Please use this identifier to cite or link to this item:
Scopus Web of Science® Altmetric
Type: Journal article
Title: Methotrexate toxicity in growing long bones of young rats: A model for studying cancer chemotherapy-induced bone growth defects in children
Author: Fan, C.
Georgiou, K.
King, T.
Xian, C.
Citation: Journal of Biomedicine and Biotechnology, 2011; 2011:1-8
Publisher: Hindawi Publishing Corporation
Issue Date: 2011
ISSN: 1110-7243
Statement of
Chiaming Fan, Kristen R. Georgiou, Tristan J. King, and Cory J. Xian
Abstract: The advancement and intensive use of chemotherapy in treating childhood cancers has led to a growing population of young cancer survivors who face increased bone health risks. However, the underlying mechanisms for chemotherapy-induced skeletal defects remain largely unclear. Methotrexate (MTX), the most commonly used antimetabolite in paediatric cancer treatment, is known to cause bone growth defects in children undergoing chemotherapy. Animal studies not only have confirmed the clinical observations but also have increased our understanding of the mechanisms underlying chemotherapy-induced skeletal damage. These models revealed that high-dose MTX can cause growth plate dysfunction, damage osteoprogenitor cells, suppress bone formation, and increase bone resorption and marrow adipogenesis, resulting in overall bone loss. While recent rat studies have shown that antidote folinic acid can reduce MTX damage in the growth plate and bone, future studies should investigate potential adjuvant treatments to reduce chemotherapy-induced skeletal toxicities.
Keywords: Animals; Humans; Rats; Neoplasms; Bone Diseases; Disease Models, Animal; Methotrexate; Antineoplastic Agents; Bone Development; Child
Rights: Copyright © 2011 Chiaming Fan et al.
RMID: 0020107337
DOI: 10.1155/2011/903097
Appears in Collections:Paediatrics publications

Files in This Item:
There are no files associated with this item.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.