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PubMed1988

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↗
PubMed1985

Tac-positive, HTLV-negative, T helper phenotype chronic lymphocytic leukemia cells.

In this report we describe an Italian patient with chronic T cell leukemia whose proliferating cells were mature T lymphocytes with a helper phenotype (T helper phenotype chronic lymphocytic leukemia, or Thp-CLL). Unlike other reported cases of Thp-CLL, fresh leukemic cells from this patient were positive with the anti-Tac monoclonal antibody, which recognizes the receptor for interleukin-2 (IL-2). Thus, the phenotype of these cells was similar to that expressed by Japanese patients with adult T cell leukemia (ATL) (OKT3+, OKT4+, OKT8-, Tac+). However, the Italian patient had Thp-CLL, not ATL, since his cells, unlike ATL cells, lacked human T cell leukemia virus (HTLV-I)-related DNA sequences. The Tac receptor, which appears to be modulated in vitro by the anti-Tac antibody, was biologically inactive, since the patient's cells did not respond in vitro to IL-2. In addition, they also failed to demonstrate in vitro functional activities. The clinical course was aggressive, as usual, for both Thp-CLL and ATL. Taking advantage of the description of this case, some similarities and differences between Thp-CLL and ATL are discussed, focusing on the importance of screening of HTLV-I in the differential diagnosis.

Aged↗
PubMed1988

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↗
PubMed1988

Leukemic cells from some adult T-cell leukemia patients proliferate in response to interleukin-4.

The proliferative response of fresh peripheral blood leukemic cells from eight adult T cell leukemia (ATL) patients to interleukin-4 (IL-4) was studied to determine the possibility that the IL-4-mediated T-cell growth pathway is involved in the cell growth of leukemic cells in ATL. Resting lymphocytes from ten normal individuals did not proliferate in response to IL-4. Leukemic cells from two ATL patients did not respond to interleukin-2 (IL-2) or IL-4. Leukemic cells from two patients did respond to IL-2, but not to IL-4. In contrast, a strong proliferative response was observed in the IL-4 culture, but not in the IL-2 culture in the remaining four patients. Chromosome analysis of mitotic cells, performed in one of four patients, confirmed that the cells dividing in response to IL-4 were leukemic cells, but not activated normal lymphocytes. These results indicate the activation of IL-4/IL-4 receptor system in leukemic cells from some ATL patients and suggest the possible involvement of the system in the proliferation of leukemic cells and the leukemogenesis in ATL.

Adult↗
PubMed1987

Treatment of adult T cell leukemia with mega-dose cyclophosphamide and total body irradiation followed by allogeneic bone marrow transplantation.

A 43-year-old patient with adult T cell leukemia (ATL) was treated with mega-dose cyclophosphamide and total body irradiation (TBI) followed by bone marrow transplantation (BMT) from his HLA-identical sibling who was not a carrier of ATL virus. After BMT, ATL cells rapidly decreased and disappeared, and the engraftment of marrow was confirmed on day 20. The patient showed normal hematologic recovery. However, he died on day 205 with interstitial pneumonitis caused by cytomegalovirus infection. Neither autopsy findings nor serologic and cytologic examinations showed any evidence of ATL relapse after BMT. This pilot study suggests that mega-dose chemotherapy and TBI followed by allogeneic BMT should be considered for such treatment of ATL.

Adult↗
PubMed1984

Adult T-cell leukemia-lymphoma in the Hokuriku District and presentation of a case in hematological remission after cryptococcus infection.

Ten cases of adult T-cell leukemia-lymphoma (ATL/L) in the Hokuriku district were studied. Five patients were born in endemic areas and later moved to Hokuriku. Five patients were from nonendemic areas, and have not lived in endemic areas. All of the five patients from nonendemic areas had antibody to the adult T-cell leukemia cell-associated antigen (anti-ATLA), and they had anti-ATLA-positive members in their families. Four of the six patients examined had ATL virus (ATLV) proviral DNA in their leukemic cells and type C virus particles were found in the cultured cell line from one of them (case S.D.). The incidence of anti-ATLA in the control population was 0.93% in Ishikawa Prefecture, 0.39% in Toyama Prefecture and 0% in Fukui Prefecture. The overall positive rate in the controls in Hokuriku was 0.49%. The rate of positive anti-ATLA among family members of seven ATL patients (patients are excluded) was 43.5% (17/39). The pedigree study of ATL patients very strongly suggested transmission of ATLV between spouses and transmission from mother to children. We also report a case of ATL from an endemic area, who has been in remission without antileukemic therapy for about one year. He is on 5 FC (5-fluorocytosine), Minomycin (minocycline hydrochloride), and Baktar (trimethoprim-sulfamethoxazole). Possibility that the therapeutic effect of 5 FC on ATL or the remission is due to enhanced cellular immunity after cryptococcus infection is discussed.

