By Pier Paolo Pandolfi (Editor), Peter K. Vogt (Editor)
During the last 10 years, paintings on acute promyelocytic leukemia (APL) has turn into the paradigm of translational learn that started with the invention of a recurrent chromosomal translocation, via the identity of the genes and proteins concerned, discovering their molecular features in transcriptional keep watch over, developing mouse versions and culminating within the improvement of specific remedy.
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Additional info for Acute Promyelocytic Leukemia: Molecular Genetics, Mouse Models and Targeted Therapy (Current Topics in Microbiology and Immunology 313)
Animal models of leukemia can be used to assess the potential role of the immune system in controlling malignant cell growth, and to examine strategies to boost the immune response to AML. The use of mouse models in which the leukemic oncoproteins are themselves expressed from murine genes may enhance the relevance of such studies to future human clinical investigation. 2. APL models have been used in preclinical studies to assess the potential value of new AML therapies. 3. Many agents that enter human clinical trials are initially assessed as single agent therapies in phase I trials.
2001). In this model, oral ATRA administration at the dose used had a moderate effect on subcutaneous growth of NB4 cells, and although NB4 cells are sensitive to ATRA, ATRA did not prolong survival of mice that received NB4 cells intravenously. The addition of the histone deacetylase inhibitor FK228 (also known as depsipeptide) to ATRA strongly suppressed subcutaneous growth. Further, when NB4 cells were injected intravenously, 3 of 7 dual-treated mice experienced long-term survival, in contrast to untreated or single-agent-treated animals.
A few cases also had Auer rods. Like the usual cases of APL, the promyelocytes were CD34− /CD13+ /CD33+ but were sometimes positive for the CD56 natural killer (NK) cell antigen. It was proposed that due to their characteristic regular nuclei and unusual immunophenotype, cases of APL with t(11;17)(q23;q21) should be given the subclassiﬁcation M3r . The PLZF gene is located on chromosome 11q23, about 1 Mb centromeric to the MLL (mixed lineage leukemia) gene. The PLZF locus was completely 32 M.