Poorly expressed CD2 antigen on the leukemic cells of adult T-cell leukemia implicate more aggressive clinical course?

1990 ◽  
Vol 14 (11-12) ◽  
pp. 1071 ◽  
Author(s):  
Fumio Kawano ◽  
Atsuko Tsukamoto ◽  
Masahiko Satoh ◽  
Isao Sanada ◽  
Tadahiro Shido ◽  
...  
Keyword(s):  
T Cell ◽  
Clinical Course ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Aggressive Clinical Course

scholarly journals Evidence for the interleukin-2 dependent expansion of leukemic cells in adult T cell leukemia

Blood ◽  
1987 ◽  
Vol 70 (5) ◽  
pp. 1407-1411 ◽  
Author(s):  
M Maeda ◽  
N Arima ◽  
Y Daitoku ◽  
M Kashihara ◽  
H Okamoto ◽  
...  
Keyword(s):  
T Cell ◽  
Receptor Gene ◽  
Interleukin 2 ◽  
Leukemic Cells ◽  
Type I ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
In Vitro Proliferation ◽  
Adult T Cell Leukemia

Abstract Interleukin 2 (IL-2) receptor/Tac antigen is abnormally expressed on cells of patients with adult T cell leukemia (ATL) caused by infection with human T lymphotropic virus type I (HTLV-I). Twenty-five patients with ATL were examined to determine whether their leukemic cells continued to show IL-2-dependent proliferation. In 21 patients, the in vitro proliferation of HTLV-I-infected nonleukemic T cell clones was found to be dependent on IL-2. However, clonality analysis based on T cell receptor gene rearrangement profiles and the site of HTLV-I provirus integration revealed IL-2-dependent growth in leukemic cells in four patients with ATL. These results provide evidence for the IL-2- dependent proliferation of leukemic cells in some ATL patients.

Comparative genomic hybridization analysis in adult T-cell leukemia/lymphoma: correlation with clinical course

Blood ◽  
2001 ◽  
Vol 97 (12) ◽  
pp. 3875-3881 ◽  
Author(s):  
Kunihiro Tsukasaki ◽  
Johannes Krebs ◽  
Kazuhiro Nagai ◽  
Masao Tomonaga ◽  
H. Phillip Koeffler ◽  
...  
Keyword(s):  
T Cell ◽  
Comparative Genomic Hybridization ◽  
Clinical Course ◽  
Comparative Genomic ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Genomic Hybridization ◽  
Adult T Cell Leukemia ◽  
Paired Samples ◽  
Sequential Samples

Sixty-four patients with adult T-cell leukemia/lymphoma (ATL; 18 patients with indolent subtype and 46 with aggressive subtype) associated with human T-lymphotropic virus type 1 (HTLV-1) were analyzed using comparative genomic hybridization (CGH). The most frequent observations were gains at chromosomes 14q, 7q, and 3p and losses at chromosomes 6q and 13q. Chromosome imbalances, losses, and gains were more frequently observed in aggressive ATL than in indolent ATL, with significant differences between the 2 ATL subtypes at gains of 1q and 4q. An increased number of chromosomal imbalances was associated with a significantly shorter survival in all patients. A high number of chromosomal losses was associated with a poor prognosis in indolent ATL, whereas the presence of 7q+ was marginally associated with a good prognosis in aggressive ATL. Paired samples (ie, samples obtained at different sites from 4 patients) and sequential samples from 13 patients (from 6 during both chronic disease and acute crisis and from 7 during both acute onset and relapse) were examined by CGH and Southern blotting for HTLV-1. All but 2 paired samples showed differences on CGH assessment. Two chronic/crisis samples showed distinct results regarding both CGH and HTLV-1 integration sites, indicating clonal changes in ATL at crisis. In 11 patients, the finding of identical HTLV-1 sites and clonally related CGH results suggested a common origin of sequential samples. In contrast to chronic/crisis samples, CGH results with all acute/relapse sample pairs showed the presence of clonally related but not evolutional subclones at relapse, thereby suggesting marked chromosomal instability. In summary, clonal diversity is common during progression of ATL, and CGH alterations are associated with clinical course.

