ArticleOncotarget2016
Speed of leukemia development and genetic diversity in xenograft models of T cell acute lymphoblastic leukemia.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Nonclinical evaluation of renizgamglogene autogedtemcel for SCD and TDT.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- CDKN1A is a target for phagocytosis-mediated cellular immunotherapy in acute leukemia.Nature communications · 2022Article
- Modified quasispecies model: the analysis of a periodic therapy.Journal of mathematical biology · 2022Article
- Oncogene-Induced Reprogramming in Acute Lymphoblastic Leukemia: Towards Targeted Therapy of Leukemia-Initiating Cells.Cancers · 2021Review
- Xenograft and cell culture models of Sézary syndrome reveal cell of origin diversity and subclonal heterogeneity.Leukemia · 2021Article
- Dissecting molecular mechanisms of resistance to NOTCH1-targeted therapy in T-cell acute lymphoblastic leukemia xenografts.Haematologica · 2020Article
- Bone marrow sites differently imprint dormancy and chemoresistance to T-cell acute lymphoblastic leukemia.Blood advances · 2017Article
Corrections and comments
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Authors and funding
13 authors at 9 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell acute lymphoblastic leukemia (T-ALL) develops through accumulation of multiple genomic alterations within T-cell progenitors resulting in clonal heterogeneity among leukemic cells. Human T-ALL xeno-transplantation in immunodeficient mice is a gold standard approach to study leukemia biology and we recently uncovered that the leukemia development is more or less rapid depending on T-ALL sample. The resulting human leukemia may arise through genetic selection and we previously showed that human T-ALL development in immune-deficient mice is significantly enhanced upon CD7+/CD34+ leukemic cell transplantations. Here we investigated the genetic characteristics of CD7+/CD34+ and CD7+/CD34- cells from newly diagnosed human T-ALL and correlated it to the speed of leukemia development. We observed that CD7+/CD34+ or CD7+/CD34- T-ALL cells that promote leukemia within a short-time period are genetically similar, as well as xenograft-derived leukemia resulting from both cell fractions. In the case of delayed T-ALL growth CD7+/CD34+ or CD7+/CD34- cells were either genetically diverse, the resulting xenograft leukemia arising from different but branched subclones present in the original sample, or similar, indicating decreased fitness to mouse micro-environment. Altogether, our work provides new information relating the speed of leukemia development in xenografts to the genetic diversity of T-ALL cell compartments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.