ArticleDisease models & mechanisms2019
Therapeutic targeting of Notch signaling and immune checkpoint blockade in a spontaneous, genetically heterogeneous mouse model of T-cell acute lymphoblastic leukemia.
Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 11 citations in OpenAlex.
- Overexpression of Lmo2 initiates T-lymphoblastic leukemia via impaired thymocyte competition.The Journal of experimental medicine · 2023Article
- Identification of an Immune-Related Nine-lncRNA Signature Predictive of Overall Survival in Colon Cancer.Frontiers in genetics · 2020Article
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic cancer derived from the malignant transformation of T-cell progenitors. Outcomes remain poor for T-ALL patients who have either primary resistance to standard-of-care chemotherapy or disease relapse. Notably, there are currently no targeted therapies available in T-ALL. This lack of next-generation therapies highlights the need for relevant preclinical disease modeling to identify and validate new targets and treatment approaches. Here, we adapted a spontaneously arising, genetically heterogeneous, thymic transplantation-based murine model of T-ALL, recapitulating key histopathological and genetic features of the human disease, to the preclinical testing of targeted and immune-directed therapies. Genetic engineering of the murine
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