Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Feb;62(1):47-60.
doi: 10.1016/j.pcl.2014.09.004.

Biology of childhood acute lymphoblastic leukemia

Affiliations
Review

Biology of childhood acute lymphoblastic leukemia

Deepa Bhojwani et al. Pediatr Clin North Am. 2015 Feb.

Abstract

Giant strides have been made in the management of childhood acute lymphoblastic leukemia (ALL) over previous decades. Extensive collaborative efforts internationally have played a vital role in the remarkable progress made in not only improving therapeutic outcomes but also deciphering the complex biology of childhood ALL. This review summarizes various insights gained from biological studies of childhood ALL, with a focus on recent studies, and also discusses genomic lesions and epigenetic regulatory mechanisms associated with leukemic transformation. The importance of studying the biology of the host so as to understand additional heterogeneity in treatment response and toxicities is highlighted.

Keywords: Childhood acute lymphoblastic leukemia; Chromosomal alterations; Genomics; Host germline polymorphisms.

PubMed Disclaimer

Figures

Figure 1
Figure 1. Distribution of molecular subtypes of childhood B-ALL
The pie chart on the left depicts molecular subtypes that were identified prior to 2004, incorporated in the 2008 WHO classification and are currently used for risk stratification. Subtype was unknown in 22% of patients (termed B-other). Since then, various novel molecular subtypes have been characterized shown in the bar graph on the right. Data has been modified from Pui CH, Relling MV, Downing JR. Acute lymphoblastic leukemia. N Engl J Med. 2004;350: 1535–1548; and from Pui CH, Mullighan CG, Evans WE, Relling MV. Pediatric acute lymphoblastic leukemia: Where are we going and how do we get there? Blood. 2012;120: 1165–1174. NOS: not otherwise specified
Figure 2
Figure 2. Pathogenesis of ALL
Several inherited variants associated with susceptibility to ALL have been identified by genome– wide association studies and studies of familial ALL. Within hematopoietic cells, in addition to a sentinel event such as a chromosomal translocation, a multitude of secondary genetic events contribute to leukemic transformation.

References

    1. Ward E, DeSantis C, Robbins A, Kohler B, Jemal A. Childhood and adolescent cancer statistics, 2014. CA Cancer J Clin. 2014;64:83–103. - PubMed
    1. Pui CH, Evans WE. A 50-year journey to cure childhood acute lymphoblastic leukemia. Semin Hematol. 2013;50:185–196. - PMC - PubMed
    1. Hunger SP, Lu X, Devidas M, et al. Improved survival for children and adolescents with acute lymphoblastic leukemia between 1990 and 2005: a report from the children's oncology group. J Clin Oncol. 2012;30:1663–1669. - PMC - PubMed
    1. Schultz KR, Carroll A, Heerema NA, et al. Long-term follow-up of imatinib in pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia: Children's Oncology Group study AALL0031. Leukemia. 2014;28:1467–1471. - PMC - PubMed
    1. Pui CH, Yang JJ, Hunger SP, et al. Childhoof Acute Lymphoblastic Leukemia: Progress Through Collaboration. J Clin Oncol. 2014 (in press) - PMC - PubMed

Publication types

MeSH terms