scholarly journals S-100 beta positive T cell leukemia

Blood ◽  
1988 ◽  
Vol 71 (5) ◽  
pp. 1299-1303 ◽  
Author(s):  
K Takahashi ◽  
Y Ohtsuki ◽  
H Sonobe ◽  
K Hayashi ◽  
S Nakamura ◽  
...  
Keyword(s):  
T Cell ◽  
Human Peripheral Blood ◽  
Leukemic Cell ◽  
Cell Receptor ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
S 100 ◽  
T Cell Phenotypes

Abstract We reported a peculiar case with T cell leukemia. The patient was a 34- year-old woman showing extensive splenomegaly and marked leukemic cell proliferation and running a rapid fatal clinical course. The leukemic cells were morphologically ordinary lymphocytes showing suppressor/cytotoxic(s/c) T cell phenotypes and containing S-100b protein. Southern blot analysis revealed rearrangement of the beta chain genes of the T cell receptor (TcR) of the leukemic cells. Because these phenotypic and morphologic features were identical with those of S-100 beta+T lymphocytes (S-100 beta +TL) in normal human peripheral blood, we regarded this case as S-100 beta +T cell leukemia. We discussed clinicopathological features of S-100 beta +T cell leukemia/lymphoma by assessing similar cases reported so far. S-100 beta +T cell leukemia/lymphoma is a new type of s/c T lymphocytic leukemia/lymphoma with aggressive features.

scholarly journals S-100 beta positive T cell leukemia

Blood ◽  
1988 ◽  
Vol 71 (5) ◽  
pp. 1299-1303
Author(s):  
K Takahashi ◽  
Y Ohtsuki ◽  
H Sonobe ◽  
K Hayashi ◽  
S Nakamura ◽  
...  
Keyword(s):  
T Cell ◽  
Human Peripheral Blood ◽  
Leukemic Cell ◽  
Cell Receptor ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
S 100 ◽  
T Cell Phenotypes

We reported a peculiar case with T cell leukemia. The patient was a 34- year-old woman showing extensive splenomegaly and marked leukemic cell proliferation and running a rapid fatal clinical course. The leukemic cells were morphologically ordinary lymphocytes showing suppressor/cytotoxic(s/c) T cell phenotypes and containing S-100b protein. Southern blot analysis revealed rearrangement of the beta chain genes of the T cell receptor (TcR) of the leukemic cells. Because these phenotypic and morphologic features were identical with those of S-100 beta+T lymphocytes (S-100 beta +TL) in normal human peripheral blood, we regarded this case as S-100 beta +T cell leukemia. We discussed clinicopathological features of S-100 beta +T cell leukemia/lymphoma by assessing similar cases reported so far. S-100 beta +T cell leukemia/lymphoma is a new type of s/c T lymphocytic leukemia/lymphoma with aggressive features.

scholarly journals OX40 Expressed on Fresh Leukemic Cells From Adult T-Cell Leukemia Patients Mediates Cell Adhesion to Vascular Endothelial Cells: Implication for the Possible Involvement of OX40 in Leukemic Cell Infiltration

Blood ◽  
1997 ◽  
Vol 89 (8) ◽  
pp. 2951-2958 ◽  
Author(s):  
Akihiro Imura ◽  
Toshiyuki Hori ◽  
Kazunori Imada ◽  
Shin Kawamata ◽  
Yuetsu Tanaka ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
T Cell ◽  
Mononuclear Cells ◽  
Vascular Endothelial Cells ◽  
Leukemic Cell ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia

Abstract We demonstrated previously that OX40 and its ligand, gp34, directly mediate adhesion of activated normal CD4+ T cells, as well as human T-cell leukemia virus type I (HTLV-I)–transformed T cells to vascular endothelial cells. In the present study, we examined expression of OX40 on fresh leukemic cells from patients with adult T-cell leukemia (ATL) and its possible involvement in cell adhesion. Flow cytometric analysis showed that peripheral blood mononuclear cells (PBMC) or lymph node tumor cells from 15 of 17 cases expressed significant levels of OX40 without stimulation. On the other hand, gp34 was not expressed on these cells, although its expression is also known to be associated with HTLV-I-infection. In Western blot analysis, a 50-kD protein band was detected by anti-OX40 monoclonal antibody (MoAb) in two ATL cases examined, as well as phytohemagglutinin (PHA) blasts and Hut102, an HTLV-I–infected T-cell line, but not in resting PBMC or Jurkat. Expression of OX40 mRNA was shown by reverse transcriptase-polymerase chain reaction in all ATL cases tested, PHA-blasts, and Hut102, but not in resting PBMC or Jurkat. We could not detect expression of HTLV-I viral mRNA in any of the cases tested. Cell adhesion assay was performed and in at least three cases, fresh ATL cells exhibited adhesion to human umbilical vein endothelial cells that could be considerably inhibited by either anti-OX40 MoAb or anti-gp34 MoAb. Immunohistochemical staining of skin biopsy specimens indicated that infiltrating mononuclear cells express OX40 in vivo. Taken together, these data indicate that leukemic cells from most, but not all, ATL patients constitutively express OX40, which may play a role in leukemic cell infiltration in addition to cell adhesion in vivo.

