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At least 883 records · Page 49Linked to original sources
PubMed1993

Successful treatment of a patient with adult T-cell leukemia by daily oral administration of low-dose etoposide. Decrease in the amount of HTLV-I proviral DNA revealed by the polymerase chain reaction method.

BACKGROUND: Oral administration of low-dose etoposide is known to be effective against various malignancies, including malignant lymphoma. However, the effectiveness of low-dose etoposide as a treatment for adult T-cell leukemia (ATL) has not been established. METHODS: A 74-year-old woman with ATL in acute phase was treated by daily oral administration of low-dose etoposide (25 mg/m2). The authors assayed changes in the surface markers and the amount of human T-cell lymphotropic virus type I (HTLV-I) proviral DNA in peripheral blood mononuclear cells (PBMC) by using flow cytometry and the polymerase chain reaction (PCR) method, respectively. RESULTS: Before treatment, generalized lymphadenopathy and hepatomegaly were observed. In laboratory examination, the leukocyte count was 13.7 x 10(3)/microliters, with 65% abnormal lymphocytes. The percentages of CD3-, CD4-, and CD25-positive cells in PBMC were 84.4%, 84.4%, and 76.5%, respectively. The serum lactic dehydrogenase (LDH) level was 1376 IU/l (normal range, less than 520 IU/l). After the initiation of treatment, lymph-adenopathy and hepatomegaly disappeared, and the serum LDH level was reduced to the normal level before the 20th day of the treatment. On the 55th day of the treatment, CD25-positive cells had virtually disappeared. In addition, the amount of the proviral DNA in PBMC was reduced to approximately one-tenth by this treatment. Subsequently, the patient was in remission for more than 16 months. No side effects were observed. CONCLUSIONS: Daily oral administration of low-dose etoposide can be a safe and effective treatment for patients with ATL. The authors believe this to be the first report of a patient with ATL in whom complete remission (CR) was achieved by this treatment.

Administration, Oral↗
PubMed1992

Presence of HTLV-I proviral DNA in central nervous system of patients with HTLV-I-associated myelopathy.

The polymerase chain reaction (PCR) method was used to determine the presence and amount of human T lymphotropic virus type I (HTLV-I) proviral DNA in central nervous system (CNS) tissue obtained at autopsy from 6 patients with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP), 1 patient with adult T-cell leukemia (ATL) and CNS infiltration of leukemic cells, and 9 control subjects with other neurological disorders. HTLV-I pX and env but not pol DNA were detected in CNS tissue from 5 of 6 patients with HAM/TSP. The ATL samples were positive for pX, env, and pol DNA by PCR. None of the control samples was consistently positive for HTLV-I by PCR, but all showed positive bands on beta-globin PCR. Quantitative PCR combined with histological studies showed no correlation between HTLV-I proviral DNA amounts and extent of perivascular mononuclear cell infiltration in the HAM/TSP CNS. Also, the amounts of pX and probably env DNA were greater in the HAM/TSP samples than in the ATL sample, although the extent of mononuclear cell infiltration was far less in the HAM/TSP samples than in the ATL sample. Therefore, in addition to infiltrating mononuclear cells, constituent cells of the CNS may harbor the HTLV-I genome, at least in the pX and env regions, in patients with HAM/TSP.

Base Sequence↗
PubMed2004

Elevated expression of CCL5/RANTES in adult T-cell leukemia cells: possible transactivation of the CCL5 gene by human T-cell leukemia virus type I tax.

HTLV-I is the etiologic agent of ATL and of tropical spastic paraparesis/HTLV-I-associated myelopathy. Infiltration of various tissues by circulating leukemic cells and HTLV-I-infected T cells is a characteristic of ATL and HTLV-I-associated inflammatory diseases. Chemokines play important roles in migration and tissue localization of various lymphocyte subsets. Here, we report the highly frequent expression of CCL5 (RANTES) in ATL and HTLV-I-infected T-cell lines. Among various human T-cell lines, those infected with HTLV-I selectively expressed the CCL5 gene and secreted CCL5. Furthermore, CCL5 was expressed by leukemic cells in peripheral blood and lymph nodes from patients with ATL. Inducible expression of HTLV-I transcriptional activator Tax in a human T-cell line Jurkat, up-regulated CCL5 mRNA and induced CCL5 secretion. Analysis of the CCL5 promoter revealed that this gene is activated by Tax, via the activation of NF-kappaB, whose responsive element, R(A/B), is located at positions -71 to -43 relative to the putative transcription start site. Aberrant expression of CCL5 by HTLV-I-infected T cells may impact on the pathophysiology of HTLV-I-associated diseases.

