[HTLV-I negative T helper/inducer phenotype chronic lymphocytic leukemia associated with OKT3 epitope deficiency--a case report].
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Aged↗
Biomedical subjects
K Takatsuki
Publications and source records attributed to K Takatsuki.
Gene rearrangements of T cell receptor beta and gamma chains in HTLV-I infected primary neoplastic T cells.
Rearrangements of T cell receptor beta and gamma chain (T beta and T gamma) genes were analyzed by Southern blot method in samples from 30 patients with adult T cell leukemia (ATL) and 17 patients with non-ATL T cell neoplasms. The DNA probes used were the constant and joining region of T beta gene and the joining region of T gamma gene. Rearranged bands of T beta gene on one or both allelic chromosomes were detected in all neoplastic T cells, even those of smoldering ATL, in which only a small percentage of peripheral blood T cells were detected as leukemic. T gamma gene was rearranged in the cells of all but one patient, the exception being one ATL patient. In order to test whether any given variable region (V) of T beta gene was expressed in ATL cells, two functionally rearranged V beta sequences of ATL were compared with a V beta sequence from T cells acute lymphoblastic leukemia cells. No significant homologies were noted among the three deduced gene product amino acid sequences, confirming that T beta molecules of ATL cells contained no specific structures in common. The observed heterogeneity of T beta and T gamma gene rearrangements in ATL cells further supported these findings.
Amino Acid Sequence↗
Clinical evaluation of calcium metabolism in adult T-cell leukemia/lymphoma.
To clarify the mechanism of development of hypercalcemia in adult T-cell leukemia/lymphoma (ATLL), ten patients with a serum creatinine level less than 177 mumol/L (2 mg/dL) were examined. Although hypercalcemia was seen in only four (40%) of these patients, four of six normocalcemic patients showed hypercalciuria (greater than 5 mmol/d [greater than 200 mg/24 h]). All hypercalcemic patients exhibited high nephrogenous cyclic adenosine monophosphate (NcAMP) levels in the face of low-normal immunoreactive parathyroid hormone and reduced serum 1,25-dihydroxyvitamin D [1,25(OH)2D] concentration. Half of the hypercalciuric patients with normocalcemia also showed high NcAMP and reduced serum 1,25(OH)2D levels. Furthermore, the changes in NcAMP and serum 1,25(OH)2D concentration closely paralleled the development of hypercalcemia and hypercalciuria in two patients. These results are reminiscent of the syndrome of humoral hypercalcemia of malignancy and suggest that derangements in calcium metabolism develop by a similar mechanism in patients with ATLL. The present data also indicate the importance of the measurement of urinary calcium excretion for early detection and prevention of fatal hypercalcemia in patients with ATLL.
Adult↗
Soluble interleukin 2 receptors in sera of Japanese patients with adult T cell leukemia mark activity of disease.
Serum concentrations of soluble interleukin 2 receptors (sIL 2R) were measured by an enzyme-linked immunosorbent assay (ELISA) in 30 patients with adult T cell leukemia (ATL), in 9 patients with other hematopoietic malignancies, and in 17 asymptomatic individuals seropositive for human T cell leukemia virus type I (HTLV-I). Sixty HTLV-I seronegative, age-matched controls showed a normal range of form 63.2 to 480.8 U/mL. All asymptomatic carriers of HTLV-I had sIL 2R in their sera within the normal range. sIL 2R in sera was not related to the anti-HTLV-I antibody titer. Eleven patients with acute ATL, a clinical phenotype with median survival rate of 4.4 months, had markedly elevated sIL 2R (11,100 to 99,000 U/mL), but eight patients with smoldering ATL had low sIL 2R values (less than 480.8 U/mL) comparable to controls. Eleven patients with chronic ATL had intermediate elevated levels of sIL 2R (480.8 to 37,300.0 U/mL). Serum levels of sIL 2R correlated with the number of ATL cells (r = 0.812) and CD25-positive cells (r = 0.725) circulating in the peripheral blood. Longitudinal studies performed in four patients with ATL showed significant correlation between serum concentration of sIL 2R and activity of the malignancy. These findings suggest that the level of sIL 2R in serum indicated tumor load and, possibly, prognosis.
