In vitro growth response to G-CSF and GM-CSF by bone marrow cells of patients with acute myeloid leukemia

Jinnai, Itsuro

doi:10.1016/0145-2126(90)90130-2

Cited by 10 publications

(4 citation statements)

References 27 publications

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“…The broad range of expression of these receptors could, however, correlate with the heterogeneous response of the cells to growth factors described in other reports. IL-3 (38,39), SCF (31,41), IL-6 (35, 42) and G-CSF (36,43) stimulated the proliferation of the leukaemic cells in only some of the AML patients. IL-3 (40,44,45) and IL-7 (46±48) induced a proliferative response in part of the B-lineage ALL samples.…”

Section: Discussionmentioning

confidence: 99%

Growth factor receptor profile of CD34⁺ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Waele¹,

Renmans²,

Gucht³

et al. 2001

European J of Haematology

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Leukaemic cells show a low clonogenic activity and a heterogeneous proliferative response to growth factors. We investigated whether this could be due to an altered expression of growth factor receptors on the leukaemic precursors. Receptors for G-CSF, stem cell factor (SCF), IL-3, IL-6 and IL-7 were detected on CD34+ cells in AML and B-lineage ALL with monoclonal antibodies and flow cytometry. The expression was compared with that on myeloid and B-lymphoid CD34+ cells in normal bone marrow. Leukaemic CD34+ cells expressed the same receptors as their normal counterparts. AML and B-lineage ALL could be distinguished by the growth factor receptor profile of their CD34+ cells. SCFR, G-CSFR and IL-6Ralpha were found in AML, IL-7R in B-lineage ALL and IL-3Ralpha in both. IL-3Ralpha was upregulated in AML and B-lineage ALL CD34+ cells, while samples with low or high expression were present for the other receptors. This variable expression could correlate with the heterogeneous response of leukaemic cells to growth factors. Functional studies on isolated CD34+ cells are needed to investigate this further.

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Section: Discussionmentioning

confidence: 99%

Growth factor receptor profile of CD34⁺ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Waele¹,

Renmans²,

Gucht³

et al. 2001

European J of Haematology

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“…For example, HLAs are hardly detected on the surface of APL cells. 17,35,36 Studies on the expression of the immunosubunits have shown that the APL cell line NB4 exhibits barely detectable PSMB8 and PSMB9 levels. 17 PSMB10 expression data were absent from that study because PSMB10, unlike PSMB8 and PSMB9, is located outside of the MHC cluster, 37 and was therefore not identified during the investigation.…”

Section: Discussionmentioning

confidence: 99%

Coordinated regulation of the immunoproteasome subunits by PML/RARα and PU.1 in acute promyelocytic leukemia

Wang

et al. 2013

Oncogene

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Recognition and elimination of malignant cells by cytotoxic T lymphocytes depends on antigenic peptides generated by proteasomes. It has been established that impairment of the immunoproteasome subunits, that is, PSMB8, PSMB9 and PSMB10 (PSMBs), is critical for malignant cells to escape immune recognition. We report here the regulatory mechanism of the repression of PU.1-dependent activation of PSMBs by PML/RARα in the pathogenesis of acute promyelocytic leukemia (APL) and the unidentified function of all-trans retinoic acid (ATRA) as an immunomodulator in the treatment of APL. Chromatin immunoprecipitation and luciferase reporter assays showed that PU.1 directly bound to and coordinately transactivated the promoters of PSMBs, indicating that PSMBs were transcriptional targets of PU.1 and PU.1 regulated their basal expression. Analysis of expression profiling data from a large population of acute myeloid leukemia (AML) patients revealed that the expression levels of PSMBs were significantly lower in APL patients than in non-APL AML patients. Further evidence demonstrated that the decrease in their expression was achieved through PML/RARα-mediated repression of both PU.1-dependent transactivation and PU.1 expression. Moreover, ATRA but not arsenic trioxide induced the expression of PSMBs in APL cells, indicating that ATRA treatment might activate the antigen-processing/presentation machinery. Finally, the above observations were confirmed in primary APL samples. Collectively, our data demonstrate that PML/RARα suppresses PU.1-dependent activation of the immunosubunits, which may facilitate the escape of APL cells from immune surveillance in leukemia development, and ATRA treatment is able to reactivate their expression, which would promote more efficient T-cell-mediated recognition in the treatment.

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“…The possibility that fusion proteins deriving from chromosomal translocations represent a candidate target for an HLA restricted T cellmediated antitumor response has been already suggested for CML patients. 6,7 Since APL cells do not express HLA class II molecules, 8,9 it is more likely that any direct killing of such cells by cytotoxic T cells involves class I molecules and CD8 + T cell recognition. Thus, HLA alleles coding for molecules that bind bcr1 or bcr3 fusion peptides should be under-represented among the patients of either bcr1 or bcr3 type.…”

Section: Introductionmentioning

confidence: 99%

HLA class I in acute promyelocytic leukemia (APL): possible correlation with clinical outcome

et al. 2000

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The majority of patients with acute promyelocytic leukemia (APL) possess either a bcr1 or a bcr3 type fusion between PML and RAR␣ genes. The junction sequences may possibly be a target for immune response and influence susceptibility to the disease. In this case, HLA class I allele frequencies would be different between bcr1 and bcr3 patients. To test this hypothesis, we typed 102 APL patients for HLA-A, -B and -Cw alleles. The A*1, A*30, B*51, B*41, Cw*0602, and Cw*1701 alleles showed a different distribution between bcr1 and bcr3 patients, but in no case was this statistically significant after correction for the number of comparisons or was confirmed in an independent panel. Moreover, no difference was detected between bcr1 and bcr3 when HLA alleles were grouped according to their peptide binding specificities. Comparing HLA frequencies, clinical features at diagnosis and clinical outcome of the 64 patients homogeneously treated with all-trans retinoic acid and idarubicin (AIDA protocol) we observed a statistically significant association between HLA-B*13 and risk of relapse by univariate and multivariate regression analysis. Should this finding be confirmed in larger future studies, this observation would be of outmost importance in identifying patients at high risk of relapse in which more aggressive consolidation therapies should be used. Leukemia (2000) 14, 393-398.

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In vitro growth response to G-CSF and GM-CSF by bone marrow cells of patients with acute myeloid leukemia

Cited by 10 publications

References 27 publications

Growth factor receptor profile of CD34⁺ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Growth factor receptor profile of CD34⁺ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Coordinated regulation of the immunoproteasome subunits by PML/RARα and PU.1 in acute promyelocytic leukemia

HLA class I in acute promyelocytic leukemia (APL): possible correlation with clinical outcome

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In vitro growth response to G-CSF and GM-CSF by bone marrow cells of patients with acute myeloid leukemia

Cited by 10 publications

References 27 publications

Growth factor receptor profile of CD34+ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Growth factor receptor profile of CD34+ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Coordinated regulation of the immunoproteasome subunits by PML/RARα and PU.1 in acute promyelocytic leukemia

HLA class I in acute promyelocytic leukemia (APL): possible correlation with clinical outcome

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Product

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Growth factor receptor profile of CD34⁺ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts

Growth factor receptor profile of CD34⁺ cells in AML and B‐lineage ALL and in their normal bone marrow counterparts