scholarly journals Expression of Cytokine mRNA in Leukemic Cells from Adult T Cell Leukemia Patients

1989 ◽  
Vol 80 (6) ◽  
pp. 531-536 ◽  
Author(s):  
Taiichi Kodaka ◽  
Takashi Uchiyama ◽  
Hiroshi Umadome ◽  
Haruto Uchino
Keyword(s):  
T Cell ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Cytokine Mrna ◽  
Adult T Cell Leukemia

scholarly journals Phenotypic and functional analysis of leukemic cells from 16 patients with adult T-cell leukemia/lymphoma

Blood ◽  
1983 ◽  
Vol 61 (1) ◽  
pp. 192-199 ◽  
Author(s):  
Y Yamada
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
B Cell ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
B Cell Differentiation ◽  
Cell Leukemia ◽  
Suppressor Activity ◽  
Surface Phenotype ◽  
Adult T Cell Leukemia

Abstract Surface phenotypes of leukemic cells from 16 patients with adult T-cell leukemia/lymphoma (ATLL) were analyzed by using monoclonal antibodies (anti-Leu-1, anti-Leu-2a, anti-Leu-3a, anti-HLA-DR and MAS 036 c), and the effect of leukemic cells on PWM-induced normal B-cell differentiation was also studied. The majority of ATLL cells bear Leu-1 and Leu-3a antigen on cell surface but lack Leu-2a antigen and were unreactive with MAS 036 c. These results indicate that ATLL cells are of peripheral inducer/helper T-cell origin. However, contrary to the surface phenotype, ATLL cells from 10 patients showed potent suppressor activity on PWM-induced normal B-cell differentiation to immunoglobulin- producing cells (Ig-PC) and no case showed helper activity. The dissociation between surface phenotype and function of ATLL cells is discussed in this article.

Constitutive activation of LIL-Stat in adult T-cell leukemia cells

Blood ◽  
2000 ◽  
Vol 95 (8) ◽  
pp. 2715-2718 ◽  
Author(s):  
Junichi Tsukada ◽  
Yoko Toda ◽  
Masahiro Misago ◽  
Yoshiya Tanaka ◽  
Philip E. Auron ◽  
...  
Keyword(s):  
T Cell ◽  
Dna Binding ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Mobility Shift ◽  
Adult T Cell Leukemia ◽  
Nuclear Extracts ◽  
Responsive Element ◽  
Electrophoretic Mobility Shift Assays

Abstract The activation status of a recently identified STAT (signal transducers and activators of transcription) factor, LIL-Stat (lipopolysaccharide [LPS]/IL-1–inducible Stat) in adult T-cell leukemia (ATL) cells was investigated by electrophoretic mobility shift assays using nuclear extracts of leukemic cells from 7 patients with ATL and a GAS (gamma interferon activation site)-like element termed LILRE (LPS/IL-1–responsive element), which is found in the human prointerleukin 1β (IL1B) gene. Spontaneous DNA binding of LIL-Stat was observed in all ATL cells examined. However, in normal human peripheral lymphocytes, DNA binding of LIL-Stat was detected only after stimulation with IL-1. These results demonstrated that LIL-Stat is constitutively activated in ATL cells. Furthermore, our transient transfection studies using LILRE chloramphenicol acetyltransferase (CAT) reporters argue that LIL-Stat in ATL cells functions as a transcriptional activator through binding to the LILRE in theIL1B gene.

scholarly journals A model of in vivo cell proliferation of adult T-cell leukemia

Blood ◽  
1993 ◽  
Vol 82 (8) ◽  
pp. 2501-2509 ◽  
Author(s):  
A Kondo ◽  
K Imada ◽  
T Hattori ◽  
H Yamabe ◽  
T Tanaka ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cell ◽  
Scid Mice ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Beta Chain ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Human T Cell

