scholarly journals Maturation of acute T-lymphoblastic leukemia cells after CD2 ligation and subsequent treatment with interleukin-2

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1182-1192 ◽  
Author(s):  
F Mentz ◽  
F Ouaaz ◽  
A Michel ◽  
C Blanc ◽  
P Herve ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Phosphorylation ◽  
Lymphoblastic Leukemia ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Subsequent Treatment ◽  
Leukemic Cells ◽  
Cell Phenotype ◽  
Cell Functions

Abstract In this study, we have investigated the ability of various cytokines to induce the maturation of acute lymphoblastic leukemia (T-ALL) cells with early T-cell phenotype. Leukemic blasts from 17 untreated T-ALL patients were assayed for their ability to acquire mature T-cell markers, CD3/T-cell receptor (TCR) in particular, after incubation with one or a combination of recombinant human interleukin-1 (IL-1), IL-2, IL-4, IL-7, and CD2-specific monoclonal antibody (MoAb). IL-7 or IL-2 induced the proliferation of some leukemic cells, whereas sequential cell treatment with CD2-MoAb and then IL-2 promoted CD3/TCR expression on nearly all CD2+ cells (15 of 16), except for 1 T-ALL that developed into CD3-CD16+CD56+ cells. Differentiation of T-ALL cells was also evidenced through the downregulation of CD34 precursor cell antigen, the generation of CD4+ and CD8+ cells from CD4+ CD8+ precursors, and the acquisition of mature T-cell functions. CD2 ligation induced a progressive increase of surface expression of IL-2 receptor alpha (IL- 2R alpha) and IL-2R beta and an accelerated in vitro death of leukemic cells. The ligation of IL-2R by IL-2 rescued T-ALL cells from death and promoted their progression toward more mature cells expressing extracellular CD3/TCR alpha beta complexes. Intracellular analysis indicates that TCR alpha transcription and membrane translocation of both TCR alpha and TCR beta were promoted in these conditions. Analysis of intracellular signals transduced during T-ALL differentiation indicated that CD2-ligation induced Ca2+ influx and that the ligation of CD2 and IL-2R induced distinct tyrosine phosphorylation patterns. The addition of inhibitors of tyrosine phosphorylation abolished T-ALL cell differentiation, which suggests the involvement of tyrosine kinases in this phenomenon. Together, we showed the constant maturation of leukemic early T cells after stimulation of surface CD2 and the high- affinity IL-2R.

scholarly journals Maturation of acute T-lymphoblastic leukemia cells after CD2 ligation and subsequent treatment with interleukin-2

Blood ◽  
1994 ◽  
Vol 84 (4) ◽  
pp. 1182-1192 ◽  
Author(s):  
F Mentz ◽  
F Ouaaz ◽  
A Michel ◽  
C Blanc ◽  
P Herve ◽  
...  
Keyword(s):  
T Cell ◽  
Tyrosine Phosphorylation ◽  
Lymphoblastic Leukemia ◽  
Interleukin 1 ◽  
Interleukin 2 ◽  
Subsequent Treatment ◽  
Leukemic Cells ◽  
Cell Phenotype ◽  
Cell Functions

