

Human lymphoid cells express epithelial membrane antigen. Implications for diagnosis of human neoplasms.

Epithelial membrane antigen (EMA) is generally assumed to be expressed only on epithelial cells. However, EMA was also found on reactive and neoplastic plasma cells, on some non-Hodgkin's lymphomas (particularly cases of T-cell lymphoma and "malignant histiocytosis"), and on Reed-Sternberg cells in cases of lymphocyte-predominant Hodgkin's disease. EMA was also induced on normal blood lymphocytes by exposure to human T-lymphotropic virus type II or phytohaemagglutinin. The specificity of these aberrant reactions was confirmed by the use of three different monoclonal anti-EMA antibodies (E29, HMFG2, and LICR.LON/M8), and by showing that EMA in lymphoid tissue is similar in molecular weight to EMA in human milk. These results indicate that additional anti-epithelial antibodies (eg, anti-cytokeratins) should be used in conjunction with anti-EMA for tumour diagnosis.

Antibodies, Monoclonal↗
PubMed1984

Reactivity of Leu 1 and T101 monoclonal antibodies with B cell lymphomas (correlations with other immunological markers).

The reactivity of Leu 1/T101 monoclonal antibodies (MoAb) was studied in a series of 69 lymphomas with B cell differentiation and was correlated with other cell markers. A three step immunoperoxidase technique on frozen sections was used to test a panel of 20 MoAb: anti-human Ig (heavy and light chains), To 15 (Pan B cells), Leu 1, T101, Leu 4, Leu 3a, Leu 5, OKT 8, OKT 6, Leu 7, anti-CALLA (IOT 5), Leu 10, anti-HLA-DR, OKM 1 and anti-dendritic reticulum cells (R 4/23). T101/Leu 1 antigen was detected in 24 cases: CLL (11 of 11), diffuse centrocytic lymphomas (four of 11), follicular lymphomas (none of 12), follicular and diffuse lymphomas (seven of 10) and one unclassified low grade lymphoma. This antigen was observed in only one high grade malignant lymphoma. In follicular lymphomas, two results deserve attention: (1) T101+ lymphomas showed most frequently IgM+, IgD+ surface Ig. Inversely, T101 unreactive lymphomas displayed IgM+, IgD+ phenotype. (2) Tp67 antigen (T101, Leu 1) and CALLA (GP 100) were found to be mutually exclusive in these lymphomas. These results suggest that follicular lymphomas could be derived from two distinct germinal center cell populations: IgM+ Ig'D-, Calla+, Leu 1-/T101- and IgM+, IgD+, CALLA-, Leu+/T101+.

Antibodies, Monoclonal↗
PubMed1984

Metastases of human tumor xenografts in nude mice.

In the present study, using systematic microscopic examination, we tried to determine the true incidence of metastases in nude mice bearing a wide variety of human tumors. A total of 63 malignant tumors were successfully transplanted subcutaneously and 831 nude mice bearing tumors were examined. It appeared that 17 of the 63 tumors (26.9%) retained their metastatic ability in nude mice. Most of these tumors were adenocarcinomas (11/17 cases). Generally the metastatic deposits in the lungs and, to a lesser extent, in the lymph nodes were small and thus only detectable on microscopic examination. We also found a positive correlation between the presence of metastases and neoplastic infiltration of the lymphatic and/or blood vessels around the subcutaneous tumors. Metastatic human tumors, including neoplastic cells from effusion, exhibited higher metastatic ability than primary tumors (p less than 0.005). However, the expression of this metastatic potential depends on several factors including tumor volume, survival time after inoculation and murine hepatitis infection. Thus, animals with metastases bore larger tumors (9.56 cm3) than those without metastasis (6.35 cm3; p less than 0.0001). Moreover, survival time after inoculation was longer in mice with metastases (104 days) than in mice without metastases (81 days; p less than 0.0001). A negative influence of viral hepatitis on the incidence of metastases was observed. This may simply be related to the shortened life span of the animals. Death due to this infection may precede the expression of the metastatic potential.

Animals↗
PubMed1982

[Angioimmunoblastic lymphadenopathy with cutaneous leukocytoclastic vasculitis. 2 cases].

In two patients with similar symptoms (fever, very poor general condition, skin rash, pulmonary involvement, multiple lymphadenopathy and phlebitis) pathological examination disclosed angioimmunoblastic lesions in lymph nodes and leucocytoblastic vascularities in the skin. While all cases published so far were exceptional, the clinical and pathophysiological findings were strikingly similar in these two cases, and the possibility of a special nosological entity is considered. If relapses are to be avoided, both patients will require continuous high dosage corticosteroid therapy, which aggravates the long-term prognosis.

Aged↗
PubMed1982

Warthin-Finkeldey-like cells in benign and malignant lymphoid proliferations.

