What is the pathophysiology of postradiation sarcoma (PRS)?

Updated: Jul 01, 2020
  • Author: Nagarjun Rao, MD, FRCPath; Chief Editor: Omohodion (Odion) Binitie, MD  more...
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PRS can occur with orthovoltage (low-energy) and megavoltage (high-energy) radiation. With orthovoltage radiation, the dosages are lower and the latent periods longer. The threshold dose for PRS is not known, though in most published series, a dose of 40-60 Gy has been reported. [2, 11, 12] Development of PRS also is influenced by other factors, including genetic tendency and influence of chemotherapeutic agents.

Ionizing radiation is thought to act via genetic alterations, including mutations of p53 and retinoblastoma (Rb) genes. Experimental studies revealed p53 gene alterations or increased p53 messenger ribonucleic acid (mRNA) levels in murine PRS. [13]

A study by Mentzel et al used fluorescence in situ hybridization (FISH) to analyze angiosarcomas and atypical vascular lesions occurring after treatment of breast cancer. [14] In all postradiation cutaneous angiosarcomas, FISH analysis revealed MYC amplification in a variable number of counted nuclei; MYC amplification was not seen in any of the other cases. The authors concluded that MYC amplification may be an important diagnostic tool for distinguishing postradiation cutaneous angiosarcomas from atypical vascular lesions after radiotherapy.

A study by Laé et al found that C-MYC amplification was able to distinguish postradiation breast angiosarcomas from primary breast angiosarcomas, even though the two lesions were morphologically indistinguishable. [15]

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