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Biomedical subjects

H Stein

Publications and source records attributed to H Stein.

At least 559 records · Page 31Linked to original sources
PubMed1986

A review of nephrotic syndrome associated with chronic lymphocytic leukemia.

Four patients had the nephrotic syndrome and chronic lymphocytic leukemia (CLL), which may be pathogenetically related. Membranoproliferative glomerulonephritis appears to be the most common glomerular lesion in patients with CLL. Available evidence suggests that nephrotic syndrome associated with CLL is often related to immune-complex disease. It is also possible that disorders of immunoglobulin production and cellular immunity contribute to renal disease in patients with CLL.

Aged↗
PubMed1985

Malignant histiocytosis of the intestine: a T-cell lymphoma.

Malignant lymphoma complicating coeliac disease has been characterised on morphological and immunocytochemical grounds as malignant histiocytosis of the intestine (MHI). Fresh tissue from four cases of MHI was studied by means of a panel of monoclonal antibodies; in three cases tumour DNA was studied for immunoglobulin and T-cell receptor (TCR) gene rearrangement. Immunocytochemistry showed a T-cell phenotype in all four cases, confirmed by the demonstration of a rearranged TCR beta-chain gene in the three cases studied. Lymphoma complicating coeliac disease thus appears to be of T-cell, rather than histiocyte, origin.

Adult↗
PubMed1985

Distinctions between endemic and sporadic forms of Epstein-Barr virus-positive Burkitt's lymphoma.

Tumour cell lines were established in vitro from 16 cases of Epstein-Barr (EB) virus genome-positive Burkitt's lymphoma (BL), 7 of "endemic" origin (i.e. from holoendemic malarial areas of Africa and of New Guinea) and 9 of "sporadic" origin (i.e. from outside such high-incidence areas). All the BL cell lines thus established were monoclonal by immunoglobulin isotype expression and displayed a characteristic chromosomal translocation, t(8:14) or t(8:22), confirming their malignant origin. Clear differences observed between the individual BL cell lines appeared to be related to their endemic or sporadic status. All 7 endemic cell lines began growth as a carpet of single cells, often with small, loose clumps appearing in later passage. Whilst 3 lines of sporadic origin displayed a similar pattern to the above, the majority of sporadic lines grew as large, tight clumps of cells from the first passage onwards. These differences in growth pattern were reflected by differences in cell surface phenotype, as defined in indirect immunofluorescence tests using a panel of monoclonal antibodies (MAbs) specific for B-lineage-associated antigens. BL cell lines could be classified into 3 separate groups on the basis of their reactivity with 6 particular antibodies (MHM6, AC2, Ki-1, Ki-24, J5 and 38.13). All 7 endemic BL cell lines and 2 of the 3 sporadic BL cell lines which began growth as single cells showed a group-I cell-surface phenotype (MHM6, AC2, Ki-1, Ki-24 negative; J5, 38.13 positive) in early passage. In contrast, all 6 sporadic BL cell lines which began growth in large clumps displayed a distinct group-II phenotype (MHM6, AC2, Ki-1 positive/negative; Ki-24, J5, 38.13 positive); in later passage most of these sporadic lines progressed to a group-III phenotype (MHM6, AC2, Ki-1, Ki-24 positive; J5, 38.13 negative) without loss of those immunoglobulin and chromosomal markers identifying the cells' malignant origin. These clear differences between endemic BL cell lines on the one hand and the majority of sporadic BL cell lines on the other suggest that endemic BL arises from a more restricted range of progenitor B cells than does the sporadic form of the disease.

Adult↗
PubMed1985

Normal and neoplastic Langerhans cells: phenotypic comparison with other types of macrophages.