Adult↗
PubMed1984

The pX region of HTLV-I.

Gallo and his coworkers isolated a retrovirus (HTLV) from human cells derived from T-cell leukemia and lymphoma. Hinuma and his coworkers isolated independently a similar virus from a cell line derived from adult T-cell leukemia (ATL) patient. The occurrence of ATL correlates with the formation of antibody to ATL associated antigens or ATLA. To understand the etiological relationship between ATL and HTLV, we analyzed the antigens termed ATLA and found that they are polypeptides encoded by HTLV genome. We further studied the genome of HTLV and its gene expression in cells as well as in a cell-free translation system. We focused on a defective type HTLV produced from a cell line MT-2 that transforms normal lymphocytes most efficiently. The 24S defective gene of HTLV consists of a fused gene of gag-pXs and is amplified at the proviral state. The in vitro translation experiments revealed that the 24S defective gene of HTLV directs the synthesis of p28 of ATLA. By the sequence analysis of the amplified gag-pXs fused genes, we found that a carboxy terminal portion of p28 is translated from a pX-0 region. We further investigated a function of the gag-pX-0 fusion protein, p28. The p28 has an associated protein kinase activity that requires manganese instead of magnesium and phosphorylates the serine residue specifically. Another defective HTLV with a genomic 32S RNA was analyzed. The 32S defective genomic RNA forms a subgenomic 20S RNA in cells. The 20S mRNA is a transcript of an env-pXs fused genome and directs the synthesis of a fused glycoprotein, gp68 of ATLA. The sequence analysis of a cloned cDNA derived from the subgenomic 20S mRNA revealed that a coding frame of the entire pX-IV region is translated. In fact, an antibody against synthetic polypeptides of the pX-IV, immunoprecipitated the gp68. These results demonstrate at the first time that the pX-0 and pX-IV of HTLV genome are expressed in human cells. The biological activities of the fused pXs proteins are also discussed. Human T-cell leukemia virus type I (HTLV-I), a family of human retrovirus and the predicted causative agent of human adult T-cell leukemia/lymphoma (ATL) consists of the gag, pol, env, and pX regions (1).(ABSTRACT TRUNCATED AT 400 WORDS)

Base Sequence↗
PubMed1984

The detection of human T cell leukemia virus proviral DNA and its application for classification and diagnosis of T cell malignancy.

Adult T cell leukemia virus (HTLV or ATLV) proviral DNA integrated in the cellular DNA was examined by a modified Southern blotting method in the peripheral blood mononuclear cells and/or lymph node cells from 61 patients with adult T cell leukemia (ATL) and other hematologic diseases. Serum antibodies against ATL-associated antigens (ATLA) were also examined. The presence of human T cell leukemia virus (HTLV) proviral DNA was confirmed in all 20 patients with overt ATL and in 3 patients with T cell malignant lymphoma, who were seropositive but did not show clinical features characteristic of prototypic ATL. However, it was not detected in 6 antibody-positive healthy individuals and 8 seropositive patients with various hematologic disorders. Thus, the detection of proviral DNA by the method described here seems to be useful for the diagnosis of ATL in the endemic area and may provide a powerful tool for the classification of T cell malignancies.

Acute Disease↗
PubMed1984

A case of adult T-cell leukemia initiated with central nervous system symptoms.

We treated a 52-year-old Japanese woman with adult T-cell leukemia (ATL) initiated with central nervous system (CNS) symptoms. Her chief complaints were paraplegia and left facial palsy. CNS-ATL was diagnosed because of the following three features. 1) Various sized lymphoid cells with marked nuclear convolution were numerous in her cerebrospinal fluid. 2) These cells were a monoclonal proliferation of T lymphocytes with OKT 4 marker. 3) The patient's serum was positive for anti-ATL associated antigen (ATLA). Although the neurological signs and symptoms improved markedly after intrathecal administration of combined chemotherapy (methotrexate, cytarabine and corticosteroid), these ATL cells were highly resistant to radiation therapy. The abdominal mass which developed in the course of the disease was diagnosed as a tumor formed of ATL cells, and VEPA (vincristine, endoxan, prednisolone and adriamycin) was administered with marked success.

Antigens, Neoplasm↗
PubMed1981

Surface phenotype of Japanese adult T-cell leukemia cells characterized by monoclonal antibodies.

