In vitro culture of leukemic cells in t(4;11) acute leukemia

Stong, Robin C.; Kersey, John H.

doi:10.1182/blood.v66.2.439.439

Cited by 30 publications

(7 citation statements)

References 19 publications

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“…Among approximately 300 published cases in 15 studies, no leukemic colonies were observed in one third of patients and, even if colonies were generated in the remaining two thirds, plating efficiency was much lower than in the case of AML, ranging from 0.001% to 2.76%, with an overall median value of only 0.28% [72]. It has been reported that Philadelphia chromosomeor myeloid-antigen-positive ALL cases tend to show colony formation in response to myeloid growth factors, suggesting that ALL blasts with bipotential phenotypes grow more like AML blasts [66,69,70]. The poor colony forming capability of ALL blast progenitors compared to those from AML cases could be due, in part, to culture conditions under which ALL blasts easily undergo apoptosis even in the presence of added HGFs.…”

Section: Leukemic Stem Cells In Allmentioning

confidence: 96%

“…Attempts to demonstrate the leukemic stem cells in acute lymphoblastic leukemia (ALL), particularly common ALL or pre-B-ALL, have been made, but leukemic colony assays for ALL have been difficult to establish and relatively little data reported [63][64][65][66][67][68][69][70][71]. For ALL colony assays, feeder cells from irradiated peripheral blood are required together with soluble growth stimulants, including PHA-LCM.…”

Section: Leukemic Stem Cells In Allmentioning

confidence: 99%

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Hematopoietic Growth Factors and Blast Progenitors in Acute Leukemia

Miyauchi

1997

Hematology

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Leukemic cells are maintained by a minor subpopulation of cells called leukemic stem cells (LSC) with proliferative and self-renewal capacity, both of which are detected with leukemic colony assay, with the latter being an important prognositic factor. Drug sensitivity tests employing leukemic colony assay revealed the effects of cytotoxic drugs on LSC to be diverse and that cytosine arabinoside predominantly suppresses self-renewal, which probably accounts for its effectiveness in AML therapy. Hematopoietic growth factors (HGFs) regulate the growth of LSC and various in vitro effects of HGFs on acute leukemia cells have been reported. These effects appear to reflect physiological functions of each HGF and can be categorized into groups according to their distinct functions. Endogenously produced HGFs stimulate LSC in an autocrine or a paracrine fashion, resulting in autonomous growth of these cells, which also correlates with the patients' prognosis. HGFs can enhance the cytotoxicity of anti-leukemia drugs in vitro, possibly mainly through recruitment of LSC from the dormant state into active cell cycling. HGFs have been clinically tested in leukemia therapy. Although recovery of blood leukocyte counts can consistently be accelerated with HGF treatment, the effectiveness of HGFs in sensitizing leukemia cells to chemotherapeutic agents and/or improving patient prognosis has not been clearly demonstrated. Different strategies using HGFs and related molecules must be tested in future leukemia therapy.

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Section: Leukemic Stem Cells In Allmentioning

confidence: 96%

Section: Leukemic Stem Cells In Allmentioning

confidence: 99%

Hematopoietic Growth Factors and Blast Progenitors in Acute Leukemia

Miyauchi

1997

Hematology

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“…Human cell lines studied were: RC-K8, from a B-cell lymphoma with t( 11; 14)(q23;q32) (Kubonishi et al, 1986); KOCL-33, from an infantile acute leukemia with t(11;19)(q23;p13) (Akao et al, 1991b); and RS4;11, from an acute leukemia with t(4;11)(q21;q23) (Stong and Kersey, 1985). An Epstein-Barr virus-transformed cell with a normal karyotype was used as a control.…”

Section: Cellsmentioning

confidence: 99%

Long‐range mapping of the 11q23 region involved in chromosome aberrations in human tumors by pulsed‐field gel electrophoresis with a yeast artificial chromosome

