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PubMed1988

Expression of TGF-beta gene in adult T cell leukemia.

Peripheral mononuclear cells from adult T cell leukemia (ATL) patients were analyzed in comparison with other types of leukemia cells, for the expression of transforming growth factor-beta (TGF-beta) mRNA, for the presence of TGF-beta activity (colony stimulating activity for normal rat kidney fibroblasts [NRK]) in conditioned medium and for their susceptibility to exogenous TGF-beta. Highly elevated TGF-beta mRNA levels were observed in all five ATL cell samples tested; however, in three acute myelogenous leukemia (AML) samples, in one acute lymphatic leukemia (ALL), and one chronic myelogenous leukemia (CML), TGF-beta expression was relatively lower. In normal peripheral mononuclear cells TGF-beta mRNA was weakly detectable. Colony stimulating activity for NRK found in the conditioned medium from ATL cells as well as other leukemia cells correlated well with the levels of TGF-beta mRNA expression. In all three ATL samples tested, stimulation of 3H-thymidine uptake by purified TGF-beta from platelets was apparent. These results suggest that ATL cells are secreting active TGF-beta in a relatively high amount, as compared with other leukemia cells, and may proliferate in response to the factor via an autocrine manner. Furthermore, considering that TGF-beta stimulates bone resorption, we can speculate that the relatively high amount of TGF-beta in ATL cells contributes to the hypercalcemia frequently seen in ATL patients.

Cell Division↗
PubMed1987

Effect of immunosuppressive factors produced by adult T cell leukemia cells on B cell responses.

The immunosuppressive activity of sera from adult T cell leukemia (ATL) patients and culture supernatants of ATL cells and ATL cell lines on B cell responses was examined in vitro. ATL sera and culture supernatants of ATL cells suppressed B cell proliferative and differentiative responses induced with B cell mitogens such as Staphylococcus aureus Cowan I and pokeweed mitogen. The suppressive effect was observed not only in the production of B cell growth factors (BCGF) and B cell differentiation factors (BCDF) by T cells, but also in the responsiveness of B cells to BCGF and BCDF. These results suggest that the immunosuppressive factors produced by ATL cells might act to suppress both the cellular immunity and the humoral immunity, and could have an important role in the induction of immunodeficient states in ATL patients.

B-Lymphocytes↗
PubMed1983

A proposal for smoldering adult T-cell leukemia: a clinicopathologic study of five cases.

We have observed five patients with smoldering adult T-cell leukemia (ATL) who had skin lesions as premonitory symptoms. The illness developed slowly, but flared up after several years. Skin lesions appeared in the form of erythema, papules, or nodules. Infiltration of the skin by ATL cells was slight, and the proportion of ATL cells in the peripheral blood was 0%-2%. The serum lactate dehydrogenase (LDH) value was within normal range and was not associated with hypercalcemia; lymphadenopathy, hepatosplenomegaly, and bone marrow infiltration were very slight. In most cases, hypergammaglobulinemia was seen, and in one case, monoclonal hypergammaglobulinemia was observed. All five patients had lived in an area in which ATL was endemic, and their anti-ATLA antibodies were positive; none had ever received a blood transfusion. One patient developed typical ATL after more than 13 yr of illness and died of renal insufficiency. Another patient developed typical ATL after 5 yr of illness and died of cryptococcus meningitis. Based on clinical and pathologic differences, we believe that these cases should be distinguished from typical ATL cases for the purposes of prognosis and treatment.

Antibodies↗
PubMed1983

Three cases of pre-adult T-cell leukemia.

Three patients with pre-adult T-cell leukemia (ATL) are reported. All of them were seropositive to ATL-associated antigens (ATLA) and had 3-30% abnormal lymphocytes with cleaved or lobulated nuclei in the peripheral blood in the absence of clinical symptoms of ATL. All the data on immunological tests were normal except for negative purified protein derivative skin tests. In Case 1 the patient was an elder sister of an ATL patient. Four other members of this family were also anti-ATLA positive without abnormal cells in the blood. In Cases 1 and 2, ATLA and ATL virus (ATLV) were expressed in the lymphocytes cultured with phytohemagglutinin or T-cell growth factor. Moreover, an ATLV-producing cell line was established from Case 1 by mixed lymphocyte culture with lymphocytes obtained from a normal anti-ATLA negative person. Investigation of pre-ATL cases may clarify factors leading to the development of ATL in ATLV-infected persons.

