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Discovery of the targets of the immune response to chronic myeloid leukemia in 3 patients using protein microarrays

ABSTRACT: Three patients who had relapsed chronic myeloid leukemia after allogeneic bone marrow transplant and received an immunotherapeutic intervention (donor lymphocyte infusion, or DLI) without further treatment were studied. The binding of serum immunoglobulins to proteins after immunotherapy was compared to before in two patients using Invitrogen ProtoArrays from a single lot. For a third patient, comparison was made between two timepoints after immunotherapy against one timepoint before using Invitrogen ProtoArrays from a separate lot. Significant interactions were determined by comparing each after sample separately against the before sample from that patient, using the Concentration-Dependent Analysis described in Marina et al., J Proteome Res, 2008. The goal was to identify proteins with significantly-increased reactivity after donor lymphocyte infusion. Keywords: Immune response discovery

ORGANISM(S): Homo sapiens

PROVIDER: GSE11565 | GEO | 2008/05/31

SECONDARY ACCESSION(S): PRJNA109145

REPOSITORIES: GEO

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Discovery of the targets of the immune response to chronic myeloid leukemia in 3 patients using protein microarrays

Project description:Three patients who had relapsed chronic myeloid leukemia after allogeneic bone marrow transplant and received an immunotherapeutic intervention (donor lymphocyte infusion, or DLI) without further treatment were studied. The binding of serum immunoglobulins to proteins after immunotherapy was compared to before in two patients using Invitrogen ProtoArrays from a single lot. For a third patient, comparison was made between two timepoints after immunotherapy against one timepoint before using Invitrogen ProtoArrays from a separate lot. Significant interactions were determined by comparing each after sample separately against the before sample from that patient, using the Concentration-Dependent Analysis described in Marina et al., J Proteome Res, 2008. The goal was to identify proteins with significantly-increased reactivity after donor lymphocyte infusion. Keywords: Immune response discovery One sample from before and one sample from after immunotherapy were tested for 2 patients, and one sample from before and two samples from after immunotherapy were tested for a third patient.

2008-05-31 | E-GEOD-11565 | biostudies-arrayexpress

Discovery of the targets of the immune response to chronic lymphocytic leukemia in 2 patients using protein microarrays

Project description:The binding of serum immunoglobulins to proteins was compared using serum from after and before an immunotherapeutic intervention (donor lymphocyte infusion) in two patients who had relapsed chronic lymphocytic leukemia (CLL) after bone marrow transplant. One Invitrogen ProtoArray was used for each sample. Significant interactions were determined by comparing the before and after samples for each patient separately, using the Concentration-Dependent Analysis described in Marina et al., J Proteome Res, 2008. One sample from before and one sample from after immunotherapy were tested for each patient. Keywords: Immune response discovery

2008-05-31 | GSE11564 | GEO

Discovery of the targets of the immune response to chronic lymphocytic leukemia in 2 patients using protein microarrays

2008-05-31 | E-GEOD-11564 | biostudies-arrayexpress

Expression data from responders/nonresponders before/after receiving DLI for relapse of CML s/p BMT

Project description:Increasing evidence across malignancies suggests that infiltrating T cells at the site of disease are crucial to tumor control. We hypothesized that marrow-infiltrating immune populations play a critical role in response to donor lymphocyte infusion (DLI), an established and potentially curative immune therapy whose precise mechanism remains unknown. We therefore analyzed marrow-infiltrating immune populations in 29 patients (22 responders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4+ DLI in the pre-tyrosine kinase inhibitor era. We used microarrays to detail the global programme of gene expression underlying T cell infiltration into bone marrow of responders and nonresponders to DLI. mRNA expression profiling of marrow-infiltrating CD3+ positively selected T cells of 4 responders compared to 2 non-responders, before and after DLI, was performed on Affymetrix microarrays.