Adult↗
Adult T cell leukemia cell lines that originated from primary leukemic clones also had a defect of expression of CD3-T cell receptor complex.
Surface phenotypes and genotypes of six T cell lines established from four patients with adult T cell leukemia (ATL) were compared with those of fresh ATL cells. The surface antigen densities of CD3 and T cell receptor (TCR) complex examined by OKT3 and WT-31 mAbs on fresh ATL cells were low. But three IL-2-dependent cell lines, SKT-2, SKT-5, and ATL-17-2, established from three patients expressed a high density of CD3-TCR complex on their surfaces. On the contrary, three other cell lines (SKT-1A, SKT-1B, and MMT-2), established from two other patients, expressed a low density of CD3-TCR complex. Genotypic analysis of TCR beta chain (T beta) gene and integration sites of the proviral genome of human T cell lymphotropic virus type 1 demonstrated that SKT-1A, SKT-1B, and MMT-2 were derived from the original leukemic clones. These apparent associations between a defect of expression of CD3-TCR complex and identical genotypes of fresh and cultured cells suggest that the defect of expression of CD3-TCR complex may play a key role for development of ATL.
Adult↗
ATL and AIDS.
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Acquired Immunodeficiency Syndrome↗
[ATL and AIDS].
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Acquired Immunodeficiency Syndrome↗
Gastroduodenal complications in patients with adult T-cell leukemia.
Gastroduodenal endoscopic examinations were performed on 15 patients with adult T-cell leukemia (ATL). Twelve had the disease in acute form, two in chronic form and one patient was in crisis. Eight patients had gastroduodenal lesions, four esophageal candidiasis, three gastric infiltration and two duodenal ATL-cell infiltration. Four out of the five patients who had the gastroduodenal ATL-cell infiltration complained of gastroduodenal symptoms such as anorexia, upper abdominal pain, diarrhea and melena. Our observations suggested that these gastroduodenal symptoms were related to the gastroduodenal ATL-cell infiltration. Esophageal candidiasis in ATL could be related to immunodeficiency.
Adult↗
Major prognostic factors of adult patients with advanced B-cell lymphoma treated with vincristine, cyclophosphamide, prednisone and doxorubicin (VEPA) or VEPA plus methotrexate (VEPA-M).
Eighty-two adult patients with advanced B-lymphoma, treated between 1981 and 1983 with VEPA (vincristine, cyclophosphamide, prednisolone and doxorubicin) or VEPA-M (VEPA plus methotrexate) in a prospective randomized fashion, were evaluated for pretreatment characteristics. The overall complete response (CR) and the 4-year survival rates were 74% and 45%, respectively. The relapse rate was 51%. Stage of disease only was negatively associated with the CR rate in a multivariate analysis. The primary extranodal tumor site other than upper gastrointestinal (GI) tract and high grade pathology were found to affect disease-free survival adversely in a Cox proportional hazards model. Poor performance status, advanced stage, primary extranodal tumor site other than upper GI tract, advanced age, high grade pathology and prior therapy by either surgery or radiation, were significantly associated with shortened survival in a Cox proportional hazards model. These results indicate advanced B-lymphoma in Japan to be generally similar to advanced non-Hodgkin's lymphoma in the West in terms of prognostic factor characteristics, but the importance of the primary site in predicting survival has not been reported in the West. Also, the lack of a survival plateau in patients with diffuse large cell lymphoma indicates more intensive chemotherapy regimens than VEPA or VEPA-M to be needed. It was also found that the significant prognostic factors in patients with advanced B-lymphoma were very different from those with T-lymphoma. The five factors: pathology, stage, primary site, age, prior therapy by surgery or radiation, for which the risk ratio was more than 2.3, were used to construct a model containing 23 categories of patients running an increasing risk of shortened survival; this divided patients into three groups. The CR and 4-year survival rates of low-, moderate- and high-risk groups were 90% and 74%, 74% and 58%, and 50% and 5%, respectively. The risk-grouping provides indications for determining optimal therapy for individual patients and the need for new therapeutic trials in patients at high risk.