Adult↗
PubMed1984

Changes of adult T cell leukemia cell surface antigens at relapse or at exacerbation phase after chemotherapy defined by use of monoclonal antibodies.

Surface phenotypes of leukemic cells from six patients with adult T cell leukemia (ATL) were analyzed by the use of monoclonal antibodies, both at the time of initial diagnosis and at either relapse or exacerbation phase after chemotherapy. Changes of cell surface antigens were observed in four of the six cases. The majority of the leukemic cells of these patients were reactive with anti-Leu-1 and anti-Leu-3a, but unreactive with anti-Leu-2a and MAS 036c monoclonal antibodies at the time of initial diagnosis, indicating that ATL cells are of peripheral inducer/helper T cell origin. In three cases, the Leu-1 antigen disappeared at relapse or at exacerbation phase, and in one of these cases, a small percentage of ATL cells became reactive with MAS 036c, which identifies cortical thymocyte antigen. ATL cells of one other case did not have Leu-1 antigen from the start, but gained Leu-2a antigen at exacerbation phase and became double-labeled cells (Leu-2a+, 3a+), which is known to be a feature of thymocytes. Thus, it appeared that ATL cells sometimes change their surface phenotype to that of an earlier stage of T cell differentiation at relapse or at exacerbation phase. Chronic myelocytic leukemia (CML) cells also usually change to immature cells at blastic crisis involving morphological change. However, this morphological change was not so prominent in the ATL cases studied, except one, in which typical ATL cells with nuclear indentation changed to large immature cells with basophilic cytoplasm at relapse.

Adult↗
PubMed1994

Improving trauma care in Trinidad and Tobago.

Identification of trauma as a major cause of morbidity and mortality in Trinidad and Tobago prompted the establishment of a training programme aimed at improving trauma care in this developing country. An Advanced Trauma Life Support (ATLS) programme for physicians, funded through the Canadian International Development Agency resulted in a statistically significant improvement of in-hospital trauma patient outcome at the Port-of-Spain General Hospital (observed to expected mortality ratio of 3.16 pre-ATLS compared to 1.94 post-ATLS). A recent analysis of all motor vehicle injuries for a shorter period did not confirm this positive impact of the ATLS programme, primarily because a large number of these patients died in the pre-hospital period. Pre-hospital trauma care therefore required urgent attention to complement the positive in-hospital impact of the ATLS programme. A second training programme (the Pre-Hospital Trauma Life Support or PHTLS) for paramedical personnel was thus instituted in 1990. Over 250 physicians have been trained in the ATLS programme and to date over 100 paramedical personnel have been trained in the PHTLS programme. Attempts have also been made to equip the ambulances with more appropriate resuscitative devices in order to improve pre-hospital care. The combination of the PHTLS and the ATLS programme should result in further improvement in the care of patients sustaining major injuries in Trinidad and Tobago.

Emergency Medical Services↗
PubMed1996

Differential patterns of serum biomarkers of immune activation in human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis, and adult T-cell leukemia/lymphoma.

Adult T-cell leukemia/lymphoma (ATL) and human T-cell lymphotropic virus type I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) are associated with differing patterns of immune dysfunction. Biomarkers of immune activation may correlate with perturbations of immune function associated with these diseases. We conducted a pilot cross-sectional study to assess four candidate biomarkers of immune activation. beta 2-microglobulin, neopterin, tryptophan, and kynurenine levels were assayed in stored sera from asymptomatic, human T-cell leukemia virus type I (HTL V-I)-seronegative (HTLV-I-) and HTLV-I-seropositive (HTLV-I+) individuals, and ATL and HAM/TSP patients previously enrolled in seroepidemiological studies in Jamaica. Mean levels of beta 2-microglobulin, neopterin, and kynurenine were significantly elevated among ATL patients compared to the other study groups. Mean tryptophan levels were significantly lower among ATL and HAM/TSP patients than HTLV-I- and HTLV-I+ groups. No significant differences in biomarkers were found between the HTLV-I- and HTLV-I+ groups. Among HAM/TSP patients, a significant association was found between elevated neopterin levels and symptoms of less than 4 years duration. In Cox proportional hazards regression modeling, neopterin and tryptophan were found to be independent predictors of survival among ATL patients. This study demonstrates a differential pattern of biomarkers of immune activation among ATL and HAM/TSP patients compared to HTLV-I- and HTLV-I+ individuals. Neopterin and tryptophan may be useful clinical indicators of disease severity and prognosis among HAM/TSP and ATL patients.

