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11 - Molecular genetics of acute myeloid leukemia

from Part II - Cell biology and pathobiology

Published online by Cambridge University Press:  01 July 2010

Robert B. Lorsbach
Affiliation:
Assistant Member, Department of Pathology St. Jude Children's Research Hospital, St. Jude Children's Research Hospital, Memphis, TN, USA
James R. Downing
Affiliation:
Member and Chair, Department of Pathology, Scientific Director, St. Jude Children's Research Hospital, Memphis, TN, USA
Ching-Hon Pui
Affiliation:
St. Jude Children's Research Hospital, Memphis
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Summary

Introduction

One of the goals of modern leukemia research has been to gain a clearer understanding of the nature of the underlying molecular genetic lesions responsible for the establishment of the leukemic clone. This pursuit is fueled by the hope that the information obtained will not only help us understand the variability in clinical response that is observed among leukemia patients, but will also lead to the identification of rational molecular targets for novel chemotherapeutic agents. This goal is starting to be realized through recent advances in our understanding of the pathogenesis of acute myeloid leukemia (AML). Specifically, molecular genetic and genomic data are beginning to provide the initial framework for the subclassification of AML into clinically meaningful subgroups, and rationally designed compounds that inhibit novel molecular targets in leukemic cells are beginning to be assessed clinically for their utility as antileukemic therapeutics.

In this chapter, we provide a summary of the recent advances that have been made in elucidating the molecular genetic lesions involved in the pathogenesis of de novo AML. Our approach is to describe the structure of identified genetic lesions and explain at a molecular level how these alterations lead to cellular transformation. Because of the distinct clinical and biologic differences that exist between de novo AML and myelodysplasia-related AML, we largely restrict our discussion to de novo AML, which lacks any evidence of a prior or concurrent myelodysplastic phase.

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Childhood Leukemias , pp. 298 - 338
Publisher: Cambridge University Press
Print publication year: 2006

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  • Molecular genetics of acute myeloid leukemia
    • By Robert B. Lorsbach, Assistant Member, Department of Pathology St. Jude Children's Research Hospital, St. Jude Children's Research Hospital, Memphis, TN, USA, James R. Downing, Member and Chair, Department of Pathology, Scientific Director, St. Jude Children's Research Hospital, Memphis, TN, USA
  • Edited by Ching-Hon Pui
  • Book: Childhood Leukemias
  • Online publication: 01 July 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511471001.012
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  • Molecular genetics of acute myeloid leukemia
    • By Robert B. Lorsbach, Assistant Member, Department of Pathology St. Jude Children's Research Hospital, St. Jude Children's Research Hospital, Memphis, TN, USA, James R. Downing, Member and Chair, Department of Pathology, Scientific Director, St. Jude Children's Research Hospital, Memphis, TN, USA
  • Edited by Ching-Hon Pui
  • Book: Childhood Leukemias
  • Online publication: 01 July 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511471001.012
Available formats
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  • Molecular genetics of acute myeloid leukemia
    • By Robert B. Lorsbach, Assistant Member, Department of Pathology St. Jude Children's Research Hospital, St. Jude Children's Research Hospital, Memphis, TN, USA, James R. Downing, Member and Chair, Department of Pathology, Scientific Director, St. Jude Children's Research Hospital, Memphis, TN, USA
  • Edited by Ching-Hon Pui
  • Book: Childhood Leukemias
  • Online publication: 01 July 2010
  • Chapter DOI: https://doi.org/10.1017/CBO9780511471001.012
Available formats
×