Chemotherapeutic Remissions in Wistar Furth Rat Acute Myelogenous Leukemia: A Model for Human AML

Greenberger, Joel S.; Bocaccino, Carol A.; Szot, Susan J.; Moloney, William C.

doi:10.1159/000207886

Cited by 8 publications

(1 citation statement)

References 11 publications

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“…Following initial inductions of myelogenous leukaemia employing largely polynuclear aromatic hydrocarbons, 128,129 several transplantable AML rat models 9,130-149 became available (Table 3 and reviewed 150,151 ). Primarily, the Wistar/Furth, 152 L5222 acute rat leukaemia in BDIX 142 and the BNML 9 rat models, all with predictable growth characteristics, 138,153,154 analogous biology to human AML, 142,143,155,156 ease of transplantability with excellent levels of engraftment 9,138 and similar susceptibility to clinical chemotherapeutic regimes employed in human AML 138,157,158 emerged as suitable experimental models. However, in comparative colony-forming (CFU-s) studies, 143,159 it was soon Insertional mutagenesis.…”

Section: Transplantable Modelsmentioning

confidence: 99%

Animal models of acute myelogenous leukaemia – development, application and future perspectives

2005

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From the early inception of the transplant models through to contemporary genetic and xenograft models, evolution of murine leukaemic model systems have been critical to our general comprehension and treatment of cancer, and, more specifically, disease states such as acute myelogenous leukaemia (AML). However, even with modern advances in therapeutics and molecular diagnostics, the majority of AML patients die from their disease. Thus, in the absence of definitive in vitro models which precisely recapitulate the in vivo setting of human AMLs and failure of significant numbers of new drugs late in clinical trials, it is essential that murine AML models are developed to exploit more specific, targeted therapeutics. While various model systems are described and discussed in the literature from initial transplant models such as BNML and spontaneous murine leukaemia virus models, to the more definitive genetic and clinically significant NOD/SCID xenograft models, there exists no single compendium which directly assesses, reviews or compares the relevance of these models. Thus, the function of this article is to provide clinicians and experimentalists a chronological, comprehensive appraisal of all AML model systems, critical discussion on the elucidation of their roles in our understanding of AML and consideration to their efficacy in the development of AML chemotherapeutics.

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