Adult↗
PubMed1997

Kenneth MacGredie Memorial Lectureship. Adult T-cell leukemia/lymphoma.

Adult T-cell leukemia (ATL) was first reported in Japan, where it has a high incidence in the southwestern region. The retrovirus, human T-lymphotropic virus type I (HTLV-I), is the causative agent of ATL. In ATL-endemic areas, the rate of HTLV-I carriers is high. A definite diagnosis of ATL is based on the presence of HTLV-I proviral DNA in the tumor cell DNA. ATL cells originate from the CD4 subset of peripheral T cells. ATL shows diverse clinical features but can be divided into four subtypes: acute, chronic, smoldering, and lymphoma type. Chemotherapy is not effective; the acute and lymphoma types have a poor prognosis. Familial occurrence of ATL is common. HTLV-I infection is caused by transmission of live infected lymphocytes from mother to child, from man to female, or by blood transfusion. Infection with HTLV-I can lead to other diseases, including HTLV-I-associated myelopathy/tropical spastic paraparesis and HTLV-I uveitis.

Adult↗
PubMed1997

Non-Hodgkin's lymphoma of Waldeyer's ring as a manifestation of lymphoproliferative diseases associated with human T-cell leukemia virus type 1 in southwestern Japan.

Adult T-cell leukemia/lymphoma (ATL) usually presents with node- and/or cutaneous-based diseases, with a leukemic picture. It is not clear whether ATL initially manifests with lesions in Waldeyer's ring (WR) in an ATL-endemic area. In the present study, we examined distributions of immunophenotypes and the presence of human T-cell leukemia virus type 1 (HTLV-1) and Epstein-Barr virus (EBV) genomes in 62 cases of non-Hodgkin's lymphoma (NHL) of WR (NHL-WR) from two areas of Japan: Osaka, an ATL-nonendemic area (25 cases), and Okinawa, an ATL-endemic area (37 cases). In both areas, age ranged from 10 to 94 years (median, 64 yr), with a male-to-female ratio of 1.81:1. Twelve patients were in Stage I, 34 in Stage II, and 6 in Stage III; stage was unknown in 10. The 25 Osaka cases were B-cell type (16 diffuse immunoblastic type (DIB), 8 diffuse large cell predominantly noncleaved cell (DLNC), 1 cleaved cell (DLC)). Of the 37 Okinawa cases, 20 were B-cell type (3 DIB, 10 DLNC, 2 DLC, 5 other). The remaining 17 cases showed T-cell phenotype (4 DIB, 3 DLC, 3 diffuse large cell not otherwise specified, 7 other). There was a significant difference in the distribution of immunophenotypes between these two areas (P < .001). Combined studies of polymerase chain reaction (PCR) and in situ hybridization revealed the presence of EBV genome in 1 (4%) of 24 Osaka cases, 2 (13%) of 16 B-cell NHLs from Okinawa, and 3 (23%) of 13 T-cell NHLs from Okinawa. HTLV-1 proviral genome was found in 11 (85%) of 13 T-cell lymphomas from Okinawa but could not be detected in B-cell lymphomas from Osaka and Okinawa. Combined clinical, histologic, serologic, and PCR findings suggest that NHL-WR in an ATL-endemic area could be an initial manifestation of ATL.

Adolescent↗
PubMed1998

Mutation of CD95 (Fas/Apo-1) gene in adult T-cell leukemia cells.