Cell Line↗
PubMed1983

Natural infection in non-human primates with adult T-cell leukemia virus or a closely related agent.

A total of 703 sera from 10 species of monkeys were examined for the presence of antibodies to adult T-cell leukemia (ATL)-associated antigens (ATLA). ATLA represent core protein(s) of ATL virus (ATLV) and ATLV-determined polypeptides. Anti-ATLA antibodies were found in all seven macaque species tested but not in three non-macaque species. The frequencies of seropositive macaques ranged from 10 to 50%. In three macaque species (Japanese monkeys, rhesus monkeys, and crab-eating monkeys) in which sufficient numbers of animals were studied, more females than males were anti-ATLA positive and the antibody-positive rate increased with age. In Japanese monkeys, over 70% were seropositive after the age of 10 years. A family study of Japanese monkeys suggested maternal transmission of ATLV or a closely related agent. These seroepidemiological features are consistent with those of Japanese in the ATL-endemic area. Three of 10 rhesus monkeys were found to be anti-ATLA-positive 13 days after arrival in Japan, suggesting that they had been infected with ATLV in Indonesia where they were captured. Thus, ATLV appears to be prevalent among several macaque species as well as in man, and its pathogenetic role in these non-human primates should be explored in relation to ATL in man.

Animals↗
PubMed1988

Differential effects on expression of IL-2 receptors (p55 and p70) by the HTLV-I pX DNA.

Abnormal expression of the low-affinity receptor for interleukin-2 (IL-2R) is a characteristic of the HTLV-I (+) leukemic T cells in adult T-cell leukemia (ATL). Despite the expression of IL-2R bearing Tac antigen (IL-2R/p55), leukemic cells of the majority of ATL patients do not proliferate in response to IL-2. In the human NK cell line, YT, as well as in ATL-derived T cells, the co-expression of IL-2R/p55 and the second IL-2R without the Tac epitope (IL-2R/p70) is required to produce high-affinity IL-2R. To study the effect of HTLV-I on both of the IL-2Rs, we transfected a fragment of HTLV-I containing the p40X gene into YT cells. One of the 2 transfected YT clones (YT/pX-5.1) had an increased level of expression of IL-2R/p55. In contrast, expression of IL-2R/p70 was unaffected, as determined by Scatchard analysis and the cross-linking study using 125I-IL-2. Our results show that the T-cell phenotype is not required for induction of IL-2R/p55 by p40X. We suggest that HTLV-I infection induces a disproportionate induction of IL-2R/p55 without significant enhancement of IL-2R/p70 expression, resulting in the predominant expression of low-affinity IL-2R in ATL. IL-2R/p70 may be a critical parameter determining the IL-2 reactivity of HTLV-I-infected T cells as well as of normal lymphocytes.

Antigens, Differentiation↗
PubMed1994

Adult T-cell leukemia/lymphoma: a working point-score classification for epidemiological studies.

Adult T-cell leukemia/lymphoma (ATL) is a malignancy that occurs most frequently in south-western Japan and the Caribbean basin. The primary etiologic agent for this disease, human T-lymphotropic virus type I (HTLV-I), is endemic in these areas. Only a small percentage of individuals infected with HTLV-I develop ATL. The factors that determine the development of malignant disease as an outcome of HTLV-I infection in an individual are unknown. ATL is histopathologically heterogeneous and firm diagnosis is made on the contribution of clinical, laboratory and histopathologic features. The wide variety of laboratory assays available to geographically diverse populations has led to a need to standardize the criteria for determining the diagnosis of this disease for epidemiologic studies. This report summarizes current information regarding ATL and proposes a classification facilitating comparison of case series in geographically and ethnically different populations.

Adult↗
PubMed2000

Production of functionally deficient dendritic cells from HTLV-I-infected monocytes: implications for the dendritic cell defect in adult T cell leukemia.

