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Biomedical subjects

L B Vogler

Publications and source records attributed to L B Vogler.

At least 19 recordsLinked to original sources

A comparative analysis of cytoplasmic mu (C mu) expression in acute lymphoblastic leukemia by molecular and immunologic techniques. Identification of leukemia cases expressing C mu mRNA transcripts in the absence of detectable C mu proteins.

Among acute lymphoblastic leukemias derived from the B-cell lineage, the subset of cases expressing cytoplasmic mu heavy chain proteins (C mu) in the absence of surface immunoglobulin has been designated pre-B-cell acute lymphoblastic leukemia. This group, traditionally identified using immunologic smear techniques, has been associated with a poor prognosis in some series. In a comparative study, 25 cases of B-lineage acute lymphoblastic leukemia were analyzed for C mu expression using molecular and immunologic techniques. RNA derived from cryopreserved blast cells was hybridized in both Northern and slot-blot analyses using a probe (pBZ311) containing four exons of the human immunoglobulin heavy chain mu constant region gene. Expression of C mu proteins was assessed simultaneously by slide immunofluorescence and flow cytometric techniques in all samples. These studies were correlated with immunoglobulin heavy and light chain gene rearrangements, cell-surface immunophenotype, cytogenetics, and other clinicopathologic features. C mu mRNA transcripts were detected in 14 of 25 cases, whereas C mu proteins were detected in only 9 of these cases using flow cytometric techniques. Only four of these nine cases were positive by slide immunofluorescence techniques. These studies imply that molecular and flow cytometric techniques may be a more sensitive means to assess C mu expression. The identification of five cases that expressed C mu mRNA transcripts in the absence of detectable C mu proteins also suggests that molecular techniques may be valuable in identifying a unique subgroup of pre-B-cell acute lymphoblastic leukemia cases that contain C mu mRNA transcripts, but lack C mu proteins.

Adolescent

Human B-lymphocyte precursors do not express the N-myc gene.

N-myc expression has been reported in neuroblastoma, retinoblastoma and small cell lung carcinoma. Increased expression associated with gene amplification in neuroblastoma correlates with disease stage and prognosis. N-myc expression has been observed in diverse murine tissues during early stages of development with loss of expression in later stages. Abelson murine leukemia virus (A-MuLV)-transformed pre-B cells express N-myc, whereas mature B cells do not. To determine whether human B-lymphocyte precursors also have increased N-myc expression, we extracted DNA and RNA from representative cell lines, prepared Southern and Northern blots and examined them with the N-myc probe, pNB-1. RNA from the following B-cell developmental stages were examined. One null, 1 pre-pre-B, 3 pre-B (including pre-B-lymphoblastic leukemia, a poor prognostic category) and 5 mature B. Neuroblastoma cells and tissues served as positive controls; negative controls included human muscle, placenta, epithelial cell lines, monocytic, promyelocytic, and T-cell lines. N-myc expression was detected in neuroblastoma cells, but in none of the mature human B or B-lymphocyte precursor cells. Additional immunocytochemical studies performed for N-myc nuclear protein likewise failed to detect this gene product. We conclude that human pre-B cells, unlike murine B-cell precursors, do not express increased levels of N-myc RNA. Expression of this oncogene in human neoplastic B cells does not appear to correlate with developmental stage or prognostic group.

B-Lymphocytes

Response of neoplasms of B cell lineage to the proliferative effects of B cell growth factor and the phorbol ester TPA.

