Short communication: normal tissue injury after cancer therapy is a local response exacerbated by an endocrine effect of TGF beta.
The sensitivity of normal tissues rather than of the tumour usually limits the effectiveness of cancer treatment. The normal tissue side effects from chemotherapy and/or radiotherapy result from both direct cellular loss and the extensive fibrosis that develops at the site of injury. Recent evidence suggests that the cytokine, transforming growth factor beta (TGF beta), mediates this fibrogenic process. Herein, we provide evidence in support of the hypothesis that the fibrosis formation following therapy results not only from TGF beta produced locally in the injured normal tissue, but also from circulating TGF beta released by the tumour. Thus, therapy-induced normal tissue damage appears in part to be a local manifestation of a systemic condition.
Anscher
M S
MS
Department of Radiation Oncology, Duke University Medical Center, Durham, NC 27710, USA.
Kong
F M
FM
Murase
T
T
Jirtle
R L
RL
D000970:Antineoplastic Agents / Q000009:adverse effects*; D005355:Fibrosis; D006801:Humans; D008168:Lung / Q000528:radiation effects; D009369:Neoplasms / Q000097:blood / Q000628:therapy*; D011832:Radiation Injuries / Q000378:metabolism; D011878:Radiotherapy / Q000009:adverse effects*; D016212:Transforming Growth Factor beta / Q000009:adverse effects* / Q000097:blood
D000970:Antineoplastic Agents; D016212:Transforming Growth Factor beta