Adult T cell leukemia (ATL) is induced by an infection with human T lymphotropic virus type I (HTLV-I) and is accompanied by immunodeficiency. Monocyte-derived immature dendritic cells (DCs) donated by 11 ATL patients were suppressed in the ability to take up fluorescein isothiocyanate (FITC)-dextran and were down-regulated in the expression of CD1a and CD86 antigens (Ags). Monocytes from the patients showed impaired expression of CD14 and HLA-DR Ags. These results suggest intrinsic abnormalities of monocytes and a defect of DC maturation in ATL patients. Therefore, we examined the influence of HTLV-I infection of monocytes on their differentiation to DCs. Monocytes obtained from healthy donors were susceptible to HTLV-I infection in vitro. HTLV-I-infected monocytes were down-regulated in the expression of CD14 Ags, and immature DCs obtained from them expressed CD1a poorly and were impaired in the ability to take up FITC-dextran. Mature DCs differentiated from these cells could not stimulate autologous CD4(+) T cell or CD8(+) T cell proliferation, even after being secondarily pulsed with HTLV-I at an immature DC stage. These results suggest that HTLV-I-infected monocytes cannot properly differentiate to DCs and that this might be one of the important mechanisms producing dysfunctional DCs in ATL patients.

Adult↗
PubMed1994

Acute tumor lysis syndrome in poor-risk germ cell tumors: does it exist?

Acute tumor lysis syndrome (ATLS) is a well-known adverse event described after effective chemotherapy for extensive, highly proliferative, and chemosensitive tumors. While its occurrence with hematological malignancies is frequently described, there have been scattered case reports documenting ATLS in solid tumors. However, such events have not been reported in poor-risk germ cell tumors. We reviewed retrospectively 46 cases of such tumors treated in our department between 1988 and 1993 by aggressive cisplatin-based chemotherapy. All patients received systematically 6 l/24 h hydration according to the cisplatin- protocol administration. Blood chemistry data for potassium, phosphorus, calcium, alkaline reserve, uric acid, creatinine and lactate dehydrogenase were obtained before treatment and during the 7 days of the induction chemotherapy. No metabolic abnormalities suggestive of ATLS were observed. Nevertheless, 2 patients with bulky disease of the chest experienced early death from respiratory distress complicated by multiorgan failure. ATLS seems to be an unlikely event in poor-risk germ cell tumors and therefore special prophylactic therapy may be unnecessary.

Acute Disease↗
PubMed2002

OX40 signaling renders adult T-cell leukemia cells resistant to Fas-induced apoptosis.

We reported previously that OX40, a member of the tumor necrosis factor receptor family, is expressed constitutively on fresh leukemia/lymphoma cells isolated from patients with adult T-cell leukemia (ATL). In this study, we tested whether OX40 signaling affects the Fas-mediated apoptosis of fresh ATL cells isolated from 7 patients (3 acute type, 3 chronic type, and 1 smoldering type). In all these patients, the coculture of ATL cells with MMCE/OX40 ligand gp34, a stable human gp34 transfectant of a mouse epithelial cell line, resulted in a decrease in the percentage of apoptotic cells after treatment with anti-Fas monoclonal antibody, compared to coculture with MMCE/mock controls. Similar findings were obtained in OX40(+)- human T-cell leukemia virus type I-transformed T-cell lines. To elucidate the molecular mechanism of this phenomenon, we used Kit225/OX40, a stable OX40 transfectant of an IL-2-dependent T-cell line, and its deletion mutant, Kit225/del-OX40, in which the intracytoplasmic domain of OX40 had been deleted. Coculture with MMCE/gp34 inhibited the apoptosis of Kit225/OX40, but Kit225/del-OX40 apoptosis was hardly affected. These results suggest that ATL cells may escape Fas-mediated destruction of the immune system through OX40 signaling.

Adult↗
PubMed1999

Serum levels of parathyroid hormone-related protein are not elevated in patients with T-cell prolymphocytic leukemia.

