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Biomedical subjects

V K Lui

Publications and source records attributed to V K Lui.

14 recordsLinked to original sources
PubMed1981

Pretreatment testicular biopsy in childhood acute lymphocytic leukaemia.

Between August, 1978, and March, 1981, 24 boys with acute lymphocytic leukaemia (ALL) (14 non-B-cell non-T-cell, 6 pre-B-cell, and 4 T-cell) underwent bilateral wedge testicular biopsy at initial diagnosis. All testes were of normal size. Histological analysis was performed independently by three pathologists, 4 (3 non-B non-T, and 1 pre-B) of 20 patients with non-T-cell ALL demonstrated testicular focal lymphoblastic involvement. Successful induction chemotherapy without concomitant testicular irradiation completely eradicated testicular infiltrates in all 4 patients. Only 1 of the 4 T-cell patients had pre-treatment testicular infiltrates. Unlike boys with non-B non-T leukaemia, attainment of bone-marrow remission in this patient was associated with persistent testicular disease. These preliminary data indicate that in patients with ALL of non-T-cell type, systemic induction chemotherapy eradicates the small testicular infiltrates of lymphoblasts. Prophylactic testicular irradiation in this group of patients does not seem to be warranted.

Biopsy↗
PubMed1981

Bone marrow cultures in acute leukemia of childhood.

The technique of bone marrow cultures has been shown to be of value in childhood acute leukemia. It now appears that acute myelogenous leukemia may be due to defective maturation of normal progenitor cells. The pattern of growth of these cells has been demonstrated to be of prognostic value. In contrast, the growth of normal progenitor cells from the bone marrow cultures of children with acute lymphocytic leukemia (ALL) may be due to the few remaining normal cells. The cause of granulocytopenia in childhood ALL is still unclear.

Acute Disease↗
PubMed1980

Essential thrombocythemia in a child: platelet ultrastructure and function.

A nine-year-old black girl with essential thrombocythemia developed hemoptysis. Only two other cases in the English literature have been described. Ultrastructure and functional characteristics of this patient's platelets were studied. Twenty-six percent of the patient's platelets were very large (megathrombocytes). Spontaneous aggregated from the patient's platelets were not compact, and the pseudopods did not interdigitate. Both qualitative and quantitative defects in platelet organelles were detected. The microtubular system was faulty in organization. Furthermore, the number of granules (especially alpha granules) was reduced. Platelet aggregation studies demonstrated subnormal aggregation in response to ADP, epinephrine, and collagen, but aggregation with ristocetin was normal. It is postulated that a platelet membrane abnormality may be the cause of their defective platelet aggregation.

Blood Platelets↗
PubMed1980

Myelopoiesis in immunologically classified subgroups of childhood acute lymphocytic leukemia.

Soft agar culture studies of 43 immunologically characterized patients with childhood acute lymphocytic leukemias (ALL) are presented. The immunologic subsets studied include "null"-cell, pre-B-cell, and T-cell leukemias. Abnormal myelopoiesis, including high peripheral blood and low marrow, colony-forming cell numbers, low colony-stimulating activity, and normal maturation of colony-forming cells in vitro was noted in each group as previously described for immunologically uncharacterized ALL. We conclude that immunologic subsets of childhood lymphoblastic leukemia cause similar abnormalities of myelopoiesis. Lack of differences in growth characteristics among immunologic subsets of ALL make it impossible to use this tissue culture technique in subclassification of these leukemic disorders.

Adolescent↗
PubMed1980

Congenital dysgranulopoietic neutropenia: clinical, serologic, ultrastructural, and in vitro proliferative characteristics.

Six children with severe congenital neutropenia and repeated life-threatening infections were investigated by examining clinical features and myeloid cell ultrastructure, cytochemistry, and in vitro proliferation. Despite the presence of neutropenia, normal numbers of colony-forming cells (CFC) were present in blood and marrow specimens, and colony-stimulating activities (CSA) from blood cells and serum were normal or slightly increased in all patients. In vitro maturation of the progenitors to neutrophils was also uniformly present in the colonies. No patients had demonstrable antineutrophil antibodies or serum inhibitors of myelopoiesis. Serum lysozyme levels were normal. Ultrastructural and cytochemical studies of directly sampled marrow cells revealed several abnormalities in most neutrophilic myeloid cells from each of the patients consistent with an intrinsic myeloid precursor cell defect. These included (1) the defective synthesis or degeneration of primary granules, (2) an absence or marked decrease of secondary granules in the few late neutrophils observed in the bone marrow, and (3) the presence of autophagy. Phagocytosis of intact myeloid cells with subsequent degeneration was not observed; however, neutrophil debris was evident in phagocytic vacuoles of marrow macrophages. Our demonstration of ultrastructurally dysmorphic neutrophilic granulocytes, intramedullary cell lysis, normal stem cell numbers, and negative serology is comparable to similar observations of erythroid cells from patients with congenital dyserythropoietic anemia. We therefore hypothesize that the dysgranulopoiesis in these children results in neutropenia and propose the descriptive name congenital dysgranulopoietic neutropenia.

Agranulocytosis↗
PubMed1979

The effect of leukemic human serum on normal granulopoiesis.