CD95 antigen (also known as Fas or Apo-1) and Fas ligand play key roles in apoptosis of cells of the immune system, function as effector molecules of cytotoxic T lymphocytes, and function in the elimination of activated lymphocytes during the downregulation of the immune response. The critical roles of the Fas-Fas ligand system in apoptosis suggest that its inactivation may be involved in malignant transformation. We analyzed the expression of Fas antigen on adult T-cell leukemia (ATL) cells by flow cytometry and found that Fas antigen expression was absent in a case of ATL and markedly decreased in another case among 47 cases examined. Apoptosis could not be induced in the Fas-negative ATL cells by antibody against Fas antigen. Sequencing of reverse transcription-polymerase chain reaction products of the Fas genes in the Fas negative cells showed two types of aberrant transcripts: one had a 5-bp deletion and a 1-bp insertion in exon 2, and the other transcript lacked exon 4. These mutations caused the premature termination of both alleles, resulting in the loss of expression of surface Fas antigen. These aberrant transcripts were not detected in a nonleukemic B-cell line from the same patient. An RNase protection assay of the Fas gene showed mutations in 2 additional cases with Fas-positive ATL cells of 35 cases examined: 1 case lacked exon 4 and the other was a silent mutation. In the Fas antigen-negative case, leukemic cells were resistant to anticancer drugs in vivo, indicating that the loss of expression of Fas antigen may be associated with a poor response to anticancer drugs. Indeed, Fas-negative ATL cells were resistant to adriamycin-induced apoptosis in vitro, which is consistent with the finding that ATL in this case was resistant to chemotherapy. These findings indicate that mutation of the Fas gene may be associated with the progression of ATL and with resistance to anticancer drugs.

Adult↗
PubMed1999

Arsenic trioxide and interferon-alpha synergize to induce cell cycle arrest and apoptosis in human T-cell lymphotropic virus type I-transformed cells.

Human T-cell lymphotropic virus type I (HTLV-I) is the causative agent of adult T-cell leukemia/lymphoma (ATL). ATL is an aggressive proliferation of mature activated T cells associated with a poor prognosis. The combination of the antiviral agents, zidovudine (AZT) and interferon (IFN), is a potent treatment of ATL. Recently, arsenic trioxide (As) was shown to be an effective treatment of acute promyelocytic leukemia (APL). We have tested the effects of the combination of As and IFN on cell proliferation, cell cycle phases distribution, and apoptosis in ATL-derived or control T-cell lines. A high synergistic effect between IFN and As was observed in ATL-derived cell lines in comparison to the control cell lines, with a dramatic inhibition of cell proliferation, G1 arrest, and induction of apoptosis. Similar results were obtained with fresh leukemia cells derived from an ATL patient. Although the mechanisms involved are unclear, these results could provide a rational basis for combined As and IFN treatments in ATL.

Antineoplastic Agents↗
PubMed2026

The tumor suppressor NDRG2 recruits protein phosphatase 2A to suppress STAT5 phosphorylation in adult T-cell leukemia/lymphoma.

Adult T-cell leukemia/lymphoma (ATL) is an aggressive T-cell malignancy with a poor prognosis that is caused by human T-cell leukemia virus type 1 infection. We previously demonstrated that N-myc downstream-regulated gene 2 (NDRG2) is significantly downregulated in ATL, resulting in aberrant activation of the signal transduction pathways through the dissociation of serine/threonine protein phosphatase 2A. To identify potential targets of NDRG2, we performed comprehensive mass spectrometry of differentially phosphorylated peptides in ATL cells with overexpression of NDRG2 using a TiO2-based enrichment method. Kyoto Encyclopedia of Genes and Genomes and gene ontology analysis revealed that the downregulated phosphopeptides correlated with signaling pathways, T-cell differentiation, and proliferation. Our results identified signal transducer and activator of transcription 5B as a novel NDRG2-regulated protein that is dephosphorylated at serine 193 and tyrosine 699. Although enforced expression of NDRG2 in ATL cell lines does not change the phosphorylation of Janus kinase 3, an upstream regulator of STAT5, phosphorylated STAT5 at tyrosine and serine is significantly suppressed by the direct binding to STAT5 with NDRG2 leading to the inhibition of STAT5 downstream gene expression. Furthermore, NDRG2 binds to STAT5B with alanine replacement of Y699 (Y699A), but only weakly associates with S193A, suggesting that NDRG2 is directly involved in serine phosphorylation through the recruitment of serine/threonine protein phosphatase 2A to STAT5. Because S193 A remarkably induces reduced phosphorylation of Y699 and subsequent transcriptional activity, the induction of serine phosphorylation through the loss of NDRG2 expression is dispensable for STAT5 tyrosine phosphorylation and activity. Since the loss of NDRG2 expression is essential factor to maintenance of ATL cells by STAT5 activity through phosphorylation of serine and tyrosine, targeting STAT5 becomes a feasible and effective strategy in NDRG2-deficient ATL.