Adult↗
[Glomerular diseases secondary to plasma cell dyscrasia].
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Female↗
Autocrine stimulation of interleukin 1 beta in acute myelogenous leukemia cells.
A significant increase in CD25 antigen-positive cells by IL-1 was observed in cells of a patient with M7 acute myelogenous leukemia. Basal proliferation and expression of CD25 antigen by the M7 leukemic cells were inhibited by addition of anti-IL-1 beta antibody in a dose-dependent manner, but not by rabbit anti-IL-1 alpha antibody. Culture supernatants of these leukemic cells contained IL-1 activity, which was specifically inhibited by addition of anti-IL-1 beta antibody, and Northern blot analysis detected intracellular IL-1 beta mRNA. These results indicated that autocrine secretion of IL-1 beta was involved in proliferation of some myelogenous leukemic cells.
Antigens, Surface↗
Biochemical and functional characterization of MCS-2 antigen (CD13) on myeloid leukemic cells and polymorphonuclear leukocytes.
The antigen defined by MCS-2 monoclonal antibody (mAb) was characterized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis of surface and internally labeled cells. Surface iodination revealed that MCS-2 antigen on the surfaces of acute myelogenous leukemia cells, HL-60 cells, and polymorphonuclear leukocytes (PMN) had the same molecular weight (Mr 150,000) and that their autoradiographic bands were also the same. Internal labeling of HL-60 cells with [35S]methionine followed by immunoprecipitation revealed two bands whose molecular weights were 150,000 and 130,000. HL-60 cells gave stronger bands than did PMN. The intensity of the Mr 130,000 band became weaker, when internally pulse-labeled cells were cultured in the absence of labeled methionine, suggesting that Mr 130,000 glycoprotein was a precursor protein of Mr 150,000 glycoprotein. MCS-2 mAb precipitated two bands from tunicamycin-treated HL-60 cells whose apparent molecular weights were 100,000 and 110,000. When cells were cultured with MCS-2 mAb, expression of the antigen decreased rapidly (within 10 min). The degree of suppression was more prominent in PMN than in acute myelogenous leukemia and in myelomonocytic cell lines. Reexpression of MCS-2 antigen by PMN after removal of the mAb from the culture medium was not observed, but it occurred rapidly in myelomonocytic cell lines, although it was blocked by pretreatment of the cells with cycloheximide. These findings suggested that the less-marked suppression of MCS-2 antigen expression by cell lines was due to its greater synthesis by these cells. These findings suggested that MCS-2 mAb reacted with identical molecules, which were recognized by other mAbs belonging to CD13. Furthermore, modulation of MCS-2 antigen was observed by MCS-2 mAb itself.
Antibodies, Monoclonal↗
Human T-cell leukemia virus type I infection in hemodialysis patients.
Human T-cell leukemia virus Type I (HTLV-I) has been detected in a high proportion of individuals in Kumamoto prefecture (Kyushu) and Okinawa, where adult T-cell leukemia (ATL) is more likely to occur. The seroprevalence of antibody to HTLV-I was evaluated in hemodialysis patients and healthy individuals in the ATL endemic area. The prevalence of antibody to HTLV-I in 13,329 healthy controls was 3.6%, compared with 19.7% in 949 chronic hemodialysis patients. The prevalence of hemodialysis patients was significantly higher (P less than 0.01) than that in healthy individuals. Of 681 blood transfused patients who had undergone hemodialysis, 153 (22.5%) were seropositive, compared with 34 (12.7%) of the 268 who had not received the blood transfusion. The incidence was higher in dialysis patients who had been transfused than in those who had never received blood transfusions. Immune defects associated with uremia may have predisposed the patients to HTLV-I infection. Repeated antigenic stimulation from multiple infectious agents may have also played a role. The findings suggest an association between maintenance hemodialysis and HTLV-I infection, which can not be explained solely by blood or blood products.