In this study, we have investigated the ability of various cytokines to induce the maturation of acute lymphoblastic leukemia (T-ALL) cells with early T-cell phenotype. Leukemic blasts from 17 untreated T-ALL patients were assayed for their ability to acquire mature T-cell markers, CD3/T-cell receptor (TCR) in particular, after incubation with one or a combination of recombinant human interleukin-1 (IL-1), IL-2, IL-4, IL-7, and CD2-specific monoclonal antibody (MoAb). IL-7 or IL-2 induced the proliferation of some leukemic cells, whereas sequential cell treatment with CD2-MoAb and then IL-2 promoted CD3/TCR expression on nearly all CD2+ cells (15 of 16), except for 1 T-ALL that developed into CD3-CD16+CD56+ cells. Differentiation of T-ALL cells was also evidenced through the downregulation of CD34 precursor cell antigen, the generation of CD4+ and CD8+ cells from CD4+ CD8+ precursors, and the acquisition of mature T-cell functions. CD2 ligation induced a progressive increase of surface expression of IL-2 receptor alpha (IL- 2R alpha) and IL-2R beta and an accelerated in vitro death of leukemic cells. The ligation of IL-2R by IL-2 rescued T-ALL cells from death and promoted their progression toward more mature cells expressing extracellular CD3/TCR alpha beta complexes. Intracellular analysis indicates that TCR alpha transcription and membrane translocation of both TCR alpha and TCR beta were promoted in these conditions. Analysis of intracellular signals transduced during T-ALL differentiation indicated that CD2-ligation induced Ca2+ influx and that the ligation of CD2 and IL-2R induced distinct tyrosine phosphorylation patterns. The addition of inhibitors of tyrosine phosphorylation abolished T-ALL cell differentiation, which suggests the involvement of tyrosine kinases in this phenomenon. Together, we showed the constant maturation of leukemic early T cells after stimulation of surface CD2 and the high- affinity IL-2R.

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 Common and pre-B acute lymphoblastic leukemia cells express interleukin 2 receptors, and interleukin 2 stimulates in vitro colony formation

Blood ◽  
1985 ◽  
Vol 66 (3) ◽  
pp. 556-561 ◽  
Author(s):  
I Touw ◽  
R Delwel ◽  
R Bolhuis ◽  
G van Zanen ◽  
B Lowenberg
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Colony Formation ◽  
B Lymphocyte ◽  
Lymphoblastic Leukemia ◽  
Interleukin 2 ◽  
Colony Growth ◽  
Leukemic Cells ◽  
In Vitro Proliferation ◽  
Proliferation And Differentiation

Abstract The role of interleukin 2 (IL 2) as a possible regulator of in vitro proliferation and differentiation of non-T acute lymphoblastic leukemia (ALL) cells was investigated. For this purpose, leukemic cells from the blood or bone marrow of eight untreated patients with common or pre-B ALL were analyzed using the anti-Tac monoclonal antibody (reactive with the IL 2 receptor) in indirect immunofluorescence. The receptors for IL 2, which were initially absent from the cell surface, were induced on high percentages of the ALL cells after the in vitro exposure to the lectin phytohemagglutinin or the phorbol ester 12-O- tetradecanoylphorbol-13-acetate in six patients, suggesting that the cells had become sensitive to IL 2. In colony cultures to which feeder leukocytes and IL 2 had been added, colony growth was obtained in five of eight cases. Whereas the cells from one patient formed colonies in the absence of exogenous stimuli, the cells from others were dependent on the addition of feeder leukocytes plus IL 2. In the latter cases, feeder leukocytes alone, releasing some IL 2, stimulated growth suboptimally at different cell concentrations. Their stimulative effect was significantly enhanced when leukocyte-derived IL 2 or pure recombinant IL 2 was supplemented. Alone, IL 2 (up to 500 U/mL) did not support colony formation. Apparently, IL 2 and feeder leukocytes are both required for the induction of colonies in these cases of ALL. From cell sorting of fluorescent anti-common ALL antigen (CALLA) stained cells it appeared that colonies descended from cells with high as well as low or negative CALLA expression. Immunophenotyping demonstrated the presence of the original leukemia markers on colony cells, but was not indicative of maturation of ALL toward more differentiated B cells. We suggest that IL 2 can stimulate the in vitro proliferation of certain neoplastic B lymphocyte progenitors.

Analysis of In Vitro Effects of Bortezomib (Velcade) on T Cell Prolymphocytic Leukemia (T-PLL).