Akao

Tsujimoto

Seto

et al. 1993

Genes Chromosomes & Cancer

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We have previously demonstrated that the RCK gene involved in t(11;14)(q23;q32) and the more centromeric MLL/ALL1 gene involved in t(4;11)(q21;q23) and t(11;19)(q23;p13) are localized on different adjacent NotI fragments by using pulsed-field gel electrophoresis (PFGE) analysis with the yeast artificial chromosome (YAC) clone yB22B2. The PFGE analysis using the YACs of YTY17 containing the prophobilinogen deaminase (PBGD), CBL2 and THY1 genes and yB22B2 allowed the following ordering of genes and breakpoints from CD3 to THY1 on 11q23: cent-CD3-ALL/MLL1-RCK-PBGD-CBL2-THY1, and the establishment of a long-range restriction map covering these genes. In addition, we showed that the FLI1 region involved in the t(11;22)(q24;q12) in Ewing's sarcoma was more telomeric region that the THY1 gene by analyzing somatic cell hybrids carrying the 11q- and/or 14q+ chromosome of the t(11;14)(q23;q32) translocation, and by PFGE analysis of the YAC clone YTY17.

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“…We (14-17, 24, 25) and others (7,9,10,26) have discussed the problems inherent in using established ceil lines in vitro as a model system for evaluating the antileukemic efficacy of a purging reagent. These problems have received little attention because of the difficulty in growing freshly obtained ALL cells in vitro (26,27). To our knowledge, none of the reagents currently under clinical evaluation have been tested directly against clonogenic blasts from ALL patients, and therefore there is no evidence that they can effectively eliminate leukemic progenitor cells.…”

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confidence: 99%

Use of a novel colony assay to evaluate the cytotoxicity of an immunotoxin containing pokeweed antiviral protein against blast progenitor cells freshly obtained from patients with common B-lineage acute lymphoblastic leukemia.

Uckun¹,

Gajl‐Peczalska²,

Kersey³

et al. 1986

The Journal of Experimental Medicine

104

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We report a novel colony assay for B-lineage progenitor cells in acute lymphoblastic leukemia (ALL). The primary plating efficiency of blast progenitors freshly obtained from common B-lineage ALL patients varied between 0.09 and 2.63%. Morphological, cytochemical, and immunological analyses of cells from day 7 colonies provided the evidence that they are B-lineage lymphoblasts. Immunological marker analyses of cultured blasts using BA-2 (anti-CD9), BA-3 (anti-CD10), BA-1 (anti-CD24), and B43 mAb have allowed us to define two distinct immunological groups. The first group had BA-2+, BA-3+, BA-1+, B43+ marker profiles, consistent with the phenotype of uncultured bone marrow blasts. The second group differed in that the cells in the blast colonies were BA-3 (anti-CD10)-negative, although many of the cells in the bulk population were BA-3+ before culture. Blasts from both groups were able to proliferate and form secondary colonies when recultured. A pan-B immunotoxin was synthesized by linking B43, a human B cell-specific mAb, to pokeweed antiviral protein (PAP). This study showed that B43-PAP can effectively eradicate leukemic progenitor cells freshly obtained from patients with common B-lineage ALL. B43-PAP eliminated greater than 99.96% of blast progenitors under conditions in which only minimal inhibition of normal bone marrow progenitor cells (CFU-GM, CFU-E, CFU-MK, CFU-GEMM) was observed. Our results establish that the surface determinant recognized by B43 is expressed on B-lineage progenitor cells in ALL, and that these cells are sensitive to PAP at the ribosomal level. To our knowledge, B43-PAP is the first IT to prove effective against common B-lineage ALL cells.

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In vitro culture of leukemic cells in t(4;11) acute leukemia

Cited by 30 publications

References 19 publications

Hematopoietic Growth Factors and Blast Progenitors in Acute Leukemia

Hematopoietic Growth Factors and Blast Progenitors in Acute Leukemia

Long‐range mapping of the 11q23 region involved in chromosome aberrations in human tumors by pulsed‐field gel electrophoresis with a yeast artificial chromosome

Use of a novel colony assay to evaluate the cytotoxicity of an immunotoxin containing pokeweed antiviral protein against blast progenitor cells freshly obtained from patients with common B-lineage acute lymphoblastic leukemia.

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