The antigenic properties of normal epidermal Langerhans cells and their neoplastic counterparts (histiocytosis X cells) were compared with those of other types of macrophages, by immunohistochemical staining of skin and lymph node biopsies with a panel of mono-clonal antibodies. The phenotype of Langerhans cells, histiocytosis X cells, dermal macrophages and interdigitating reticulum cells were similar (HLA-DR+, OKT 6+/-, Leu3+/-, C3-receptor-, Ig-complex-, R4/23-, MO2-), and differed markedly from those of follicular dendritic cells (HLA-DR-, OKT6-, Leu3-, C3 receptor+, Ig+, R4/23+, MO2-, and histiocytic reticulum cells (HLA-DR+/-, OKT6-, Leu3+/-, C3-receptor+, Ig-complex+, R4/23-, MO2+/-). This indicates that Langerhans cells are related to the interdigitating reticulum cells found in the T cell areas of lymphoid organs, and demonstrates that Langerhans cells do not express C3b, C3bi or C3d receptor molecules. Our data also emphasise that the Leu3 antigen is not restricted to cells of the T cell lineage.

Antibodies, Monoclonal↗
PubMed1985

Benign and malignant lymphocytic skin infiltrates: immunological patterns recognized by immunohistochemical staining with monoclonal antibodies.

Skin biopsies from 150 patients with cutaneous lymphoma, premalignant or "pseudolymphomatous" conditions and benign dermatoses were examined by immunoenzymatic staining of frozen sections with a panel of monoclonal antibodies against lymphocytes, macrophages and accessory cells. Two patterns of infiltration were identified. In one of these T cells associated with Langerhans cells and HLA-DR-positive macrophages of dendritic morphology, were seen. In the other B cell follicles were present in addition to the above type of infiltrate. The latter pattern was restricted to patch tests biopsies, cutaneous lymphocytomas, and malignant lymphomas of B-cell origin. It is concluded that lymphocytic skin infiltrates are divisible into different patterns of immunological reactions similar to those seen in lymphoid organs.

Antibodies, Monoclonal↗
PubMed1985

The differential diagnosis of hairy cell leukemia with a panel of monoclonal antibodies.

A panel of monoclonal antibodies reactive with normal human lymphoid cells and with hairy cells has been applied to the immunocytochemical analysis of hairy cell leukemia. Staining was performed by immunoenzymatic methods on frozen sections of bone marrow trephines and extramedullary tissues and on cell smears. Hairy cells reacted with antibodies against HLA-DR, leukocyte common antigen, B-cell antigens (antibodies To15 and B1) and with three anti-hairy cell monoclonal antibodies (S-HCL3, HC1, and HC2). Neoplastic cells in other B-cell lymphoproliferative disorders also expressed HLA-DR, leukocyte common, and B-cell antigens but were consistently negative for the antigen detected by monoclonal antibody S-HCL3. Furthermore, hairy cells differed from other neoplastic B-cells in that they were unreactive with monoclonal antibodies against C3b receptors, anti-Leu-1, Tü1, Tü33, and lacked a meshwork of dendritic reticulum cells. These findings establish a distinctive antigenic phenotype for hairy cell leukemia and indicate that it may be diagnosed reliably by immunoenzymatic labeling of tissue sections or cell smears.

Acute Disease↗
PubMed1985

Lymphomatoid papulosis. Characterization of skin infiltrates by monoclonal antibodies.

Cryostat sections from fully developed papular lesions of lymphomatoid papulosis (histologic subtype A or B) have been examined by immunoenzymatic staining with 24 monoclonal antibodies against lymphoid cells and their subsets. The lesions demonstrated essentially identical cellular compositions and consisted of T-lymphocytes with a peripheral phenotype (Lyt3+, anti-Leu-4+, OKT6-), macrophages (HLA-DR+, EB11+, OKM1+), and Langerhans cells (HLA-DR+, OKT6+). T-helper/inducer cells (anti-Leu-3+) usually dominated over T-suppressor/cytotoxic cells (anti-Leu-2+). In all cases, proportions of the infiltrating T-cells expressed markers associated with activation (HLA-DR, the OKT1O antigen, interleukin-2 receptor) or proliferation (transferrin receptor, the Ki-67 antigen) of lymphoid cells. Furthermore, the infiltrates contained clusters and/or sheets of large cells reactive with antibodies (Ki-1, Ki-24, Ki-27), which recognize Hodgkin's and Reed-Sternberg cells. These data indicate an origin of the cellular infiltrate from transformed or activated lymphoid cells and suggest an interrelationship of lymphomatoid papulosis to Hodgkin's disease.