We studies the surface phenotype and the functional activities of leukemic cells from three patients with Japanese adult T-cell leukemic (ATL) using the panel of OK and anti-Tac monoclonal antibodies, which react with differentiation antigens and define functionally distinct T-cell subsets or activated and terminally differentiated T cells. The phenotype of ATL cells were determined to be OKT1+T3+T4+T10+T5-T8-Okla1-, although cells from two patients suppressed pokeweed mitogen (PWM) induced normal B-cell differentiation, and cells from all patients lacked helper activity in this system. In addition, after cultivation with PWM, ATL cells from all patients were reactive with anti-Tac monoclonal antibody, and cells from one patient were reactive with OKlal. These findings suggest that ATL cells arise from peripheral mature T-cell subsets and also suggest that the transition of surface phenotype of ATL cells to functionally mature and activated T cells occurs in culture.

Adult↗
PubMed1983

Seroepidemiological studies on the effects of filarial parasites on infestation of adult T-cell leukemia virus in the Goto Islands, Japan.

Patients with filariasis were commonly observed until 1961-1970 in the Goto Islands, an area where adult T-cell leukemia (ATL) is endemic. The positive rate of antibodies to ATL virus-associated antigen among persons with a high antibody titer to filarial antigen was higher than that among persons with a low antibody titer in both sexes. Thus, filarial parasites might have some promoting effects on ATL virus infection and/or ATL virus proliferation among inhabitants in the endemic areas of filariasis and ATL.

Adolescent↗
PubMed1983

Adult T-cell leukemia-lymphoma-related diseases in the Nagasaki District.

The clinical, hematological and pathological features of the adult T-cell leukemia (ATL)-related diseases and their cell membrane phenotypes in the Nagasaki district, one of the ATL-endemic areas, were delineated to compare them with those of adult T-cell leukemia-lymphoma (ATLL). In addition, the participation of ATL virus (ATLV) in the ATL-related diseases was investigated on the basis of a study of ATLV-associated antigen (ATLA) and anti-ATLA antibody. ATLA and/or anti-ATLA antibody could be detected in the ATL-related diseases, including persistent T-lymphocytosis with morphologically abnormal T-lymphocytes, T-cell chronic lymphocytic leukemia (T-CLL) of helper T-cells, T-cell malignant lymphoma of the skin, some seronegative helper T-cell malignant lymphomas and monomorphic T-cell leukemia with round nuclei. These results suggest that those cases in the Nagasaki district, though clinically different from each other, might be the same T-lymphoproliferative disease of possible viral etiology associated with ATLV. On the other hand, persistent T-lymphocytosis seems to be an infectious condition caused by ATLV and partly a preclinical stage of ATLL in view of the clinicohematological features.

Aged↗
PubMed1982

Progress in adult T cell leukemia research.

The clustering incidence of adult T cell leukemia (ATL) is found in adult populations who were born in southwest Japan and showed impairment of cell-mediated immunity; all patients with ATL contain antibody for specific ATL associated antigen in their sera. This ATLA positive T cell leukemia is morphologically characterized by leukemic cells in various sizes showing unique nuclear polymorphism. The neoplastic cells bear common immunocytologic markers with inducer T cell subset among the peripheral T2 cell group and functionally show the suppressor inducer activity. Histologic features of lymph nodes were classified to diffuse lymphoma, pleomorphic type in many cases of ATL. The prognosis of patients with ATL is the worst among lymphoid malignancies and almost all patients died within a year accompanied by pulmonary lesions or other infectious inflammatory lesions.

Adult↗
PubMed1995

Alterations of the p27KIP1 gene in non-Hodgkin's lymphomas and adult T-cell leukemia/lymphoma.

The protein p27KIP1 belongs to a recently identified family of proteins termed cyclin-dependent kinase inhibitors (CDKIs). These proteins play an important role in regulating cell-cycle progression and loss of their function has been implicated in tumorigenesis. Transforming growth factor beta (TGF-beta) may induce cell growth arrest through p27 activation. TGF-beta often loses its ability to arrest growth of transformed cells; this could potentially occur through a defect in p27. To determine the role of p27 in tumorigenesis, we examined its mutational status in 74 non-Hodgkin's lymphomas (NHLs) (52 of B-cell phenotype, 22 of T-cell phenotype), 5 lymphoma cell lines, and 42 adult T-cell leukemias/lymphomas (ATLs) using polymerase chain reaction-single strand conformational polymorphism (PCR-SSCP) and Southern blot analyses. A nonsense mutation (stop codon) that could result in expression of a truncated nonfunctional p27 protein was detected at codon 76 in one case of acute lymphomatous ATL, but not in matched normal tissues. Previously undescribed polymorphisms were also identified at codon 109 in the lymphomas and at codon 55 in the ATLs. Two homozygous deletions of the p27 gene were detected in one case of B-immunoblastic NHL and in one case of acute ATL by Southern blot hybridization. These results indicate that p27 gene alterations are rare events in NHLs and ATLs, but may play an important role in the pathogenesis of some hematologic malignancies.