2013-09-30 | E-GEOD-49067 | biostudies-arrayexpress

Expression data from responders/nonresponders before/after receiving DLI for relapse of CML s/p BMT

2013-09-30 | GSE49067 | GEO

LV-Induced Dendritic Cells for AML Immunotherapy

Project description:Wilms’ tumor 1 antigen (WT1) is overexpressed in acute myeloid leukemia (AML). Unfortunately, clinical immunotherapeutic use of WT1 peptides against AML has been inconclusive. A tricistronic lentiviral vector co-expressing a truncated form of WT1 (lacking the DNA-binding domain), GM-CSF and IL-4 was used to transduce human monocytes. The overnight transduction procedure induced the self-differentiation of monocytes into highly viable and immunophenotypically stable “SmartDC/tWT1” (GM-CSF+, IL-4+, WT1+, IL-6+, IL-8+, TNF-?+, MCP-1+, HLA-DR+, CD86+, CCR2+, CCR5+). RNA expression pattern analyses revealed up-regulation of several toll-like receptors, interferons and interferon-stimulated genes in lentivirally-reprogrammed SmartDC/tWT1 in comparison with conventional DCs. Remission samples from a FLT3-ITD+ AML patient and surplus material from the donor lymphocyte infusion (DLI) obtained from the matched related donor were used to produce SmartDC/tWT1. In our donor-patient model, donor T cells expanded with SmartDC/tWT1 showed high reactivity against WT1 and against primary AML. Intracellular processing of WT1 peptides by SmartDC/tWT1 resulted in superior WT1-specific CD8+ cytotoxicity against the primary leukemia blasts than exogenous peptide pulsing. Therefore, SmartDC/tWT1 produced in a single day of ex vivo culture with broad homeostatic, innate immunity, antigenic presentation and cytotoxic T cell stimulation properties can be clinically developed in combination with DLI for boosting anti-leukemia responses.

2012-12-31 | GSE37231 | GEO

Sorafenib promotes graft-versus-leukemia activity in mice and humans through IL-15 production in FLT3-ITD mutant leukemia cells

Project description:Patients relapsing with FLT3-ITD mutant acute myeloid leukemia (AML) after allogeneic hematopoietic cell transplantation (allo-HCT) have a one-year-survival below 20%. We observed that sorafenib increased IL-15 production by FLT3-ITD+-leukemia cells, which synergized with the allogeneic CD8+T-cell response, leading to long-term survival in murine and humanized FLT3-ITD+AML models. Using IL-15 deficiency in recipient tissues or leukemia cells, IL-15 production upon sorafenib-treatment could be attributed to leukemia cells. Sorafenib treatment-related IL-15 production caused an increase in CD8+CD107a+IFN-γ+ T-cells with features of longevity (Bcl-2high/reduced PD-1-levels), which eradicated leukemia in secondary recipients. Mechanistically, sorafenib reduced ATF4 expression, thereby blocking negative regulation of IRF7-activation, which enhances IL-15 transcription. Consistent with the mouse data, IL-15 and pIRF7 levels increased in leukemic blasts of FLT3-ITD+AML patients upon sorafenib treatment. Analysis of 130 patients with FLT3-ITD-mutant AML relapsing after allo-HCT showed the highest complete remission-rate and median overall-survival-rate in the sorafenib/donor lymphocyte infusion (DLI) group compared to all other groups (chemotherapy, chemotherapy/DLI, sorafenib alone). Our findings indicate that the synergism of DLI and sorafenib is mediated via reduced ATF4 expression, causing activation of the pIRF7/IL-15-axis in leukemia cells. The sorafenib/DLI strategy therefore has the potential for an immune-mediated cure of FLT3-ITD-mutant AML- relapse, an otherwise fatal complication after allo-HCT.

