T-cell acute lymphobalstic leukemia xenografts in NOD/SCID mouse
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE153717 | GEO | 2020/07/03
REPOSITORIES: GEO
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Project description:T-cell acute lymphobalstic leukemia xenografts in NOD/SCID mouse
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Project description:Leukemic cells from either peripheral blood or bone marrow were obtained from 6 patients with acute lymphocytic leukemia. These cells were used to generate mouse xenografts and a comparison was made between those two sample sources. Six pairs of human leukemia and associated xenografts are compared.
2010-10-18 | E-GEOD-15621 | biostudies-arrayexpress
Project description:Novel therapies are needed for pediatric acute lymphoblastic leukemia resistant to conventional therapy. While emerging data suggest leukemias as possible targets of oncolytic attenuated measles virus, it is unknown whether measles virus can eradicate disseminated leukemia, in particular pediatric acute lymphoblastic leukemia. We evaluated the efficacy of attenuated measles virus against a large panel of pediatric xenografted and native primary acute lymphoblastic leukemias ex vivo, and against four different acute lymphoblastic leukemia xenografts of B-lineage in non-obese diabetic/severe combined immunodeficient mice. Ex vivo, attenuated measles virus readily spread among and effectively killed leukemia cells while sparing normal human blood cells and their progenitors. In immunodeficient mice with disseminated acute lymphoblastic leukemia a few intravenous injections of attenuated measles virus sufficed to eradicate leukemic blasts in the hematopoietic system and to control central nervous system disease resulting in long-term survival in three of the four xenografted B-lineage leukemias. Differential sensitivity of leukemia cells did not require increased expression of the measles entry receptors CD150 or CD46 nor absence of the anti-viral retinoic acid-inducible gene I/melanoma differentiation associated gene-5 /interferon pathway. Attenuated oncolytic measles virus is dramatically effective against pediatric B-lineage acute lymphoblastic leukemia in the pre-clinical setting warranting further investigations towards clinical translation.
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Project description:Xenografts are useful in vivo tumour models for investigating cancer progression, therapeutic responses and predicting anti-cancer drug response in patients with cancer of a similar phenotype. We have generated bulk RNA-seq data from LNCaP xenografts of a large and well-annotated prostate cancer progression study, investigating responsiveness and subsequent resistance to therapies targeting the androgen receptor (AR). LNCaP xenograft tumour establishment and initial growth are dependent on androgens in male mice (PRE-CX / pre-castration group). Upon castration, AR activity and tumour growth are suppressed (POST-CX / post-castration group), however, this initial responsiveness to castration reproducibly gives way to castration-resistance (CRPC / castration-resistant prostate cancer). Further treatment of CRPC with the AR targeting drug enzalutamide (ENZ) initially provides a therapeutic response (ENZ Sensitive; ENZS), however, resistance emerges in time (ENZ Resistant; ENZR).
2022-09-07 | GSE211856 | GEO
Project description:Acute Myeloid Leukemia (AML) patient xenografts
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Project description:Acute lymphoblastic leukemia (ALL) is a heterogeneous disorder, and primary drug resistance and relapse are thought to be the main causes for treatment failure in ALL patients. For these refractory or relapsed patients, there is an increasing demand to identify novel therapeutic approaches, which will highly rely on the use of xenotransplantation models in translational research. Given the critical role that the spleen plays in the hematopoiesis and lymphopoiesis in adult mice, intrasplenic inoculation of ALL cells into immunodeficient mice may represent a feasible route for leukemic xenotransplantation. In the present study, engraftments via intrasplenic inoculation in anti-mCD122 mAb conditioned NOD/SCID mice were achieved in 5 out of 11 cases, and the engrafted cells reconstituted a complete leukemic phenotype. The engrafted cells sustained the self-renewal capacity of leukemia-initiating cells as tested by serial xenotransplantation and can be used for evaluation of antileukemic drugs. These data suggest that the combination of intrasplenic inoculation and the targeted depletion of CD122(+) cells could provide a novel approach for the xenotransplantation of ALL cells in NOD/SCID mice. Furthermore, this model can be used for stem cell research, long-term analysis of engraftment kinetics and in vivo drug tests.
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Project description:Leukemic cells from either peripheral blood or bone marrow were obtained from 6 patients with acute lymphocytic leukemia. These cells were used to generate mouse xenografts and a comparison was made between those two sample sources.
2010-10-18 | GSE15621 | GEO
Project description:Human leukemic stem cells, like other cancer stem cells, are hypothesized to be rare, capable of incomplete differentiation, and restricted to a phenotype associated with early hematopoietic progenitors or stem cells. However, recent work in other types of tumors has challenged the cancer stem cell model. Using a robust model of xenotransplantation based on NOD/SCID/IL2Rγc-deficient mice, we confirmed that human leukemic stem cells, functionally defined by us as SCID leukemia-initiating cells (SL-ICs), are rare in acute myelogenous leukemia (AML). In contrast to previous results, SL-ICs were found among cells expressing lineage markers (i.e., among Lin+ cells), CD38, or CD45RA, all markers associated with normal committed progenitors. Remarkably, each engrafting fraction consistently recapitulated the original phenotypic diversity of the primary AML specimen and contained self-renewing leukemic stem cells, as demonstrated by secondary transplants. While SL-ICs were enriched in the Lin-CD38- fraction compared with the other fractions analyzed, SL-ICs in this fraction represented only one-third of all SL-ICs present in the unfractionated specimen. These results indicate that human AML stem cells are rare and enriched but not restricted to the phenotype associated with normal primitive hematopoietic cells. These results suggest a plasticity of the cancer stem cell phenotype that we believe has not been previously described.
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Project description:Glucocorticoids are critical components of combination chemotherapy regimens in pediatric acute lymphoblastic leukemia (ALL). The pro-apoptotic BIM protein is an important mediator of glucocorticoid-induced apoptosis in normal and malignant lymphocytes, while the anti-apoptotic BCL2 confers resistance. The signaling pathways regulating BIM and BCL2 expression in glucocorticoid-treated lymphoid cells remain unclear. In this study, pediatric ALL patient-derived xenografts (PDXs) inherently sensitive or resistant to glucocorticoids were exposed to dexamethasone in vivo. In order to understand the basis for differential in vivo glucocorticoid sensitivity of PDXs, microarray analysis of gene expression was carried out on 5 each of dexamethasone-sensitive and resistant PDXs . This provided a global understanding of dexamethasone-induced signaling cascades in ALL cells in vivo, and especialy identified the genes that are involved in transducing the apoptotic signal, upstream of BIM/BCL2 dynamic interactions.
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Project description:In this study, pediatric ALL patient-derived xenografts (PDXs) inherently resistant to glucocorticoids were cultured in vitro. The study aims to determine discrepancy in gene expressions between different xeno strains.
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