Acute lymphoblastic leukemia (ALL) in children is often characterized by defective granulopoiesis during initial and relapse stages of the disease, resulting in absolute neutropenia in vivo and in low or absent production of granulocyte-macrophage colonies in vitro. The purpose of this study was to determine if serum from leukemic children with ALL could inhibit normal granulopoiesis. Several concentrations of serum from 12 leukemic patients were mixed with normal bone marrow cells and co-cultured by the double layer agar technique. Also, serum from normal individuals and from ALL patients in remission and relapse was examined for inhibitors. Cultures without serum served as controls. The majority of ALL (initial, relapse and remission) and normal sera either stimulated or had no effect on colony formation. These groups also had similar percentages of inhibitory sera, with the exception of the somewhat higher levels of inhibition found in the remission group. Thus, ALL serum resembled normal serum in its effect on in vitro granulopoiesis at the committed granulocyte-macrophage stem cell level. It is therefore unlikely that inhibition of in vivo granulopoiesis at the committed level by serum inhibitors is responsible for ALL-associated neutropenia.

Bone Marrow Cells↗
PubMed1979

The effect of leukemic lymphoblasts on normal granulopoiesis.

Acute lymphoblastic leukemia (ALL) in children is often characterized by defective granulopoiesis during initial and relapse stages of the disease, resulting in absolute neutropenia in vivo and in low or absent production of granulocyte-macrophage colonies in vitro. The purpose of this study was to determine if leukemic lymphoblasts from untreated ALL patients could inhibit normal granulopoiesis. Several concentrations of leukemic bone marrow cells from nine patients were mixed with either normal bone marrow cells or with autologous (HLA-identical) remission bone marrow cells, incubated for 1 hour, and co-cultured by the double layer agar technique. The cells were also cultured separately as controls. No statistically significant differences occurred between observed and expected colony counts in the majority of experiments. With three patients, slight inhibition occurred at some but not all leukemic cell concentrations tested; this inhibition was not correlated with the leukemic cell concentration. These results indicate that leukemic cells from untreated ALL patients do not significantly inhibit normal in vitro granulopoiesis at the committed stem cell level or at later levels of differentiation; therefore, such inhibition does not appear to be responsible for ALL-associated neutropenia.

Bone Marrow Cells↗
PubMed1979

Bone marrow transplantation.

Bone marrow transplantation can be considered in any disease state resulting in the malfunction or absence of part or all bone marrow elements. Diseases such as aplastic anemia, leukemia, and immunodeficiency disease are being treated with bone marrow transplantation. As with any organ transplant, graft rejection is a possibility. In bone marrow transplantation, there is the additional, unique problem of graft versus host disease. In order to prevent or minimize graft rejection, the immunocompetence of the recipient and the degree of disparity between donor and recipient at the major histocompatibility complex (MHC) loci are considered. The results of bone marrow transplantation are variable, and the mortality rate is still relatively high. However, progress is being made, and in many instances, normal bone marrow function can be restored in patients with whom other treatment has failed.

Anemia, Aplastic↗
PubMed1977

Characterisation of human malignant melanoma cell lines. VI. Inhibition of 3H-thymidine uptake by normal stimulated lymphocytes.

Cultured human malignant melanoma cells, when added to normal human lymphocytes stimulated to proliferate by mitogen or antigen, were found to inhibit the uptake of 3H-thymidine (3H-T) by the lymphocytes. A heat-labile factor present in the supernatants of the melanoma cultures is responsible for inhibition. Cell viability and blastogenesis are unimpaired in the lymphocyte cultures containing the inhibitor. Inhibition of 3H-deoxyuridine uptake was also noted indicating that both salvage and de novo pathways of DNA synthesis are involved. Lymphocytes appear to be preferentially affected as cultured colon cancer cells take up 3H-T normally in the presence of the inhibitor. Normal mitotic indices and biochemical estimation of DNA content in lymphocyte cultures containing the inhibitory factor indicate that DNA synthesis does proceed normally. The mechanisms of action of the inhibitor would appear to involve alteration of exogenous nucleoside rather than a metabolic inhibition of intracellular nucleic acid synthesis.

Antigens, Neoplasm↗
PubMed1975

Cellular immunocompetence in melanoma: effect of extent of disease and immunotherapy.

Cell mediated immunocompetence was measured serially in 35 patients with malignant melanoma in order to determine the effect of extent of disease and prognosis as well as the influence of BCG immunotherapy on immune reactivity. Compared with normal adult controls, statistically significant lymphopenia occurred only in patients with widespread disease. Seventeen of 21 patients with negative pre-therapy PPD skin test converted to skin test positivity. PHA blastogenesis was depressed only in patients in the pre-terminal stages of their disease using optimal mitogen concentrations for stimulation. Threshold concentrations of this mitogen more clearly demonstrated a depressed responsiveness which correlated in severity with extent of disease. PPD induced blastogenesis was normal or increased in the majority of patients; however, the degree of stimulation by PPD was less in the BCG induced convertors than in those patients who were skin test positive before BCG treatment. Comparison of the pre- and post BCG assessments reveals no significant differences except in relation to PPD conversion. We conclude that using threshold concentrations of PHA, impaired responses are regularly associated with disease beyond the regional lymph nodes. Routine assessment of lymphocyte function by these parameters did not provide information that was not available from clinical evaluation.

BCG Vaccine↗
PubMedDate not supplied

Doxorubicin and cisplatin therapy in children with neuroblastoma resistant to conventional therapy: a Southwest Oncology Group Study.

Fifteen children with metastatic neuroblastoma resistant to vincristine and cyclophosphamide were treated with two drugs which were known to be effective as single drugs against neuroblastoma. The drugs were given in courses every 3 weeks. Doxorubicin (50 mg/m2 iv) was given on Day 1 and cisplatin (50 mg/m2) was administered on Day 2 as an 8-hour infusion, using a forced diuretic-hydration program. Three of the 15 children achieved partial or complete remission. Three children showed improvement. The other children either did not respond to the therapy or had progressive disease. The combination of doxorubicin and cisplatin given in the sequence outlined is no more effective than either drug given singly. The side effects of the drug combination were tolerable and were in keeping with previously described toxicity.

Child↗