2017-12-19 | GSE95770 | GEO

LV-Induced Dendritic Cells for AML Immunotherapy

Project description:WilmsM-bM-^@M-^Y tumor 1 antigen (WT1) is overexpressed in acute myeloid leukemia (AML). Unfortunately, clinical immunotherapeutic use of WT1 peptides against AML has been inconclusive. A tricistronic lentiviral vector co-expressing a truncated form of WT1 (lacking the DNA-binding domain), GM-CSF and IL-4 was used to transduce human monocytes. The overnight transduction procedure induced the self-differentiation of monocytes into highly viable and immunophenotypically stable M-bM-^@M-^\SmartDC/tWT1M-bM-^@M-^] (GM-CSF+, IL-4+, WT1+, IL-6+, IL-8+, TNF-?+, MCP-1+, HLA-DR+, CD86+, CCR2+, CCR5+). RNA expression pattern analyses revealed up-regulation of several toll-like receptors, interferons and interferon-stimulated genes in lentivirally-reprogrammed SmartDC/tWT1 in comparison with conventional DCs. Remission samples from a FLT3-ITD+ AML patient and surplus material from the donor lymphocyte infusion (DLI) obtained from the matched related donor were used to produce SmartDC/tWT1. In our donor-patient model, donor T cells expanded with SmartDC/tWT1 showed high reactivity against WT1 and against primary AML. Intracellular processing of WT1 peptides by SmartDC/tWT1 resulted in superior WT1-specific CD8+ cytotoxicity against the primary leukemia blasts than exogenous peptide pulsing. Therefore, SmartDC/tWT1 produced in a single day of ex vivo culture with broad homeostatic, innate immunity, antigenic presentation and cytotoxic T cell stimulation properties can be clinically developed in combination with DLI for boosting anti-leukemia responses. Seeking to better characterize possible effects of truncated WT1 over-expression in the transcriptional activity of dendritic cells, we compared the gene expression pattern of SmartDC/tWT1 with those of SmartDC and Conventional DC.

2012-12-31 | E-GEOD-37231 | biostudies-arrayexpress

Low-Dose Total Body Irradiation and Donor Peripheral Blood Stem Cell Transplant Followed by Donor Lymphocyte Infusion in Treating Patients With Non-Hodgkin Lymphoma, Chronic Lymphocytic Leukemia, or Multiple Myeloma

Project description:This pilot clinical trial studies low-dose total body irradiation and donor peripheral blood stem cell transplant followed by donor lymphocyte infusion in treatment patients with non-Hodgkin lymphoma, chronic lymphocytic leukemia, or multiple myeloma. Giving total-body irradiation before a donor peripheral blood stem cell transplant helps stop the growth of cells in the bone marrow, including normal blood-forming cells (stem cells) and cancer cells. When healthy stem cells from a donor are infused into the patient they may help the patient’s bone marrow make stem cells, red blood cells, white blood cells, and platelets. Once the donated stem cells begin working, the patient’s immune system may see the remaining cancer cells as not belonging in the patient’s body and destroy them. Giving an infusion of the donor’s white blood cells (donor lymphocyte infusion) may boost this effect.

| 2002764 | ecrin-mdr-crc

Fludarabine Phosphate, Low-Dose Total-Body Irradiation, and Donor Stem Cell Transplant Followed by Cyclosporine, Mycophenolate Mofetil, Donor Lymphocyte Infusion in Treating Patients With Hematopoietic Cancer

Project description:This clinical trial studies fludarabine phosphate, low-dose total-body irradiation, and donor stem cell transplant followed by cyclosporine, mycophenolate mofetil, and donor lymphocyte infusion in treating patients with hematopoietic cancer. Giving low doses of chemotherapy, such as fludarabine phosphate, and total body irradiation (TBI) before a donor peripheral blood stem cell transplant helps stop the growth of cancer cells. It may also keep the patient’s immune response from rejecting the donor’s stem cells. The donated stem cells may replace the patient’s immune cells and help destroy any remaining cancer cells (graft-versus-tumor effect). Giving an infusion of the donor’s T cells (donor lymphocyte infusion) after the transplant may help increase this effect. Sometimes the transplanted cells from a donor can also make an immune response against the body’s normal cells. Giving cyclosporine and mycophenolate mofetil after the transplant may stop this from happening.

| 2005296 | ecrin-mdr-crc

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