Abstract We have made a model of in vivo cell proliferation of leukemic cells from adult T-cell leukemia (ATL) patients using severe combined immunodeficiency (SCID) mice. Peripheral blood mononuclear cells (PBMC) or lymph node cells (LNC) depleted of B cells and monocytes were intraperitoneally injected into SCID mice treated with antimurine interleukin-2 receptor (IL-2+) beta chain monoclonal antibody (MoAb)(TM- beta 1), followed by daily injection of human recombinant IL-2 until 60 days after cell injection. SCID mice injected with ATL cells from 6 of 8 ATL patients were found to have the tumor or leukemia 5 to 7 weeks after the inoculation of cells. Serum levels of soluble form of human IL-2R alpha chain (Tac) were markedly elevated in such mice. The cells recovered from the mice injected with leukemic cells from four different ATL patients had the same cell surface phenotype as that of original leukemic cells which were CD4+Tac+. Furthermore, we detected the same integration site of human T-cell leukemia virus type I (HTLV- I) provirus and the same rearrangement pattern of human T-cell receptor (TCR) beta chain gene as those of ATL cells by Southern blot hybridization, indicating that the cells proliferating in SCID mice were derived from the original ATL cell clone. Histologic examination showed that the pattern of the infiltration of ATL cells into various organs in SCID mice was similar to that of an ATL patient. Such a model of in vivo cell proliferation of ATL cells will be useful for the study of the mechanism of neoplastic cell proliferation and for the development of a new and effective treatment of ATL.

Interleukin-2-mediated growth of leukemic cells in lymph nodes of patients with adult T-cell leukemia/ lymphoma

1996 ◽  
Vol 20 (2) ◽  
pp. 135-141 ◽  
Author(s):  
Kakushi Matsushita ◽  
Naomichi Arima ◽  
Toshinobu Fujiyoshi ◽  
Yasuhisa Daitoku ◽  
Shiroh Hidaka ◽  
...  
Keyword(s):  
T Cell ◽  
Lymph Nodes ◽  
Interleukin 2 ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia

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

Blood ◽  
1988 ◽  
Vol 72 (4) ◽  
pp. 1182-1186 ◽  
Author(s):  
T Uchiyama ◽  
M Kamio ◽  
T Kodaka ◽  
S Tamori ◽  
S Fukuhara ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Growth ◽  
Proliferative Response ◽  
Interleukin 2 ◽  
Leukemic Cells ◽  
Interleukin 4 ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Receptor System ◽  
Adult T Cell Leukemia

Abstract 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.

scholarly journals Autocrine growth of interleukin 2-producing leukemic cells in a patient with adult T cell leukemia

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 779-782 ◽  
Author(s):  
N Arima ◽  
Y Daitoku ◽  
S Ohgaki ◽  
J Fukumori ◽  
H Tanaka ◽  
...  
Keyword(s):  
T Cell ◽  
Interleukin 2 ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Autocrine Growth ◽  
Short Term ◽  
Adult T Cell Leukemia ◽  
Spontaneous Proliferation ◽  
Short Term Culture

Abstract Leukemic cells in the peripheral blood of a patient with adult T cell leukemia (ATL), which expressed the Tac antigen/interleukin 2 (IL2) receptor, were investigated in vitro for autocrine growth by IL 2. The cells showed spontaneous proliferation in mitogen-free medium. The spontaneous proliferation of the cells was inhibited by monoclonal anti- IL 2 or anti-Tac antibody. These cells were found to produce messenger RNA for IL 2 and secrete IL 2 during short-term culture in the same medium. Recombinant IL 2 and IL 2 secreted by the cells enhanced the proliferation of the cells in a dose-dependent manner when added to the initial culture. These findings demonstrate that an autocrine mechanism by IL 2 is involved in the proliferation of ATL cells during short-term culture.

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