Genetically mediated Nf1 loss in mice promotes diverse radiation-induced tumors modeling second malignant neoplasms.

ABSTRACT: Second malignant neoplasms (SMN) are therapy-induced malignancies and a growing problem in cancer survivors, particularly survivors of childhood cancers. The lack of experimental models of SMNs has limited understanding of their pathogenesis. It is currently not possible to predict or prevent this devastating late complication. Individuals with neurofibromatosis I (NF1) are at increased risk of developing therapy-induced cancers for unclear reasons. To model SMNs, we replicated clinical radiotherapy and delivered fractionated abdominal irradiation to Nf1(+/-) and wild-type mice. Similar to irradiated cancer survivors, irradiated wild-type and Nf1(+/-) mice developed diverse in-field malignancies. In Nf1(+/-) mice, fractionated irradiation promoted both classical NF1-associated malignancies

SUBMITTER: Choi G 

PROVIDER: S-EPMC3787120 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature