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Xu et al. Plast Aesthet Res 2017;4:116-26 Plastic and
DOI: 10.20517/2347-9264.2017.24
Aesthetic Research
www.parjournal.net
Topic: Keloid and its Treatment Open Access
The radiation therapy in keloids treatment: a
comprehensive review of pathomechanism,
damage mechanisms and cellular response
Jing Xu , Elan Yang , Nan-Ze Yu , You-Bin Wang , Xiao Long
2
1
2
2
2
1 Peking Union Medical College, Beijing 100730, China.
2 Department of Plastic Surgery, Peking Union Medical College Hospital, Beijing 100730, China.
Correspondence to: Dr. Xiao Long, Department of Plastic Surgery, Peking Union Medical College Hospital, Shuaifuyuan 1#, Beijing 100730,
China. E-mail: pumclongxiao@126.com
How to cite this article: Xu J, Yang E, Yu NZ, Wang YB, Long X. The radiation therapy in keloids treatment: a comprehensive review of pathomechanism,
damage mechanisms and cellular response. Plast Aesthet Res 2017;4:116-26.
Dr. Xiao Long is associate Professor in Peking Union Medical College Hospital (PUMCH), Division of Plastic and
Reconstructive Surgery. She received her doctor’s degree from Peking Union Medical College in 2005. Now she
serves as the vice chairman of the Youth Committee of the Chinese Medical Association of Plastic Surgeons. In
2015, she was recognized as one of the Top Ten Outstanding Young Doctors by China Youth Daily.
ABSTRACT
Article history: Keloid management has always been frustrating and challenging. The combination therapy
Received: 21-03-2017 of surgical excision and radiation therapy was deemed as the last resort for decades. The
Accepted: 15-07-2017 authors performed a thorough and comprehensive review over the mechanisms on how
Published: 28-07-2017 radiation therapy damages the keloid cells. The keloid cells’ cellular response towards
damage induced by irradiation was also studied based on original and current literatures.
Key words: Mechanisms of damage generated by radiation therapy on keloid cells remained partially
Radiation therapy, understood. However, direct damage was identified playing dominant role, in contrast to
keloids, damage involved cancer cell apoptosis. Moreover, the p53 pathway and some inflammatory
combination therapy factors like interleukin-6 were believed to function in cellular response to irradiation.
However, the transforming growth factor beta, which was the major dysregulated pathway
involved in pathogenesis of keloid formation showed no apparent correlation with cellular
response to irradiation damage. These pathways could partially explain radiation resistance
in some refractory keloid lesions. The scientific basis and experimental proof in this field was
still inadequate, which drove us to find more evidence to identify the key regulator response
to damage engendered by radiation therapy. Further pathway identification may benefit the
drug development to prevent keloid recurrence.
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