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4426-4426
Author(s):  
Fulya Ozpuyan ◽  
Paul N. Meyer ◽  
Hytham Al-Masri ◽  
Hongyu Ni ◽  
Serhan Alkan
Keyword(s):  
T Cell ◽  
Lymphoproliferative Disorder ◽  
Flow Cytometric Analysis ◽  
Leukemic Cells ◽  
Cell Phenotype ◽  
Base Line ◽  
Prolymphocytic Leukemia ◽  
Bortezomib Treatment ◽  
Flow Cytometric

Abstract T-cell prolymphocytic leukemia (T-PLL) is an aggressive lymphoproliferative disorder with postthymic T cell phenotype and prolymphocytic morphology. In the majority of patients, the leukemic process progresses rapidly and patients die shortly after diagnosis (median survival of 7 months). Bortezomib, the first proteasome inhibitor to be approved for use in haematological malignancies such as multiple myeloma, is beginning to be utilized as an effective anti-neoplastic agent in other hematopoietic and non-hematopoietic neoplastic disorders. We report here the in vitro apoptotic effects of bortezomib on leukemic cells isolated from three T-PLL patients. Interestingly, one of the patient’s leukemia developed in the setting of immunosupression due to transplant therapy (post-transplant lymphoproliferative disorder). Flow cytometric analysis of leukemic cells of the three patients showed CD8, double CD4+CD8+ and double CD4−CD8− immunophenotypic features. All cases showed monoclonal band pattern by T-cell receptor (TCR) gene rearrangement as analyzed by the PCR amplification of the TCR gamma heavy chain gene. Freshly isolated leukemic cells with the CD8 phenotype T-PLL analyzed for apoptosis after ficoll hypaque separation and cultured in the presence of various concentration of Bortezomib (0.001, 0.01, 0.1, 1, and 10 uM) for dose curve analysis. Apoptosis of the leukemic cells was determined by Annexin-V and 7-AAD staining and flow cytometric analysis after incubation at 24 and 72 hours, respectively. Samples treated for 72 hours showed higher rate of apoptosis compared to 24 hours: 10 uM (62% increase above the base line of control cells), 1 uM (58%), 0.1 uM (55%), 0.01 uM (40%) and 0.001 uM (0%) concentrations while samples treated for 24 hours with 10 uM showed (42% increase above the base line of control cells) and 1 uM (33% increase above the base line). Light microscopic analysis of leukemic cells treated with Bortezomib confirmed that the majority of cells undergo apoptosis with Bortezomib treatment as it revealed nuclear fragmentation and apoptotic bodies. Leukemic cells recovered from cryopreservation from the second and third T-PLL patient samples analyzed also showed significant increase in early and late apoptosis at 24 hours with Bortezomib treatment (10nm). These results suggest that Bortezomib may provide an alternate therapy in the treatment of T-PLL. Future collaborative efforts investigating efficacy with Bortezomib as a single agent or in combination with other therapeutic agents will be crucial to improving survival for patients with this disease.

scholarly journals CD7+, CD4-, CD8- acute leukemia: a syndrome of malignant pluripotent lymphohematopoietic cells

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 381-390
Author(s):  
J Kurtzberg ◽  
TA Waldmann ◽  
MP Davey ◽  
SH Bigner ◽  
JO Moore ◽  
...  
Keyword(s):  
Lymphoblastic Leukemia ◽  
Leukemic Cell ◽  
Leukemic Cells ◽  
Cell Phenotype ◽  
Therapeutic Approaches ◽  
Myeloid Leukemias ◽  
Cell Gene ◽  
In Vitro Data

Following our initial observation of in vivo conversion of CD7+, CD4-, CD8- acute lymphoblastic leukemia (ALL) cells from lymphoid to myeloid lineages (Proc Natl Acad Sci (USA) 81:253, 1984) we have studied eight additional cases of ALL with this leukemic cell phenotype. The CD7+, CD4-, CD8- phenotype was associated with a distinct clinical entity with those affected predominantly male (either less than 35 years or greater than 65 years of age), with frequent mediastinal and/or thymic masses, skin and CNS disease, high peripheral WBC counts, and bone marrow blasts that were morphologically L1 or not ascribable to a specific lineage. These patients did not respond to conventional chemotherapeutic regimens for either acute lymphoid or myeloid leukemias. No common karyotype or T-cell gene rearrangement pattern could be defined. Importantly, seven of eight patient's leukemic cells studied were capable of multilineage (myeloid, erythroid, monocytoid, megakaryocytoid, and lymphoid) differentiation in vitro. Data is presented suggesting that CD7+, CD4-, CD8- leukemias, in many instances, are leukemias of immature hematopoietic cells. The development of novel therapeutic approaches to this form of leukemia will be necessary to alter its poor prognosis.