Base Sequence↗
PubMed1993

APO-1-induced apoptosis of leukemia cells from patients with adult T-cell leukemia.

The 48-Kd cell-surface protein APO-1 is a new member of the nerve growth factor (NGF)/tumor necrosis factor (TNF) receptor superfamily. APO-1 is expressed on various cells, including activated T and B cells and some lymphoid and nonlymphoid cell lines. Triggering of APO-1 by the monoclonal antibody anti-APO-1 induces programmed cell death (apoptosis) in APO-1-expressing cells. APO-1 is also present on T-cell lines derived from patients with adult T-cell leukemia (ATL). Therefore, we investigated APO-1 expression and APO-1-mediated induction of apoptosis ex vivo in cells from patients with ATL. Fresh leukemic cells from nine patients with ATL were assayed for APO-1 expression by two-color immunofluorescence. The leukemic cells from all patients strongly expressed APO-1. Incubation of ATL cells with anti-APO-1 in vitro inhibited spontaneous and cytokine-mediated DNA synthesis. Furthermore, DNA isolated from cells treated with anti-APO-1 exhibited polynucleosomal DNA fragmentation (DNA ladder) characteristic for apoptotic cell death. The analysis of APO-1-mediated apoptosis may represent a new approach to the study of growth control in lymphoid malignancies. In addition, induction of apoptosis by administration of anti-APO-1 may represent a new therapeutic approach for aggressive T-cell malignancies such as ATL.

Antigens, Surface↗
PubMed1995

p53 gene mutation and loss of heterozygosity are associated with increased risk of disease progression in adult T cell leukemia.

Although the prototype of adult T cell leukemia (ATL) is an aggressive T cell neoplasm, ATL manifests four major clinical subtypes, acute, lymphoma, chronic, and smoldering. We studied the relationship between p53 gene alteration and clinical features in 34 patients with ATL, 14 acute type, 15 chronic type, and five crisis type transformed from chronic type. Using a polymerase chain reaction/single strand conformation polymorphism (PCR/SSCP) assay, followed by nucleotide sequencing, we detected mutations of the p53 gene in six of the 14 acute type patients, two of the five crisis type, and one of the 15 chronic type patients. Gene dosage studies, using PCR amplification and Southern blotting, showed loss of heterozygosity (LOH) of the p53 gene in four of the 14 acute type patients, two of the five crisis type, and one of 14 chronic type patients examined. These observations indicated that the frequency of p53 gene alterations in the acute and crisis types of ATL was markedly higher than that in chronic type, suggesting that p53 gene alteration plays a role in the disease progression of ATL.

Adult↗
PubMed1993

[Successful chronic daily administration of oral etoposide for a case of adult T cell leukemia].

A 54-year-old woman with leucocytosis and skin lesion was hospitalized and diagnosed as chronic type adult T cell leukemia (ATL) in August 1989. Since her ATL cell count and LDH level increased after hospitalization, oral administration of etoposide was started at a dose of 100 mg/day for seven days. The oral administration of etoposide induced another chronic state of ATL. After 10 months without medication, she was readmitted because of an acute ATL crisis. After daily administration of etoposide at a dose of 50 mg/day, the white blood cell count and serum LDH level decreased to the normal range, and abnormal lymphocytes of peripheral blood disappeared. The low-dose daily administration of etoposide at a dose of 25 approximately 50 mg/day could be maintained over six months. No severe side effects except for alopecia and mild myelosuppression were noted during the treatment. Chronic daily administration of oral etoposide is one candidate for the treatment of ATL in an outpatient clinic.

Administration, Oral↗
PubMed1993

[Clonal change of HTLV-1 infected lymphocytes before onset of adult T-cell leukemia/lymphoma].

A 73-year-old HTLV-1 infected male developed overt ATL following 3-years observation, and the clonality of HTLV-1 infected cells changed before overt ATL onset. 10 micrograms of DNA, extracted from mononuclear cells was digested with PstI, and the clonal proliferation of HTLV-1 infected cells was examined by Southern blotting with LTR probe. 4 bands were observed 3 years prior to ATL onset, and 2 different bands were detected 2 years and 6 months later. This suggests that in some ATL cases, the clonality of monoclonally proliferated HTLV-1 infected cells may be changeable before overt ATL onset.

Aged↗