Adult↗
PubMed1985

Phenotypic characterization of lymphocyte subsets in mycosis fungoides. Comparison with large plaque parapsoriasis and benign chronic dermatoses.

Altogether, 209 skin biopsies from 103 patients with mycosis fungoides (MF), large plaque parapsoriasis (LPP), and benign chronic dermatoses (BCD) have been examined immunohistologically with the use of a panel of 21 monoclonal antibodies against lymphoid cells and their subsets. All the infiltrates contained a mixture of T-lymphocytes, Langerhans cells, and other types of HLA-DR-positive dermal macrophages. The neoplastic T-cells in MF lesions expressed proliferation-(transferrin receptor) and activation-(the OKT10 antigen) associated markers more frequently than the T-cells in LPP and BCD. In other respects, the neoplastic T-cells in plaque lesions of MF resembled those seen in LPP and BCD; and most of these cases demonstrated a clear predominance of T-cells of helper/inducer type. The neoplastic T-cells in tumor lesions of MF were much more heterogeneous in phenotype. Only eight of these cases could be classified as T-helper neoplasms. In the remaining ten tumor cases, the neoplastic cells expressed either suppressor/cytotoxic or aberrant T-cell phenotypes. There were no phenotypic differences between the "classical" tumor stages and MF d'emblee cases. The data indicate that the early lesions of MF show an immunohistologic reaction pattern common to many immune responses of the skin and that the neoplastic cells in the advanced stages are more heterogeneous in phenotype than previously recognized.

Adult↗
PubMed1985

Use of freeze-dried paraffin-embedded sections for immunohistologic staining with monoclonal antibodies.

Most diagnostically valuable monoclonal antibodies recognize antigens that do not survive conventional tissue processing. The use of frozen tissue sections for immunohistologic studies overcomes this obstacle but introduces a number of practical problems, e.g., the necessity to store material in the frozen state, poor morphologic preservation, etc. In the present paper we report that antigenic denaturation during conventional tissue processing appears to occur during exposure to aldehyde-containing fixatives and to alcohol but not as a result of heating or exposure to melted paraffin wax. In consequence, we have developed a technique by which tissue is freeze-dried and then embedded directly in paraffin wax. All but one of the 40 monoclonal antibodies investigated stained the freeze-dried paraffin sections with an intensity equal to or greater than that observed on frozen sections. There was less diffusion artifact and less background staining than in cryostat sections, and cellular morphology was better preserved. One of the most important advantages of this new method is that antigens in freeze-dried paraffin-embedded tissue are stable, and tissue blocks may be handled in the same manner as conventional paraffin blocks. An additional finding was that, once the tissue has been freeze-dried, paraffin embedded, and sectioned, the antigens it contains are resistant to fixatives (e.g., formol, formol sublimate, alcohols) which would very rapidly cause their destruction in frozen sections.

Antibodies, Monoclonal↗
PubMed1985

[Geometry of the "true self" (Winnicott). On a psychoanalytic Leibniz study by F. Eckstein in 1931].

A psychoanalytical study of Leibniz by F. Eckstein from the year 1931 serves as starting point to confront the theory of monad with the concept of self of Winnicott. The theory of monad has given a new structure to the concepts of unity and multiplicity in the history of European philosophy. Freud's "third step in the theory of instincts" may be understood as a variation of the philosophy unity and multiplicity and may be newly interpreted in context with the philosophy of Leibniz.

Ego↗
PubMed1985

Phenotypic and genotypic analysis of Hodgkin's disease derived cell lines: histopathological and clinical implications.

