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Epigenetics in T-cell acute lymphoblastic leukemia

Sofie Peirs (UGent) , Joni Van der Meulen (UGent) , Inge Van de Walle (UGent) , Tom Taghon (UGent) , Franki Speleman (UGent) , Bruce Poppe (UGent) and Pieter Van Vlierberghe (UGent)
(2015) IMMUNOLOGICAL REVIEWS. 263(1). p.50-67
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Abstract
Normal T-cell development is a strictly regulated process in which hematopoietic progenitor cells migrate from the bone marrow to the thymus and differentiate from early T-cell progenitors toward mature and functional T cells. During this maturation process, cooperation between a variety of oncogenes and tumor suppressors can drive immature thymocytes into uncontrolled clonal expansion and cause T-cell acute lymphoblastic leukemia (T-ALL). Despite improved insights in T-ALL disease biology and comprehensive characterization of its genetic landscape, clinical care remained largely similar over the past decades and still consists of high-dose multi-agent chemotherapy potentially followed by hematopoietic stem cell transplantation. Even with such aggressive treatment regimens, which are often associated with considerable side effects, clinical outcome is still extremely poor in a significant subset of T-ALL patients as a result of therapy resistance or hematological relapses. Recent genetic studies have identified recurrent somatic alterations in genes involved in DNA methylation and post-translational histone modifications in T-ALL, suggesting that epigenetic homeostasis is critically required in restraining tumor development in the T-cell lineage. In this review, we provide an overview of the epigenetic regulators that could be implicated in T-ALL disease biology and speculate how the epigenetic landscape of T-ALL could trigger the development of epigenetic-based therapies to further improve the treatment of human T-ALL.
Keywords
epigenetics, T-ALL, therapeutics, ACUTE MYELOID-LEUKEMIA, FORSSMAN-LEHMANN-SYNDROME, HISTONE DEACETYLASE INHIBITORS, BET BROMODOMAIN INHIBITION, CHROMATIN REMODELER MI-2-BETA, GENE-EXPRESSION SIGNATURES, EMBRYONIC STEM-CELLS, DNA METHYLATION, SOMATIC MUTATIONS, IDH2 MUTATIONS

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Citation

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MLA
Peirs, Sofie, Joni Van der Meulen, Inge Van de Walle, et al. “Epigenetics in T-cell Acute Lymphoblastic Leukemia.” IMMUNOLOGICAL REVIEWS 263.1 (2015): 50–67. Print.
APA
Peirs, S., Van der Meulen, J., Van de Walle, I., Taghon, T., Speleman, F., Poppe, B., & Van Vlierberghe, P. (2015). Epigenetics in T-cell acute lymphoblastic leukemia. IMMUNOLOGICAL REVIEWS, 263(1), 50–67.
Chicago author-date
Peirs, Sofie, Joni Van der Meulen, Inge Van de Walle, Tom Taghon, Franki Speleman, Bruce Poppe, and Pieter Van Vlierberghe. 2015. “Epigenetics in T-cell Acute Lymphoblastic Leukemia.” Immunological Reviews 263 (1): 50–67.
Chicago author-date (all authors)
Peirs, Sofie, Joni Van der Meulen, Inge Van de Walle, Tom Taghon, Franki Speleman, Bruce Poppe, and Pieter Van Vlierberghe. 2015. “Epigenetics in T-cell Acute Lymphoblastic Leukemia.” Immunological Reviews 263 (1): 50–67.
Vancouver
1.
Peirs S, Van der Meulen J, Van de Walle I, Taghon T, Speleman F, Poppe B, et al. Epigenetics in T-cell acute lymphoblastic leukemia. IMMUNOLOGICAL REVIEWS. 2015;263(1):50–67.
IEEE
[1]
S. Peirs et al., “Epigenetics in T-cell acute lymphoblastic leukemia,” IMMUNOLOGICAL REVIEWS, vol. 263, no. 1, pp. 50–67, 2015.
@article{5784859,
  abstract     = {Normal T-cell development is a strictly regulated process in which hematopoietic progenitor cells migrate from the bone marrow to the thymus and differentiate from early T-cell progenitors toward mature and functional T cells. During this maturation process, cooperation between a variety of oncogenes and tumor suppressors can drive immature thymocytes into uncontrolled clonal expansion and cause T-cell acute lymphoblastic leukemia (T-ALL). Despite improved insights in T-ALL disease biology and comprehensive characterization of its genetic landscape, clinical care remained largely similar over the past decades and still consists of high-dose multi-agent chemotherapy potentially followed by hematopoietic stem cell transplantation. Even with such aggressive treatment regimens, which are often associated with considerable side effects, clinical outcome is still extremely poor in a significant subset of T-ALL patients as a result of therapy resistance or hematological relapses. Recent genetic studies have identified recurrent somatic alterations in genes involved in DNA methylation and post-translational histone modifications in T-ALL, suggesting that epigenetic homeostasis is critically required in restraining tumor development in the T-cell lineage. In this review, we provide an overview of the epigenetic regulators that could be implicated in T-ALL disease biology and speculate how the epigenetic landscape of T-ALL could trigger the development of epigenetic-based therapies to further improve the treatment of human T-ALL.},
  author       = {Peirs, Sofie and Van der Meulen, Joni and Van de Walle, Inge and Taghon, Tom and Speleman, Franki and Poppe, Bruce and Van Vlierberghe, Pieter},
  issn         = {0105-2896},
  journal      = {IMMUNOLOGICAL REVIEWS},
  keywords     = {epigenetics,T-ALL,therapeutics,ACUTE MYELOID-LEUKEMIA,FORSSMAN-LEHMANN-SYNDROME,HISTONE DEACETYLASE INHIBITORS,BET BROMODOMAIN INHIBITION,CHROMATIN REMODELER MI-2-BETA,GENE-EXPRESSION SIGNATURES,EMBRYONIC STEM-CELLS,DNA METHYLATION,SOMATIC MUTATIONS,IDH2 MUTATIONS},
  language     = {eng},
  number       = {1},
  pages        = {50--67},
  title        = {Epigenetics in T-cell acute lymphoblastic leukemia},
  url          = {http://dx.doi.org/10.1111/imr.12237},
  volume       = {263},
  year         = {2015},
}

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