Little information is available regarding the role of soluble growth factors in neoplastic B cell proliferation. The authors have measured B cell growth factor (BCGF)-induced proliferation in B lymphocytes isolated from 28 patients with malignancies representing different stages of B cell differentiation. The phorbol ester TPA (12-O-tetradecanoyl phorbol-13-acetate), a potent mitogen and inducer of BCGF receptor expression in normal B cells, was added in combination with BCGF to enhance the proliferative response. These results show that many neoplastic B cells are able to respond to BCGF (32%), particularly when combined with TPA (63%). The response was variable in frequency and magnitude within clinicopathologic groups; cells from patients with non-Hodgkin's lymphoma (NHL) were more refractory to stimulation than those from acute lymphocytic leukemia (ALL) and chronic lymphocytic leukemia (CLL). An attenuated response to BCGF plus TPA was observed in neoplastic cells with high rates of spontaneous DNA synthesis from all histologic categories. These observations suggest that some maximally stimulated cells appear incapable of responding to additional exogenous growth stimuli. Within apparently homogeneous clinicopathologic groups, distinct subgroups of B cell neoplasms can be defined by cellular responses to BCGF. The correlation of this biologic feature with the clinical behavior of the neoplasm requires additional study.

B-Lymphocytes

T4+ (helper phenotype) chronic lymphocytic leukemia: case report with liver failure and literature review.

T-cell lymphomas and leukemias are a heterogeneous group of neoplasms found in each anatomic compartment of the T system (marrow, thymus, and various peripheral tissues) and that have varying phenotypic expressions. Histopathologic features of the thymic and peripheral T neoplasms do not fit into a clearly defined pattern, and clinical expressions of T neoplasms are likewise variable. This report describes a 60-year-old man with "chronic" lymphocytic leukemia of T4+ (helper) phenotype. Rapid deterioration in liver function, presumably due to tumor infiltration, was unexpected and has not previously been reported. The unusual clinical and pathologic features are reviewed in the context of T-cell neoplasms, particularly T4+ processes.

Humans

Lymphoproliferative diseases in immunocompromised hosts: the role of Epstein-Barr virus.

Epstein-Barr virus (EBV) is a ubiquitous transforming virus of the herpes group showing tropism for B lymphocytes. Primary infection in normal hosts results in a transient lymphoproliferative disorder, acute infectious mononucleosis (IM), that is restricted by cytotoxic and suppressive lymphocytes. However, in the immunodeficient host, EBV-induced lymphoproliferation may behave in a biologically malignant fashion. Patients with primary immunodeficiencies and those with immune incompetence resulting from suppressive therapy in allograft transplantation or infection with human immunodeficiency virus (HIV) have EBV-related illness ranging from fulminant mononucleosis and invasive polyclonal B cell hyperplasia to monoclonal B cell malignancies. While the direct link between EBV and malignant B cell proliferation in these patients has not been elucidated, the association has been increasingly recognized with improved techniques of viral detection. Clinical management can be guided by the location and extent of tumor, histologic features, and clonality. Regional and node-based polyclonal proliferations may respond to prompt reduction of immunosuppressive therapy and efforts to interrupt the replicative cycle with antiviral agents. Systemic cytotoxic therapy often leads to further immunosuppression and should be reserved for patients with progressive disease, advanced visceral involvement, and monoclonal lymphoid malignancies.

Acquired Immunodeficiency Syndrome

Plasmacytic differentiation in follicular center cell (FCC) lymphomas.

Although follicular centers are the sites of production of plasma cell precursors, plasmacytic differentiation in follicular center cell (FCC) lymphomas is rarely seen, presumably because of a "block" in differentiation of the large noncleaved FCC. The authors reviewed a large number of these cases to determine the frequency of plasmacytic differentiation in FCC lymphomas. In one hundred ninety-eight, consecutive FCC lymphomas with a follicular pattern from a two-year period, 17 (9%) cases were found in which there were large numbers of plasma cells. Immunoperoxidase studies of paraffin-embedded sections (PIP) for cytoplasmic immunoglobulin showed polytypic marking in ten of these and a monotypic plasma cell population in seven. In this latter group, isotypically identical marking of the plasma cell and FCC populations could be demonstrated in three cases with immunoperoxidase (where the FCCs showed cytoplasmic marking) and in one case (of one tested) with surface typing studies. In addition, three patients had serum paraproteins identical to the plasma cell cytoplasmic immunoglobulins. These findings indicate that a small minority of FCC lymphomas contain sufficient plasma cells to be a diagnostic problem, and that in some of these cases, plasma cells are a differentiated component of the FCC lymphomas.