Five Hodgkin's disease (HD) derived cell lines were established in vitro in our laboratory in the last seven years. Morphological, cytochemical, immunological and cytogenetic marker analysis demonstrated that the in vitro cells represent genotypically and phenotypically the in vivo Hodgkin (H) and Sternberg-Reed (SR) cells in biopsy specimens. The cultured cells resemble haematolymphoid cells at different stages of maturation. Four of the five continue to grow in vitro as suspension cells after more than 50 months. Four more in vitro HD-derived lines were described recently by several authors. A summary of the various marker characteristics of these in vitro lines is given as a synopsis of the phenotypic marker spectrum and is discussed in comparison with our own cell lines. There is a striking similarity between two of the newly established lines (CO, HDLM-2) and our lines whereas the two other in vitro established cultures seem to resemble cell species further along the line of maturation to B lymphocytes (DEV) and monocytes (SU-HD-1). Gene rearrangement experiments undertaken with the L428, L540, L591 and the CO cell line show that the L428 and 591 cells have undergone gene rearrangement, the L428 being compatible with the genotypic state of a pre-B cell; the L591 cells, similarly rearranged furthermore demonstrated functional light chain rearrangement, compatible with B-cell development. By cytogenetic analysis chromosome 7 was found to be affected in all our described lines. This chromosome appears to be particularly unstable and vulnerable in patients with HD, since all tested cell lines revealed multiple abnormalities of this chromosome, a finding which is in accordance with observations made by other investigators in HD-biopsy cells. Since similar structural changes or loss of chromosome 7 is a characteristic event in cases of secondary acute non-lymphocytic leukaemia, it is speculated that this form of secondary neoplasia could resemble the blast crisis, as observed in chronic myeloid leukaemia.

Cell Line↗
PubMed1985

Monoclonal antibody patterns in lymphomatoid papulosis.

Atypical cells resembling Reed-Sternberg cells are a characteristic histologic feature of lymphomatoid papulosis. Thus far no consistent data are available on the nature of these cells, or a possible antigenic relationship between them and Reed-Sternberg cells. Twenty-four biopsy specimens from 14 patients with lymphomatoid papulosis were immunolabeled with antibodies against Ki-1 and other Reed-Sternberg cell-associated antigens. In all cases a proportion of the large, atypical cells expressed the Ki-1 antigen. In contrast, in 20 biopsy specimens of benign inflammatory skin lesions or mycosis fungoides, Ki-1-positive cells were absent or only occasionally present. Furthermore, the large atypical cells of lymphomatoid papulosis also expressed other antigens (for example, T3, T4, HLA-DR, IL-2 receptors) that have previously been demonstrated on Reed-Sternberg cells. Our findings, together with the observation that the Ki-1 antigen can be induced on peripheral blood lymphocytes after prolonged phytohemagglutinin stimulation, suggest that the Ki-1-positive cells in lymphomatoid papulosis are activated T cells closely related to the Reed-Sternberg cells of Hodgkin's disease.

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

The monoclonal antibodies alpha S-HCL 1 (alpha Leu-14) and alpha S-HCL 3 (alpha Leu-M5) allow the diagnosis of hairy cell leukemia.

To define cell surface antigens associated with hairy cell leukemia (HCL), and to gain better insight into the origin of this disease, we developed monoclonal antibodies against spleen cells of a patient with this disease. Although none of these antibodies alone proved specific for the leukemic cells, two of them, designated alpha S-HCL 1 (alpha Leu-14) and alpha S-HCL 3 (alpha Leu-M5) were found to be valuable in the diagnosis of HCL when used in combination. alpha S-HCL 1 recognizes an antigen associated with greater than 95% of B cells in the peripheral blood. Biochemical analysis identified this antigen as a single polypeptide chain with a molecular weight of 150,000 daltons (150 kilodaltons). alpha S-HCL 1 expression on hairy cells is markedly increased when compared with normal B lymphocytes isolated from peripheral blood, tonsils, and spleens. alpha S-HCL 3 reacts with an antigen present on hairy cells but also on monocytes, macrophages, in a lower density on neutrophils, and a small percentage (less than 2%) of lymphocytes. The antigen recognized by alpha S-HCL 3 is composed of a non-covalently linked biomolecular complex of 90 and 150 kilodaltons. Since the HCL 3 antigen was not detectable on other lymphomas of either T or B cell type, the co-expression of S-HCL 1 and S-HCL 3 on hairy cells is a unique marker for this disease.

Animals↗