Multinucleate giant cells resembling Warthin-Finkeldey cells have been described in various lymphoid disorders. These Warthin-Finkeldey-like cells (WFLC) with as many as 50 nuclei are of three main types: reticular, lymphocyte and intermediary. In reactive lymphoid proliferations (34 cases) WFLC were mainly observed inside germinal centres and to a lesser extent in the interfollicular zones. In neoplastic lymphoid proliferations (33 cases) WFLC were most commonly found in the lymphocytic predominance type of Hodgkin's disease (16/25 cases). All non-Hodgkin's lymphomas (13 cases) in which WFLC were detected proved to be of low grade malignancy (lymphocytic: one case, lymphoplasmacytic-plasmacytoid: six cases; and centroblastic-centrocytic, six cases). They were also found in two cases of angioimmunoblastic lymphadenopathy. Immunoperoxidase and electron microscopic studies could not elucidate the exact histogenesis of these cells, but it is assumed that they are associated with B cell proliferations.

Hodgkin Disease↗
PubMed1982

[Mononucleated phagocytes and mesothelial cells in serous peritoneal effusion fluid].

Twenty one peritoneal effusions from patients with cirrhosis were studied in order to characterize mesothelial cells, monocytes and their vacuolated forms. Morphological investigations were performed after Papanicolaou, M.G.G. and Giemsa stains; cytochemical studies by P.A.S., Alcian Blue pH 2,5 and Sudan Black B techniques. Seven enzymatic activities were appreciated: Naphtyl Acetate Esterase, Acid Phosphatase pH 5, beta Glucuronidase, Lactico-dehydrogénase, Malico D, NADH.D and Peroxidase pH 7,6. The free mesothelial cells show a metabolic and functional active phase in which their hydrolasic equipment suggests an intense lysosomal activity only correlated to pinocytosis. Monocytes in transudates show a morphologically micro-vacuolated macrophagic transformation of pinocytic type (elicited macrophages ?); they only become cytophagic when an acute inflammation occurs (activated macrophages ?). This paper emphasizes analogy of behaviour of mesothelial cells and monocytes in transudates, but demonstrates differences in their energetic metabolisms and endocytic characteristics.

Ascitic Fluid↗
PubMed1982

Spontaneous mouse erythrocyte-rosette formation in chronic lymphocytic leukaemia.

Mouse erythrocyte-rosette-forming cells (MRFC) were determined in 76 cases of chronic lymphocytic leukaemia (CLL), 19 cases of centroblastic-centrocytic follicular non-Hodgkin's lymphoma (NHL), five cases of hairy cell leukaemia (HCL) and in 62 control patients. The mean percentage of MRFC in B-CLL was 54.8% +/- 24.4%, in nodular centro-follicular NHL 2.3% +/- 3%, in hairy cell leukaemia 14.6% +/-14.7% and among the controls 3.2% +/- 1.9%. Thus, MRFC appear to be an excellent marker of B-CLL and sometimes the only B cell marker as in 11 cases of SIg negative CLL. There is no correlation between the percentage of MRFC and clinical staging according to Rai classification whereas patients with stage 2 in Binet's classification (isolated splenomegaly) have a significantly lower MRFC percentage (23.4% +/- 27.7%; P less than 0.05). There is no correlation with prognosis, nor with serum Ig levels. We found no correlation with surface phenotype IgM, IgM-IgD or IgG. Thus, this study does not confirm the hypothesis that MRFC might characterize and immature stage in the B lymphocyte differentiation. However, these results are consistent with another hypothesis which states that lymphocytes in CLL possibly originate from a clonal expansion of a normal B lymphocyte subset, characterized by a low concentration of SIg and a receptor for mouse erythrocytes.

Animals↗
PubMed1981

Richter's syndrome. Evidence for the clonal origin of the two proliferations.

A case of Richter's syndrome was investigated by several technics: light and electron microscopy, surface markers, immunohistological studies and immunoelectron microscopy. On light microscopy lymph node proliferation was composed of large lymphoid cells, some exhibiting Reed-Sternberg like features. On electron microscopy many intermediary cells, from small lymphocytes to immunoblasts and plasma cells, were noted. The circulating small lymphocytes were characterized as B cells (SIg +; MRBC+). The lymph node cells shared the same SIg phenotype (IgMK) but the percentage of MRBC was slightly lower. Immunohistological studies showed that lymph node cells were stained exclusively by anti micron and anti kappa antisera. These results are indicative of the B clonal origin of the two cell proliferations. Immunoelectron microscopy showed three staining patterns: 1) cells presenting only surface staining, 2) cells with diffuse staining presumably related to ribosomal fixation, 3) cells with endoplasmic reticulum staining. The significance of these three patterns is discussed with regard to B lymphocyte differentiation.

Aged↗