scholarly journals Establishment of a karyotypically normal cytotoxic leukemic T-cell line from a T-ALL sample engrafted in SCID mice

Blood ◽  
1993 ◽  
Vol 81 (10) ◽  
pp. 2714-2722
Author(s):  
A Cesano ◽  
R O'Connor ◽  
PC Nowell ◽  
B Lange ◽  
SC Clark ◽  
...  
Keyword(s):  
T Cell ◽  
Cell Line ◽  
Chromosomal Abnormalities ◽  
Lymphoblastic Leukemia ◽  
Interleukin 2 ◽  
Cell Subset ◽  
Scid Mice ◽  
Leukemic Cells ◽  
Cytotoxic T Cell ◽  
Tumoricidal Activity

Bone marrow (BM) cells from a child with an immature (CD3-) acute T lymphoblastic leukemia (T-ALL) bearing no chromosomal abnormalities failed to grow in long-term culture in the presence or absence of recombinant human (rh) growth factors but could be engrafted in severe combined immunodeficient (SCID) mice and induced leukemia. The leukemic cells recovered from the animal tissues could be adapted to grow in vitro in the presence of rh interleukin-2 (IL-2) and give rise to a growth factor-dependent cell line designated TALL-107. This cell line expresses T-cell-specific mature markers (CD2, CD3/T-cell receptor [TCR] alpha beta, CD8, CD56), and its growth can be inhibited by IL-4 of all the cytokines tested. Similar to the original leukemic blasts, TALL-107 cells are clonal, have rearranged TCR-beta, gamma, and delta loci, and a normal 46 XY karyotype. However, unlike the patient's BM cells, the TALL-107 cell line displays potent tumoricidal activity that is not major histocompatibility complex restricted. The magnitude of mRNA expression of perforin and serine esterases and of lytic activity depends on the doses of IL-2 added. TALL-107 cells can also be triggered by CD3- and CD2-specific monoclonal antibodies (MoAbs) to mediate reverse tumor cell lysis. In addition, this cell line produces high levels of interferon gamma and tumor necrosis factor alpha on stimulation with anti-CD3 and/or anti-CD2 MoAb both in the presence or absence of IL-2. The overall data indicate that the SCID mouse is able to support the functional maturation and expansion of a cytotoxic T- cell subset from some types of T-ALL.

Free radicals and redox signalling in T-cells during chronic inflammation and ageing

2011 ◽  
Vol 39 (5) ◽  
pp. 1273-1278 ◽  
Author(s):  
Helen R. Griffiths ◽  
Christopher R. Dunston ◽  
Stuart J. Bennett ◽  
Melissa M. Grant ◽  
Darren C. Phillips ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Chronic Inflammation ◽  
Cell Function ◽  
Cell Phenotype ◽  
Cell Functions ◽  
Cytoplasmic Proteins ◽  
Local Cell ◽  
Species Production

During chronic inflammation and ageing, the increase in oxidative stress in both intracellular and extracellular compartments is likely to influence local cell functions. Redox changes alter the T-cell proteome in a quantitative and qualitative manner, and post-translational modifications to surface and cytoplasmic proteins by increased reactive species can influence T-cell function. Previously, we have shown that RA (rheumatoid arthritis) T-cells exhibit reduced ROS (reactive oxygen species) production in response to extracellular stimulation compared with age-matched controls, and basal ROS levels [measured as DCF (2′,7′-dichlorofluorescein) fluorescence] are lower in RA T-cells. In contrast, exposing T-cells in vitro to different extracellular redox environments modulates intracellular signalling and enhances cytokine secretion. Together, these data suggest that a complex relationship exists between intra- and extra-cellular redox compartments which contribute to the T-cell phenotype.

