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A novel mouse model of radiation-induced cancer survivorship diseases of the gut.

Journal article
Authors Cecilia Bull
Dilip Malipatlolla
Marie Kalm
Fei Sjöberg
Eleftheria Alevronta
Rita Grandér
Linda Persson
Martina Boström
Yohanna Eriksson
John Swanpalmer
Agnes E Wold
Klas Blomgren
Thomas Björk-Eriksson
Gunnar Steineck
Published in American journal of physiology. Gastrointestinal and liver physiology
Volume 313
Pages G456-G466
ISSN 1522-1547
Publication year 2017
Published at Institute of Clinical Sciences, Section for Oncology, Radiation Physics, Radiology and Urology, Department of Radiation Physics
Institute of Clinical Sciences, Section for Oncology, Radiation Physics, Radiology and Urology, Department of Oncology
Institute of Neuroscience and Physiology, Department of Pharmacology
Institute of Biomedicine, Department of Infectious Medicine
Pages G456-G466
Language en
Links dx.doi.org/10.1152/ajpgi.00113.2017
Subject categories Cancer and Oncology


A deeper understanding of the radiation-induced pathophysiological processes that develop in the gut is imperative in order to prevent, alleviate or eliminate cancer survivorship diseases after radiotherapy to the pelvic area. Most rodent models of high-dose gastrointestinal radiation injury are limited by high mortality. We therefore established a model that allows for the delivering of radiation in fractions at high doses, while maintaining long-term survival. Adult male C57/BL6 mice were exposed to small-field irradiation, restricted to 1,5 cm of the colorectum using a linear accelerator. Each mouse received 6 or 8 Gy, twice daily in 12 hours intervals, in 2, 3 or 4 fractions. Acute cell death was examined at 4.5 hours post-irradiation, and histological changes at six weeks post-irradiation. Another group was given 4 fractions of 8 Gy and followed over time for development of visible symptoms. Irradiation caused immediate cell death, mainly limited to the colorectum. At six weeks post-irradiation, several crypts displayed signs of radiation-induced degeneration. The degenerating crypts were seen alongside crypts that appeared perfectly healthy. Crypt survival was reduced after the fourth fraction regardless of dose, while the number of macrophages increased. Angiogenesis was induced, likely as a compensatory mechanism for hypoxia. Four months post-irradiation, mice began to show radiation-induced symptoms, and histological examination revealed an extensive crypt loss and fibrosis. Our model is uniquely suitable for studying the long-term trajectory and underlying mechanisms of radiation-induced gastrointestinal injury.

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