T-cell prolymphocytic leukemia (T-PLL) is a rare post-thymic T-cell neoplasm which shares most clinical features with adult T-cell leukemia (ATL). We measured serum level of C-terminal parathyroid hormone-related protein (C-PTHrP) in patients with T-PLL and ATL. Serum C-PTHrP levels of eight patients with T-PLL (median 36.8 pmol/l; range 27.0-50.2 pmol/l) did not differ from those of 30 human T-lymphotropic virus type I (HTLV-I)-seronegative blood donors (median 37.0 pmol/l; range 22.6-54.0 pmol/l). The C-PTHrP levels in ten ATL patients (median 69.6 pmol/l; range 42.5-899.4 pmol/l) were significantly higher than those in healthy controls (p<0.0001) or T-PLL patients (p=0.001). We suggest that the serum level of PTHrP can provide useful information for differentiating between T-PLL and ATL.

Adult↗
PubMed2004

Control of Atm-/- thymic lymphoma cell proliferation in vitro and in vivo by dexamethasone.

AIM: Ataxia telangiectasia (A-T) is an autosomal recessive disease in humans caused by mutations in the Atm (A-T mutated) gene. The disease involves multiple organ systems, and is associated with a high incidence of leukemias and lymphomas that develop in childhood. We have reported previously that thymic lymphoma development in Atm knockout (Atm-/-) mice is associated with elevated spontaneous DNA synthesis in thymocytes, and that dexamethasone (Dex) attenuates the elevated DNA synthesis and prevents thymic lymphoma development. The primary objectives of the present study were (1) to investigate possible mechanisms underlying the tumor-suppressing effect of Dex on Atm-/- thymic lymphoma cells, and (2) to determine whether Dex is an effective tumor-suppressing treatment in mice bearing transplanted Atm-/- thymic tumors. METHODS: Establishment of a number of Atm-/- thymic lymphoma (ATL) cell lines from Atm-/- mice, cell proliferation assays, cell cycle analyses, Western blotting and Hoechst nuclear staining were used to analyze the effects of Dex on Atm-/- thymic lymphoma cells. Atm-/- tumor cells were transplanted into the right flanks of Atm+/+ mice prior to the initiation of Dex treatment. RESULTS: Atm-/- tumor cells were highly sensitive to Dex, both in culture and in vivo as ectopic tumors in mice. In cultured ATL-1 cells, Dex induced apoptosis, arrested the cell cycle at the G1 phase and downregulated NF-kappaB and multiple cell cycle regulators, while upregulating the NF-kappaB inhibitor IkappaBalpha. In Atm+/+ mice transplanted subcutaneously with ATL-1 cells, tumor growth was either prevented completely or significantly suppressed by Dex treatment. CONCLUSIONS: Our findings identify potential mechanisms by which Dex affects the proliferation and survival of ATL-1 cells in culture, and provide evidence that Dex can suppress the proliferation of Atm-/- thymic lymphoma cells growing in the body. Together these results add to our earlier published data suggesting that the cellular pathways regulated by Dex may be promising therapeutic targets for prevention and treatment of thymic lymphomas in A-T individuals.

Animals↗
PubMed2001

Regulation of intracellular pH in rat renal inner medullary thin limbs of Henle's loop.

Regulation of intracellular pH (pHi) was studied in isolated rat renal inner medullary thin limbs of Henle's loop in bicarbonate/phosphate-buffered medium with high pCO2, high osmolality ( congruent with670 mosmol/kg H2O; 270 mM urea; 180 mM NaCl), organic osmolytes, and a pH of 6.8 to approximate the physiological in vivo environment. The pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF) was used to measure pHi. Resting pHi was always acid and significantly more acid in descending thin limb (DTL) cells than in ascending thin limb (ATL) cells from pure or mixed-type thin limbs. Resting pHi was slightly but significantly higher in both DTLs and ATLs in high osmolality ( approximately 670 mosmol/kg H2O) than in low osmolality ( approximately 290 mosmol/kg H2O) medium but not when sucrose replaced urea. In both DTLs and ATLs the rate of recovery of pHi following additional acidification with an NH4Cl pulse was reduced by Na+ removal from the medium and by the addition of 60 microM HOE642 (an inhibitor of the Na+/H+ exchanger, NHE1), 55 microM S1611 (inhibitor of Na+/H+ exchanger, NHE3), 1 microM bafilomycin A1 (an inhibitor of vacuolar H+ -ATPase), or 20 microM Schering 28080 (an inhibitor of H+ -K+ -ATPase) to the medium. Resting pHi was also reduced by 60 microM HOE642, 55 microM S1611, and 20 microM Schering 28080. In both DTLs and ATLs, RT-PCR revealed message for NHE1, NHE3, and vacuolar H+ -ATPase; immunocytochemistry demonstrated the expression of the protein for NHE1 (basolateral membrane), NHE3 (luminal membrane), and H+ -K+ -ATPase (luminal membrane). These data suggest that pHi in rat inner medullary thin limbs is regulated by urea and by basolateral and luminal H+ extrusion via NHE1, NHE3, vacuolar H+ -ATPase, and H+ -K+ -ATPase.