Adolescent↗
The expression of functional erythropoietin receptors on an interleukin-3 dependent cell line.
We report the expression of the erythropoietin receptors on an interleukin-3 dependent cell line. By the transfer into medium supplemented with erythropoietin, DA-1 cells were converted to an erythropoietin dependent growth state. [125I] erythropoietin was used to detect receptors specific for this hormone on the cell surface. Binding studies revealed that erythropoietin bound to 131 +/- 23 receptors/cell with a Kd of 0.54 +/- 0.2 nM. When the cells were incubated at 37 degrees C, trichloroacetic acid soluble radioactivity appeared in the medium after [125I] erythropoietin binding began to decrease, suggesting that the decline represents the degradation of cell associated [125I] erythropoietin- receptor complexes.
Cell Line↗
Strongyloides stercoralis as candidate co-factor for HTLV-I-induced leukaemogenesis.
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Adult↗
Gas chromatographic-mass spectrometric determination of macrolide antibiotics in beef and pork using single ion monitoring.
A gas chromatographic-mass spectrometric (GC-MS) method using single ion monitoring (SIM) is described for the determination of residual macrolide antibiotics, oleandomycin, kitasamycin, spiramycin and tylosin, in beef and pork. For GC-MS determination, oleandomycin is acid hydrolysed to desoleandomycin and acetylated, in the same way as erythromycin. However, for elution from a GC column, the carbon-carbon double bonds in the antibiotics must be hydrogenated to single bonds before acid hydrolysis. Kitasamycin and spiramycin are therefore converted into hydroforocidine acetate and tylosin into hydro-O-mycaminosyl tylonolide acetate, which are determined by GC-MS with SIM.
Acetylation↗
Hypercalcemia and osteoclast proliferation in adult T-cell leukemia.
Eighteen autopsy cases of adult T-cell leukemia (ATL) were investigated clinicopathologically. Thirteen of the patients had hypercalcemia during their clinical course. Nine of the thirteen had a high level of serum calcium at the terminal stage, even after extensive chemotherapy. Microscopic examination of the bone revealed proliferation of osteoclasts and bone resorption in eight patients. No osteoclast proliferation or bone resorption was found in the other nine normocalcemic patients. The infiltration of ATL cells was observed in only two patients--one was hypercalcemic and the other, normocalcemic. The factors affecting the serum calcium level were examined in two hypercalcemic patients. Hypercalcemia could not be accounted for by parathyroid hormone or prostaglandins E levels, which were in the normal range, or by 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, which were low. Our findings are consistent with the mechanism proposed by several investigators, that the malignant T-lymphocytes produced an osteoclast-activating-factor-like substance that caused osteoclast proliferation and hypercalcemia.
Adult↗
Expression of the HT462 antigen on fresh leukemic T cells and on cells of HTLV-I infected lines.
We have examined expression of antigens defined by HT462 monoclonal antibody (mAb), together with other HTLV-I related antigens using phorbol 12-myristate 13-acetate treated leukemic mature T cells. Thirteen patients with adult T-cell leukemia (ATL), 3 patients in remission states of ATL and 5 patients with non-ATL were examined. All ATL cells expressed the HT462 antigen, however cells from patients in remission did not express the HT462 antigen. A low percentage of cells from 2 out of 5 patients with non-ATL mature leukemic T cells expressed the HT462 antigen, although these cells did not express other HTLV-I related antigens. Cells of HTLV-I infected human cell lines expressed the HT462 antigen. Three HTLV-I infected rat cell lines (TARS-1, TART-1, TARL-2) did not express the HT462 antigen, although cells of these lines expressed other HTLV-I related antigens. Characterization of the HT462 antigen by strip radioimmunoassay based on western blotting technique using cell lysates of HUT102 cells revealed two additional bands (p68, p35) together with previously reported proteins (gp52, p42). Only p68 was seen in western blots using cell lysates of the rat cell lines. These findings further suggest that the HT462 antigen is a cellular component induced in virus transformed human cells and not a virus encoded protein.
Animals↗