Humans↗
PubMed2002

A prospective phase II clinical trial with the use of zidovudine and interferon-alpha in the acute and lymphoma forms of adult T-cell leukemia/lymphoma.

Adult T-cell leukemia/lymphoma ATL is an aggressive T cells malignancy, with poor prognosis due to chemotherapy resistance. Preliminary results using zidovudine (AZT) and interferon-alpha (IFN) showed high response rate in ATL patients. We report a prospective phase II trial using AZT/IFN treatment for aggressive ATL. Nineteen ATL patients (15 acute and four lymphoma) were included in this study. Thirteen patients received AZT/IFN as initial treatment and six patients after initial chemotherapy. For the 17 patients with evaluable tumor, 13 responses were obtained with nine complete remissions (CR) and four partial remissions (PR). Response rate (RR) was 92% for patients who received AZT/IFN as initial treatment (58% CR and 33% PR). Toxicity was mild, mainly hematological. One patient died of fulminant viral hepatitis. Fifteen patients relapsed with a median event free survival (EFS) of seven months for the whole population (range 1-50+ months), 10 months for patients who received AZT/IFN as initial therapy and two months for patients who received initial chemotherapy. Median overall survival (OS) was 11 months for the whole population (range 1-82+ months) and 28 months for patients who entered CR. Three acute ATL showed prolonged CR (42, 52+ and 84+ months respectively) on maintenance therapy with AZT/IFN. This study confirms the efficacy and safety of AZT/IFN in ATL with high response and CR rates. Despite impressive prolonged CR of more than three years, most of the patients relapse stressing the need for additional therapy after achieving CR with AZT/IFN.

Adult↗
PubMed2000

Evaluation of adult T-cell leukemia/lymphoma incidence and its impact on non-Hodgkin lymphoma incidence in southwestern Japan.

The incidence of adult T-cell leukemia/lymphoma (ATL) and its impact on that of total non-Hodgkin lymphoma (NHL) were evaluated in Nagasaki, an area in southwestern Japan where human T-cell lymphotropic virus type I (HTLV-I) is endemic. The first study area comprised 4 towns located on the K Islands, which had a population of 26,870 in 1990. The overall HTLV-I seroprevalence estimated from the serologic survey of 18,485 subjects was 16.2%. By using the data from the Nagasaki Prefectural Cancer Registry (NPCR) and reviewing clinical and laboratory information, we identified 40 cases of ATL and 35 cases of other NHL diagnosed between 1985 and 1995. The crude annual incidence of ATL among 100,000 HTLV-I carriers aged 30 or older was estimated at 137.7 for men and 57.4 for women, with a significant sex difference after adjustment for age (rate ratio = 2.50, 95% confidence interval 1.32-4.73). The cumulative risk from 30 to 79 years of age was estimated at approximately 6.6% for men and 2.1% for women. Among the entire population, ATL accounted for 51 to 59% of the total NHL incidence, showing the strong impact of HTLV-I infection. The second study area comprised the whole of Nagasaki Prefecture (total population in 1990 = 1.56 million). Between 1985 and 1995, 989 cases of ATL and 1,745 cases of other NHL were registered in the NPCR. The world age-standardized annual incidence rate of ATL per 100,000 persons aged 30 or older was estimated at 10.5 for men and 6.0 for women, which accounted for approximately 37 to 41% of the total NHL incidence.

Adolescent↗
PubMed1985

Adult T-cell leukemia in two siblings. Acute crisis of smoldering disease in one patient.

Two cases of human T-cell leukemia virus (HTLV)-positive adult T-cell leukemia (ATL) in brother and sister are presented. Six of 15 members of this family were seropositive for antibodies for ATL-associated antigens (ATLA). The sister of the ATL patient developed overt ATL after 5 years and 8 months of smoldering ATL. Immunologic examinations during the smoldering phase were normal except for negative skin tests for purified protein derivative. Factors leading to the induction of ATL among HTLV carriers remain to be studied.

