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Biomedical subjects

B Koziner

Publications and source records attributed to B Koziner.

135 records · Page 8Linked to original sources
PubMed1977

Cell marker analysis in acute monocytic leukemias.

Leukemic cells from nine cases of acute monocytic leukemia (AMoL) were characterized by multiple differentiation markers. Cells in most cases were phagocytic, carried an Fc receptor, and stained positively for alpha-naphthyl acetate esterase but negatively for naphthol AS-D chloroacetate esterase. However, subtle differences in marker expression were observed which suggested different degrees of leukemic cellular maturation or activation. Cell marker analysis proved to be a useful adjunct to conventional morphology in confirming the diagnosis and the recognition of the neoplastic cells in AMoL, and may ultimately provide insight into the functional state of these cells.

Esterases↗
PubMed1975

Lymphoma presenting as bone marrow failure.

In reviewing 550 patients with non-Hodgkin's lymphoma, only 3 percent were found to present with severe leukopenia or thrombocytopenia due to bone marrow infiltration. Patients with well-differentiated lymphoma had a favorable prognosis despite the presence of cytopenia. In contrast, individuals with poorly differentiated lymphoma had a median survival of only 4 months. Thus, the critical factor in survival was the degree of differentiation of the lymphoma. Conventional therapy proved of little value in the poorly differentiated group. Trials of intensive multidrug chemotherapeutic regimens seem warranted, despite the risk of exacerbating the cytopenia.

Bone Marrow Examination↗
PubMed1975

Familial variable immunodeficiency: autosomal dominant pattern of inheritance with variable expression of the defect(s).

In 1963, Rosen and Bougas reported the case of a woman with recurrent infection, marked elevation of 19S, and virtual absence of 7S gamma globulin. Recently, members of her family were found to have similar abnormalities: Ten of the 37 family members tested had elevated levels of serum IgM accompanied by a combined deficiency of IgG and IgA in three, and by a deficiency of either IgG or IgA in two. In five, an increase in IgM was the sole abnormality. Two children had deficiencies of IgG and IgA with normal serum levels of IgM. Ten of the 12 affected individuals had no IgD detectable by radial immunodiffusion and six had a low percentage of IgG-bearing B lymphocytes. A lack of correlation between the immunochemical abnormalities and either the presence or severity of clinical illness was observed. The presence of immunodeficiency in three generations and in both sexes of this family suggests an autosomal dominant mode of inheritance with variable penetrance of the defect.

Adolescent↗
PubMed1975

Distribution of latex-ingesting cells, T cells, and B cells in the peripheral blood of patients with malignant melanoma.

The distribution among peripheral blood mononuclear cells of latex-ingesting cells, T cells, and B cells was determined with samples from 38 normal donors and 25 patients with malignant melanoma. The mean percentage of latex-ingesting cells, as well as B and T cells, was significantly reduced in the 25 patients with malignant melanoma, stages I and II, compared to the controls. Several explanations for these unexpected findings were considered; possibly the presence of occult neoplasm was responsible for the observed changes in cell distribution.

Adolescent↗
PubMedDate not supplied

Phenotypic characterization of 'non-T, non-B' acute lymphoblastic leukemia by a new panel (BL) of monoclonal antibodies.

Peripheral blood and/or bone marrow leukemic cell suspensions from 49 patients with 'non-T, non-B' acute lymphoblastic leukemia (ALL) were analysed by flow cytometry using a new panel of four monoclonal antibodies. Anti-BL1 and anti-BL2 originating from NALM-6 and B35M lymphoblastoid cell lines, respectively. These antibodies recognize B-cell differentiation antigens: a heat stable non-immunoprecipitable antigenic determinant, and a 68 000 daltons glycoprotein molecule, respectively. BL5 and BL6 were derived by immunization with the promyelocytic cell line HL-60, recognizing antigens present on early hematopoietic cells: an 85 000 daltons MW glycoprotein (Pro-Im 1) and a heat stable antigen (Pro-Im2), respectively. All ALL patients studied had L1 or L2 morphology by the FAB classification and a blast count exceeding 50 per cent. There were 25 males and 24 females. Median age was 8 years (range 1-67 years). Thirty-nine cases were studied at initial presentation and 10 at relapse. Cells from 46/49 cases expressed BL2 and/or BL1, but were not reactive with BL5 or BL6. Three of 49 cases did not express BL1 or BL2. However, a small percentage of blasts from one case was positive for BL5 (13 per cent) and the other 2 cases were reactive with BL6 (20 per cent and 36 per cent, respectively). These were one adult and 2 pediatric patients that had other ALL markers and achieved a complete remission with appropriate ALL therapy. One of the BL6+ cases relapsed after 19 months with a change in phenotype to BL1+ BL2+ BL5- BL6-. This analysis shows that the majority of 'non-T, non-B' ALL's do express B-cell associated antigens (BL1/BL2) argumentative of their B-cell origin. A small subgroup does not express such antigens and may arise from a more immature cell, since they expressed antigens on early hematopoietic stem cells.

Adolescent↗
PubMedDate not supplied

Cancers-associated with HIV infection.

The spectrum of neoplastic disease seen in patients with the acquired immune deficiency syndrome (AIDS) is similar to that seen in several congenital and iatrogenic immunodeficiency states and provides a human model for studying neoplastic transformation in the immune compromised host. High grade lymphoid neoplasia, particularly of the central nervous system (CNS), as well as a virulent form of Kaposi's sarcoma (KS) and several types of squamous cell carcinomas, are appearing at an alarming rate in patients with AIDS. There is substantial serologic, pathologic and molecular evidence linking cytomegalovirus (CMV) to KS and Epstein-Barr virus (EBV) to squamous cell carcinoma and high-grade B-cell non-Hodgkin's lymphoma (NHL). The human T-cell lymphotropic virus type III/lymphadenopathy associated virus (HTLV-III/LAV) may be responsible for the permissive immune deficient state allowing for opportunistic neoplasia and the aggressive biologic behavior and atypical anatomic distribution these neoplasms exhibit. The clinical features as well as potential etiopathogenetic mechanisms of these malignancies are reviewed.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Combination chemotherapy salvage of heavily pretreated patients with Hodgkin's disease: an analysis of prognostic factors in two chemotherapy trials and the literature.

The results of two intensive combination chemotherapy trials for heavily pretreated patients with Hodgkin's disease were markedly different. Only one of 27 patients treated with doxorubicin, bleomycin, vinblastine, and dacarbazine (ABVD) achieved a complete remission (CR), while a CR was attained by 50% of the patients (nine of 18) treated with ABVD alternating with mechlorethamine, vincristine, procarbazine, and prednisone (MOPP/ABVD). There was a significantly longer survival for patients on MOPP/ABVD. Characteristics of patients in the two trials which might have at least partially explained these differing results were identified. The patients treated with ABVD all had prior histories of multiple relapses or continuous disease activity, while the majority of responding patients treated with MOPP/ABVD had few prior relapses and long disease-free intervals immediately prior to treatment. In the MOPP/ABVD trial, a trend toward a higher CR rate was found for patients with relapses confined to lymph nodes, compared with patients who had extranodal disease, although the difference lacked statistical significance. The characteristics of the patient population undergoing treatment must be considered in the interpretation of the results of chemotherapy salvage regimens for Hodgkin's disease.

Adult↗