The role of adipose tissue and obesity in causing treatment resistance of acute lymphoblastic leukemia

Obesity is responsible for ~90,000 cancer deaths/year, increasing cancer incidence and impairing its treatment. Obesity has also been shown to impact hematological malignancies, through as yet unknown mechanisms. Adipocytes are present in bone marrow and the microenvironments of many types of cancer...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in pediatrics Vol. 2; p. 53
Main Authors Sheng, Xia, Mittelman, Steven D
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 01.01.2014
Subjects
Adipocytes, White
Apoptosis
Drug Resistance
Leukemia
Lipolysis
Obesity
Pediatrics
leukemia
pharmacokinetics
apoptosis
tumor microenvironments
drug resistance
lipolysis
adipocytes
obesity
Online AccessGet full text

Cover

More Information
Summary:Obesity is responsible for ~90,000 cancer deaths/year, increasing cancer incidence and impairing its treatment. Obesity has also been shown to impact hematological malignancies, through as yet unknown mechanisms. Adipocytes are present in bone marrow and the microenvironments of many types of cancer, and have been found to promote cancer cell survival. In this review, we explore several ways in which obesity might cause leukemia treatment resistance. Obese patients may be at a treatment disadvantage due to altered pharmacokinetics of chemotherapy and dosage "capping" based on ideal body weight. The adipose tissue provides fuel to cancer cells in the form of amino acids and free fatty acids. Adipocytes have been shown to cause cancer cells to resist chemotherapy-induced apoptosis. In addition, obese adipose tissue is phenotypically altered, producing a milieu of pro-inflammatory adipokines and cytokines, some of which have been linked to cancer progression. Given the prevalence of obesity, understanding its role and adipose tissue in acute lymphoblastic leukemia treatment is necessary for evaluating current treatment regimen and revealing new therapeutic targets.
Bibliography:Edited by: Alan Wayne, Children’s Hospital Los Angeles, USA
Reviewed by: Francis Jay Mussai, Birmingham Children’s Hospital, UK; Elizabeth Ann Raetz, The University of Utah, USA
This article was submitted to Pediatric Oncology, a section of the journal Frontiers in Pediatrics.
ISSN:2296-2360
2296-2360
DOI:10.3389/fped.2014.00053