Acute Disease↗
PubMed2004

Advanced trauma life support training for hospital staff.

BACKGROUND: Injury is responsible for an increasing global burden of death and disability. As a result, new models of trauma care have been developed. Many of these, though initially developed in high-income countries, are now being adopted in low and middle-income countries (LMICs). One such trauma care model is advanced trauma life support (ATLS) training in hospitals, which is being promoted in LMICs as a strategy for improving outcomes for victims of trauma. However, the evidence of effectiveness for this health service intervention, in either HIC or LMIC settings, has not been rigorously tested using methodology such as a systematic review. OBJECTIVES: To quantify the effectiveness of hospitals with an ATLS-trained trauma response system versus hospitals without such a response system in reducing mortality and morbidity following trauma. SEARCH STRATEGY: We searched the Cochrane Injuries Group Specialised Register (CIGSR), the Cochrane Controlled Trials Register (CCTR), MEDLINE & PubMed, EMBASE, CINAHL, Science Citation Index, National Research Register, and web-based trials databases such as Current Controlled Trials. We checked references of background papers and contacted authors to identify additional published or unpublished data. SELECTION CRITERIA: Randomised controlled trials, controlled trials, controlled before- and- after studies comparing effectiveness of hospitals with an ATLS-trained trauma response system versus hospitals without such a response system in reducing mortality and morbidity following trauma. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied eligibility criteria to trial reports for inclusion and to extract data. MAIN RESULTS: There is a limited literature relating to this topic but none of the studies identified met the inclusion criteria for this review. REVIEWERS' CONCLUSIONS: There is no clear evidence that ATLS training (or similar) impacts on the outcome for victims of trauma, although there is some evidence that educational initiatives improve knowledge of what to do in emergency situations. Further, there is no evidence that trauma management systems incorporating ATLS training impact positively on outcome. Future research should concentrate on the evaluation of trauma systems incorporating ATLS, both within hospitals and at the health system level, by using rigorous research designs.

Emergency Medical Services↗
PubMed2005

Reduced expression of human mismatch repair genes in adult T-cell leukemia.

In this study, we investigated the expression of six human DNA mismatch repair (MMR) genes, human MutS homologues 2 (hMSH2), 3 (hMSH3), and 6 (hMSH6), human MutL homologue 1 (hMLH1), human post-meiotic segregations 1 (hPMS1) and 2 (hPMS2), in primary leukemic cells obtained from 11 patients with acute-type adult T-cell leukemia (ATL) by using reverse transcription-polymerase chain reaction (RT-PCR). In contrast to normal peripheral lymphocytes, all primary ATL samples had reduced or loss of expression of two or more MMR genes, and the expression of several MMR genes was simultaneously suppressed in each ATL patient. Abnormal expression of hMSH2, hMSH3, hMSH6, hMLH1, and hPMS1 was observed more frequently than that of hPMS2. In particular, expression of hMSH2 and hPMS1 was reduced in all cases. Western blot analysis further showed reduced expression of both hMSH2 and hPMS1 proteins in all five cases examined. In three out of the 5 cases, both of the two proteins were undetectable. Interestingly, methylation-specific PCR indicated methylation of hPMS1 promoter in all of four ATL cases examined. hPMS1 expression, but not hMSH2 expression, was restored by treatment with a DNA demethylation agent, 5-aza-2'-deoxycytidine, suggesting that methylation plays a crucial role in inhibition of the hPMS1 gene expression in ATL. Our results demonstrate that defect of both human MutS and human MutL systems in primary ATL cells.

Adaptor Proteins, Signal Transducing↗
PubMed1989

Diffuse panbronchiolitis as a pulmonary complication in patients with adult T-cell leukemia.

Forty-three cases of adult T-cell leukemia (ATL) admitted to our hospital between 1982 and 1987 were studied. Three of those were found to be complicated with diffuse panbronchiolitis (DPB). The incidence of DPB is considered to be significantly higher in patients with ATL. The three DPB-complicated cases composed one case each of the smoldering, chronic, and acute type of ATL. In each type, DPB preceded overt ATL and Candida albicans was found in sputa following detection for bacteria. The DPB complication apparently worsened the prognosis of the ATL patients. We have discussed a possible relationship between ATL and DPB.

Adult↗