Acid-Base Equilibrium↗
PubMed2001

Adult T-cell leukemia associated with gastric carcinoma: report of a case.

A 67-year-old man was admitted to our hospital with nausea and epigastralgia, and a diagnosis of smoldering type adult T-cell leukemia (ATL) associated with advanced gastric carcinoma was made. The gastric carcinoma had caused pyloric stenosis, and investigations revealed regional lymph node metastasis. The patient underwent total gastrectomy, splenectomy, cholecystectomy, and lymph node dissection with a Roux-en-Y anastomosis. Histological examination of the regional lymph nodes revealed not only metastases of gastric carcinoma, but also of ATL lymphoma, indicating a final diagnosis of advanced gastric carcinoma with locoregional lymph node due to both metastasis of the gastric carcinoma and the ATL lymphoma. Despite the administration of postoperative adjuvant chemotherapy comprised of cisplatin/adriamycin/5-fluorouracil in combination with oral etoposide and immunotherapy using ubenimex, paraplegia suddenly developed caused by the metastasis of ATL to the epidural space. Resection of this metastatic tumor for decompression of the spinal cord resulted in resolution of the paraplegia; however, the patient died about 1 month later from rapid systemic tumor growth.

Adenocarcinoma↗
PubMed1999

Chromosomal imbalances in adult T-cell leukemia revealed by comparative genomic hybridization: gains at 14q32 and 2p16-22 in cell lines.

Comparative genomic hybridization was used to identify chromosomal imbalances in eight cell lines and 12 blood samples from patients with adult T-cell leukemia/lymphoma (ATL). The chromosomes most often over-represented in the cell lines were 2p (6 cases), 7q (4 cases), and 14q (4 cases), with minimal common regions at 2p16-22, 7q21-36, and 14q32, respectively. Distinct imbalances were detected in only 7 of the clinical samples. Chromosomes 14q32 and 2p16-22 harbor TCL1 and a transcription factor, HTLF (human T-cell leukemia virus enhancer factor), respectively. FISH analysis revealed that TCL1 did not juxtapose to TCRA, and we detected no expression of TCL1 in any of the ATL cell lines despite the 14q32 amplifications. Moreover, expression of HTLF was not elevated in the ATL cell lines bearing multiplication of 2p. These results suggest that chromosomal regions 2p16-22 and 14q32 harbor genes other than HTLF and TCL1 that are involved in cellular immortalization or in the pathogenesis of ATL.

Chromosome Aberrations↗
PubMed2006

Computer analysis of the significance of the effective osmolality for urea across the inner medullary collecting duct in the operation of a single effect for the counter-current multiplication system.

BACKGROUND: Although urea and water are transported across separate pathways in the apical membrane of the inner medullary collecting duct (IMCD), the existence of a cellular diffusion barrier as an unstirred layer makes it possible to use coefficients of effective osmotic force (sigma*) as equivalent to reflection coefficients. The difference in effective osmolality between urea and NaCl across the IMCD becomes a driving force for water if the compositions of solutes are different between tubular lumen and interstitium. Since reported values for sigma*(urea) are discrepant, we compared the efficiency of a single effect in the counter-current system between an ascending thin limb (ATL) and the IMCD, with the interposition of capillary networks (CNW), between two models with sigma(urea)* = 0.7 (model 1) and sigma(urea)* = 1.0 (model 2). METHODS: The time courses (within 3 s) of solute and the water transport profiles among ATL, CNW, and IMCD were simulated with a computer in the absence of flow in each compartment. RESULTS: In spite of small differences in the profiles of urea and NaCl concentrations between the two models, model 1 displayed a larger volume flux in the IMCD than model 2, resulting in an increase of osmolality in the IMCD and a decrease of osmolality in the ATL. These findings are vital for the operation of the counter-current multiplication system. CONCLUSIONS: The concept of coefficients for effective osmotic force can be applied to the counter-current model between the IMCD and the ATL with the interposition of CNW. The model of sigma(urea)* = 0.7 is more efficient than that of sigma(urea)* = 1.0.