Cell Differentiation

Immunologic markers of Burkitt's lymphoma cells.

Lymphocyte markers were studied on fresh cells from 30 patients with Burkitt (L3) leukaemia and cell lines derived from endemic and non-endemic Burkitt's lymphoma (BL) patients. We observed day-to-day variations of lymphocyte marker expression by cultured lines and, occasionally, differences between fresh and cultured cells. In L3 leukaemia, a wide range of phenotypes, including pre-B cell and mature monoclonal IgM + IgD positive B-cell phenotypes, was observed. Most often, the cells expressed high-density monoclonal surface IgM without IgD and lacked IgG Fc, complement and Epstein-Barr virus receptors. Blast cells from rare patients featured monoclonal IgG or IgA instead of IgM. Cases with light chains of the lambda type were more frequent than those with kappa chains. Monoclonal immunoglobulins were found in serum or urine from eight of 20 patients studied. These results are compared with data from the literature on endemic and non-endemic BL and discussed with respect to the maturation stage reached by the cells. In the study of both fresh and cultured cells, we demonstrated a correlation between variant chromosomal translocations and light-chain types, the cells from patients with a t(2;8) translocation expressing kappa and those with a t(8;22) expressing lambda chains, with one exception Vimentin expression was absent or weak in most BLs studied (lines or fresh cells) and in cells from patients with Langer-Giedion syndrome, in contrast to most other lymphomas and leukaemias and normal lymphoblastoid cell lines.

Burkitt Lymphoma

Diversity of immunoglobulin expression in leukaemic cells resembling B-lymphocyte precursors.

Approximately 20% of patients with acute lymphocytic leukaemia (ALL) have leukaemic blasts with features of pre-B cells which are the recently characterized precursors of B lymphocytes in normal development (for a review, see ref. 2). Pre-B cells isolated from normal bone marrow or fetal liver, and malignant cells from patients with pre-B cell leukaemia, are rapidly dividing lymphoid cells that contain cytoplasmic immunoglobulin mu heavy chains, but have no detectable surface immunoglobulin. The resemblance of immunoglobulin-containing ALL cells to normal precursors of B lymphocytes and their availability in relatively pure preparations allowed us to explore them as models of early stages in the differentiation of the B-lymphocyte line. We report here observations on the occurrence of intermediate pre-B/B-cell phenotypes, immunoglobulin isotype switching and the asynchrony of immunoglobulin heavy and light chain expression in 30 cases of ALL and 3 cases of chronic myelogenous leukaemia in lymphoblastic crisis (CML-BC).

B-Lymphocytes

An analysis of clinical and laboratory features of acute lymphocytic leukemias with emphasis on 35 children with pre-B leukemia.

In 35 of 191 patients with acute lymphocytic leukemia (ALL) malignant cells were similar in phenotype to B-lymphocyte precursors. Both these patients' lymphoblasts and normal pre-B-cells contain cytoplasmic immunoglobulin (Ig) mu heavy chains, but have no surface Ig. In patients with pre-B leukemias, lymphoblasts containing cytoplasmic mu chains alone were often accompanied by cells of identical morphology that expressed no Ig and less frequently by lymphoblasts bearing scant amounts of surface mu. This spectrum of cellular Ig expression suggests that "null," pre-B, and intermediate pre-B/B ALLs represent closely related malignancies with complete or partial arrests at different stages of maturation. When pre-B, B, T, and "null" cell categories of ALL were compared for 22 different clinical and laboratory features, including remission rate and short-term remission duration, no statistical differences were observed between the pre-B and "null" groups. These early results suggest that pre-B-cell leukemias represents a relatively good prognostic subclass of ALL, do not require more intensive treatment than that proven to be effective for "null" cell ALL, and should be distinguished from the less common, but more clinically aggressive, B-cell subclass of ALL. Longer follow-up will be required to confirm these preliminary conclusions.