Flow cytometric analysis of expression of interleukin-2 receptor beta chain (p70-75) on various leukemic cells

Blood ◽  
1990 ◽  
Vol 76 (4) ◽  
pp. 767-774 ◽  
Author(s):  
S Hoshino ◽  
K Oshimi ◽  
M Tsudo ◽  
M Miyasaka ◽  
M Teramura ◽  
...  
Keyword(s):  
T Cell ◽  
Lymphoblastic Leukemia ◽  
Interleukin 2 ◽  
Flow Cytometric Analysis ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Beta Chain ◽  
Alpha Chain ◽  
Interleukin 2 Receptor ◽  
Flow Cytometric

Abstract We analyzed the expression of the interleukin-2 receptor (IL-2R) beta chain (p70–75) on various leukemic cells from 44 patients by flow cytometric analysis using the IL-2R beta chain-specific monoclonal antibody (MoAb), designated Mik-beta 1, which has been recently developed. Flow cytometric analysis demonstrated the expression of the IL-2R beta chain on granular lymphocytes (GLs) from all eight patients with granular lymphocyte proliferative disorders (GLPDs), on adult T- cell leukemia (ATL) cells from all three patients with ATL, and on T- cell acute lymphoblastic leukemia (T-ALL) cells from one of three patients with T-ALL. Although GLs from all the GLPD patients expressed the IL-2R beta chain alone and not the IL-2R alpha chain (Tac-antigen: p55), ATL and T-ALL cells expressing the beta chain coexpressed the alpha chain. In two of seven patients with common ALL (cALL) and in both patients with B-cell chronic lymphocytic leukemia, the leukemic cells expressed the alpha chain alone. Neither the alpha chain nor the beta chain was expressed on leukemic cells from the remaining 28 patients, including all 18 patients with acute nonlymphocytic leukemia, five of seven patients with cALL, all three patients with multiple myeloma, and two of three patients with T-ALL. These results indicate that three different forms of IL-2R chain expression exist on leukemic cells: the alpha chain alone; the beta chain alone; and both the alpha and beta chains. To examine whether the results obtained by flow cytometric analysis actually reflect functional aspects of the expressed IL-2Rs, we studied the specific binding of 125I-labeled IL-2 (125I-IL-2) to leukemic cells in 18 of the 44 patients. In addition, we performed 125I-IL-2 crosslinking studies in seven patients. The results of IL-2R expression of both 125I-IL-2 binding assay and crosslinking studies were in agreement with those obtained by flow cytometric analysis. These results indicate that flow cytometric analysis using MoAbs, anti-Tac, and Mik-beta 1 is useful for detecting the expression of the IL-2R chains.

scholarly journals Expression of T-cell differentiation antigens on effector cells in cell-mediated cytotoxicity in vitro. Evidence for functional heterogeneity related to the surface phenotype of T cells.

1975 ◽  
Vol 141 (1) ◽  
pp. 227-241 ◽  
Author(s):  
H Shiku ◽  
P Kisielow ◽  
M A Bean ◽  
T Takahashi ◽  
E A Boyse ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Killer Cell ◽  
Surface Antigens ◽  
Cell Phenotype ◽  
Direct Function ◽  
Effector Cells ◽  
Cell Functions ◽  
T Cell Antigens