Poorly expressed CD2 antigen on the leukemic cells of adult T-cell leukemia and chronic lymphocytic leukemia of T-cell lineage

1989 ◽  
Vol 13 (1) ◽  
pp. 93-99 ◽  
Author(s):  
Kazuo Tamura ◽  
Kimitaka Sagawa ◽  
Hiroyuki Satoh ◽  
Junichiro Torigoe ◽  
Nobuhiro Kimura ◽  
...  
Keyword(s):  
T Cell ◽  
Chronic Lymphocytic Leukemia ◽  
Cell Lineage ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia

scholarly journals Expression of p210bcr/abl by metallothionein promoter induced T-cell leukemia in transgenic mice

Blood ◽  
1995 ◽  
Vol 85 (10) ◽  
pp. 2853-2861 ◽  
Author(s):  
H Honda ◽  
T Fujii ◽  
M Takatoku ◽  
H Mano ◽  
ON Witte ◽  
...  
Keyword(s):  
T Cell ◽  
Transgenic Mice ◽  
Philadelphia Chromosome ◽  
Chimeric Protein ◽  
Polymerase Chain Reaction Analysis ◽  
Cell Receptor ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia

The p210bcr/abl chimeric protein is considered to be implicated in the pathogenesis of Philadelphia chromosome-positive human leukemias. To investigate its biologic function in vivo, we generated transgenic mice expressing p210bcr/abl driven by the metallothionein enhancer/promoter. Two of six founder mice and the transgenic progeny developed leukemias several months after birth. In the leukemic tissues, the expression of the p210bcr/abl transgene product was detected and the increased tyrosine-phosphorylation of cellular proteins was observed. The expressed p210bcr/abl transgene product was shown to possess an enhanced kinase activity. The leukemic cells showed rearrangements in the T-cell receptor loci, indicating that the leukemic cells were monoclonal and committed to the T-cell lineage. Polymerase chain reaction analysis for tissue distribution of p210bcr/abl expression showed that, in the transgenic line that reproducibly developed leukemias, p210bcr/abl was expressed in the hematopoietic tissues such as thymus and spleen; on the other hand, in the transgenic lines that have not developed leukemias, p210bcr/abl expression was detected only in the nonhematopoietic tissues such as the brain and kidney. These results suggest that the tumorigenicity of the p210bcr/abl chimeric protein is restricted to the hematopoietic tissues in vivo and that an event enhancing p210bcr/abl expression contributed a proliferative advantage to hematopoietic precursor cells and eventually developed T-cell leukemia in transgenic mice.

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.

scholarly journals T-cell receptor chain Vbeta subunit staining to quantify the malignant clone in adult T-cell leukemia

Retrovirology ◽  
2015 ◽  
Vol 12 (S1) ◽  
Author(s):  
Aileen G Rowan ◽  
Paul Fields ◽  
Graham P Taylor ◽  
Charles RM Bangham
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Adult T Cell Leukemia ◽  
Receptor Chain

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 Enhanced MDR1 Gene Expression in Human T-Cell Leukemia Virus-I–Infected Patients Offers New Prospects for Therapy

Blood ◽  
1998 ◽  
Vol 91 (7) ◽  
pp. 2467-2474 ◽  
Author(s):  
Alan Lau ◽  
Simon Nightingale ◽  
Graham P. Taylor ◽  
Timothy W. Gant ◽  
Alan J. Cann
Keyword(s):  
Drug Resistance ◽  
T Cell ◽  
Multiple Drug Resistance ◽  
Leukemia Virus ◽  
Spastic Paraparesis ◽  
Leukemic Cells ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Human T Cell ◽  
T Cell Leukemia Virus

Overexpression of P-glycoprotein (P-gp), the protein product of the multidrug resistance gene (MDR1), confers a drug resistant phenotype on cells. This phenotype is reminiscent of human T-cell leukemia virus (HTLV)-transformed leukemic cells, for which no consistently effective chemotherapeutic regime has been found. The presence of an active multiple drug resistance (MDR) phenotype in freshly isolated peripheral blood mononuclear cells (PBMC) from HTLV-I–infected subjects was investigated. Significant P-gp–mediated efflux activity and enhanced MDR1 mRNA expression was observed in nine of 10 HTLV-infected subjects. The development of MDR phenotypes was found to be independent of disease type or status with significant MDR activities being observed in adult T-cell leukemia (ATL), HTLV-associated myelopathy (HAM)/tropical spastic paraparesis (TSP), and asymptomatic HTLV-infected individuals. P-gp–mediated drug efflux was also found to be restricted to CD3+ T-cell populations. Furthermore, we show the novel finding that theMDR1 gene promoter is transcriptionally activated by the HTLV-I tax protein, suggesting a molecular basis for the development of drug resistance in HTLV-I infections. These observations open up the possibility of new chemotherapeutic approaches to HTLV-associated diseases through the use of P-gp inhibitors.

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