B-Lymphocytes

Immunological phenotypes of human leukemias of the B-cell lineage.

The recent results are summarized of some immunological studies of various human leukemias of the B-cell lineage. The study of pre-B leukemias has outlined the diversity of immunoglobulin expression in leukemic cells resembling B-lymphocyte precursors and has provided insights into the biology of the progenitors of hematopoietic cells. Acute leukemia with Burkitt cells represents a very homogeneous group close to classical Burkitt's lymphoma. Mitogens are able to induce in vitro differentiation of leukemic cells from chronic lymphocytic-B leukemia and from hairy cell leukemia. Hairy cells become able to express new phenotypic characteristics after stimulation by phytohemagglutinin.

Antibodies, Neoplasm

Isolated marrow lymphoma: an entity of possible T-cell derivation.

Seven adults had a distinct clinicopathologic type of lymphoproliferative disorder of the bone marrow. All patients presented with weakness and pancytopenia; no evidence of gross extramedullary involvement was found. In 5 cases severe and prolonged bone marrow hypoplasia was associated with combination chemotherapy; 1 patient died of infection during initial therapy. In 6 of the 7 cases, clinical improvement occurred following therapy. As a terminal event, 2 patients developed a leukemic phase. Tumor cell from 4 patients were studied immunologically, and in 2 patients surface marker characteristics suggestive of T-cell tumor origin were found. In 2 cases, ultrastructural studies of lymphoid cells were compatible with a T-cell neoplasm. The above data suggest that these cases represent a distinct type of chemotherapy-sensitive lymphoma in which conservative initial treatment may induce a response without prolonged bone marrow hypoplasia.

Adult

Studies on the clonal origin of multiple myeloma. Use of individually specific (idiotype) antibodies to trace the oncogenic event to its earliest point of expression in B-cell differentiation.

IgA myeloma proteins of kappa- and lambda-types were isolated from two patients. These were used to produce and purify anti-idiotype antibodies of both broad (myeloma-related) and narrow (individual myeloma) specificities. The anti-idiotype antibodies were conjugated with fluorochromes and used as immunofluorescent probes to trace in the patients clonal expansion at different levels of B-cell differentiation. Our results (a) confirm that B lymphocyte precursors in IgA plasma-cell myelomas are involved in the malignant process, (b) show that B lymphocytes of the malignant clone include those expressing each of the major heavy-chain isotypes, mu, delta, gamma, and alpha, and (c) provide strong circumstantial evidence that pre-B-cell members of the malignant clone are also increased in frequency. T cells expressing idiotypic determinants were not detected. These findings argue that the initial oncogenic event may occur in a B-stem cell and is not influenced through stimulation by antigen. An interesting association was the increased frequency of related clones of B lymphocytes as detected by their reactivity with anti-idiotype antibodies of broad specificity. Neither plasma cell nor pre-B-cell members of these related clones were increased in frequency. Anti-idiotype antibodies or helper T cells reactive with myeloma-related idiotypes could be responsible for this phenomenon. We discuss other implications of these findings and speculate that all of the various phenotypes of B-lineage malignancies may result from oncogenic processes affecting stem cell targets.

Antibodies, Neoplasm

Philadelphia-chromosome-positive pre-B-cell leukemia presenting as blast crisis of chronic myelogenous leukemia.

Cytogenetic studies of chronic myelogenous leukemia (CML) have shown that the majority of hemopoietic cells originate from pluripotential stem cells affected in this disease. Evidence that lymphocytes are also progeny of these stem cells, however, has been indirect. Philadelphia-chromosome-positive leukemic blasts from a 4 10/12-yr-old boy with CML in blast crisis had features characteristic of pre-B leukemic cells, including expression of cytoplasmic IgM and absence of surface immunoglobulin. Additional immunologic, enzymatic, and pharmacologic characterization of these cells supported their pre-B-cell phenotype. Together, these features provide direct evidence for CML stem cell ancestry to lymphocytes of the B-cell lineage.

B-Lymphocytes