The cell-mediated cytotoxicity (CMC) of nonadherent cells from the peritoneal cavity (NAPC) of alloimmunized mice can be measured by the [3H]proline microassay. The exhibition of thymus-derived (T) cell antigens on these killer cells was studied by incubating them with the relevant T-cell antisera and complement (C), under optimal conditions for lysis, before performance of the CMC assay. Under these conditions, the following T-cell antigens were demonstrable on the killer population in terms of percent reduction in CMC by the respective antisera: (a) Thy-1.1 (83%) and Thy-1.2 (100%), (b) MSLA (86%), (c) NTA-RA (a T-cell antigen recognized by naturally occurring autoantibody of NZB mice) (62%), (d) Ly1.1 )58%, (e) Ly-2.1 (11%; considered a marginal result) and Ly-2.2 (63%), and (f) Ly-3.2 (77%). The following were not demonstrable: (g) TL, and (h) Ly-1.2. (i) The antigen Ly-3.1 was not studied. Omission of C deprived all T-cell antisera tested of their capacity to suppress CMC, indicating that the cell components recognized by such antisera may perform no direct function in CMC. On the assumption that all Ly+ cells are Thy-1+, it is clear that the T-cell members of the immune NAPC population must be heterogenous. This follows from the fact that the proportions of T cells lysed by different Ly antisera did not correspond with ensuing degree of loss of CMC capacity. The extremes were represented by anti-Ly-1.2 (74% Thy-1+ cells lysed, but no reduction in CMC) and Ly-3.2 (54% Thy-1+ cells lysed, with 77% reduction in CMC). From this initial survey it appears that the C57BL/6 mice killer T-cell population active in CMC in vitro is relatively rich in surface antigens of the Ly-2/Ly-3 category and relatively poor in representation of the Ly-1 surface antigens. It remains to be seen whether this killer cell phenotype, poor in Ly-1 and rich in Ly-2/Ly-3, is characteristic of the mouse generally. From these results it appears that subsets of T cells with different immunological functions may exhibit qualitative or quantitative differences in surface antigens specified by different Ly loci; this will be easier to assess in the future when the results of experiments with the same Ly antisera but dealing with T-cell functions other than CMC become available.

scholarly journals Common and pre-B acute lymphoblastic leukemia cells express interleukin 2 receptors, and interleukin 2 stimulates in vitro colony formation

Blood ◽  
1985 ◽  
Vol 66 (3) ◽  
pp. 556-561
Author(s):  
I Touw ◽  
R Delwel ◽  
R Bolhuis ◽  
G van Zanen ◽  
B Lowenberg
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Colony Formation ◽  
B Lymphocyte ◽  
Lymphoblastic Leukemia ◽  
Interleukin 2 ◽  
Colony Growth ◽  
Leukemic Cells ◽  
In Vitro Proliferation ◽  
Proliferation And Differentiation

The role of interleukin 2 (IL 2) as a possible regulator of in vitro proliferation and differentiation of non-T acute lymphoblastic leukemia (ALL) cells was investigated. For this purpose, leukemic cells from the blood or bone marrow of eight untreated patients with common or pre-B ALL were analyzed using the anti-Tac monoclonal antibody (reactive with the IL 2 receptor) in indirect immunofluorescence. The receptors for IL 2, which were initially absent from the cell surface, were induced on high percentages of the ALL cells after the in vitro exposure to the lectin phytohemagglutinin or the phorbol ester 12-O- tetradecanoylphorbol-13-acetate in six patients, suggesting that the cells had become sensitive to IL 2. In colony cultures to which feeder leukocytes and IL 2 had been added, colony growth was obtained in five of eight cases. Whereas the cells from one patient formed colonies in the absence of exogenous stimuli, the cells from others were dependent on the addition of feeder leukocytes plus IL 2. In the latter cases, feeder leukocytes alone, releasing some IL 2, stimulated growth suboptimally at different cell concentrations. Their stimulative effect was significantly enhanced when leukocyte-derived IL 2 or pure recombinant IL 2 was supplemented. Alone, IL 2 (up to 500 U/mL) did not support colony formation. Apparently, IL 2 and feeder leukocytes are both required for the induction of colonies in these cases of ALL. From cell sorting of fluorescent anti-common ALL antigen (CALLA) stained cells it appeared that colonies descended from cells with high as well as low or negative CALLA expression. Immunophenotyping demonstrated the presence of the original leukemia markers on colony cells, but was not indicative of maturation of ALL toward more differentiated B cells. We suggest that IL 2 can stimulate the in vitro proliferation of certain neoplastic B lymphocyte progenitors.

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