Animals↗
PubMed1979

Relationship of raised atherosclerotic lesions to fatty streaks in coronary heart disease and hypertension.

The abdominal aortas and right coronary arteries removed during autopsies were gathered from over 18,000 subjects in 19 location-race groups. Sudanstained intimal surfaces were graded for the percent as raised lesions (R) and fatty streaks (F). The proportions of all types of lesions (ATL = F + R) that were raised (RaL = R divided by ATL) were examined. The difference between the observed RaL (in subjects having atherosclerosis-related conditions) and the expected RaL (in age-, sex-, and ATL-matched subjects without such conditions) measured the excess of RaL, which by inference indicated the tendency for an excess of raised lesions to be produced in place of fatty streaks. In cases of coronary heart disease (CHD), a large excess of RaL was found consistently on the average. The coronary arteries and aortas of hypertensive subjects, compared with those of nonhypertensives, had only a small and inconsistent excess of RaL. Both CHD and hypertension were characterized by a marked tendency for severe involvement by ATL, including extensive fatty streaks, leaving only small remnants of normal intima. Some factors (Class A) act to form fatty streaks and also to continue advancing them into raised lesions. Once the fatty streaks are formed, some new factors (Class B2) convert them into raised lesions. We concluded that hypertension is almost, if not entirely, a Class A type of atherogenic agent, and that CHD is promoted by exceptionally strong effects of both A and B2 types of causation. This conclusion exposes a biological priniciple that, if the assumptions of the model are true, is of considerable importance: Some of the more important causes of atherosclerosis (Class B causes) begin to act only after the fatty streaks have formed.

Adult↗
PubMed1990

Adult T-cell leukemia/lymphoma of the tongue.

A case of posterior tongue lymphoma associated with adult T-cell leukemia (ATL) that occurred as a lesion in the lingual dorsal portion is reported in a 64-year-old woman. Initially, a diagnosis of Hodgkin's lymphoma was considered as no findings associated with ATL except lymphadenopathy and serum anti-ATLA antibodies were present. Combined radiotherapy and chemotherapy were administered with favorable results; however, 4 months later, Pneumocystis carinii pneumonia developed, and 2 months later, generalized lymphadenopathy and hypercalcemia evolved. At this time, a diagnosis of ATL was made. The patient died of renal dysfunction 6 months after the initial presentation. In suspected cases of ATL and malignant diseases of T-cell lineage, namely, malignant lymphoma and mycosis fungoides, the presence of HTLV-1 infection should be confirmed by testing for anti-ATLA antibodies.

Diagnosis, Differential↗
PubMed1991

Hepatocyte growth inhibitory factor derived from HTLV-I(+) T cell lines: effect on the epidermal growth factor-dependent proliferation of rat hepatocytes.

A human T cell leukemia virus-I infected T cell line, ATL-2, produces an interleukin-2 receptor inducing factor, adult T cell leukemia (ATL)-derived factor (ADF). In the conditioned medium (CM) of ATL-2, we found an inhibitory activity on the epidermal growth factor (EGF)-dependent proliferation of primary cultured rat hepatocytes, measured by cell number and [3H]thymidine incorporation. ATL-2 CM dose-dependently inhibited hepatocyte proliferation. This activity was fractionated by gel filtration at a molecular size of 15,000 to 40,000 and was tentatively called hepatocyte growth inhibitory factor (HGI). Further fractionation with the ion-exchange column indicated that HGI was separable from ADF. Nevertheless, there was a positive correlation between HGI and ADF production, because the HGI activity was also detected in the CM of another ADF producer cell line (HUT102), while no significant HGI activity was detected in the CM of low ADF producer cell lines, ED and MOLT4.

Animals↗