MYC High Level Gene Amplification Is a Distinctive Feature of Angiosarcomas after Irradiation or Chronic Lymphedema

Malignant vascular tumors—an update

“…27 Furthermore, high level MYC amplification on 8q24 is a consistent hallmark of radiation-induced and lymphedema-associated angiosarcoma. 28,29 FLT4 (encoding for VEGFR3) co-amplification on 5q35 is detected in 25% of secondary angiosarcoma. Both MYC and FLT4 gene abnormalities have not been reported in radiation-associated atypical vascular lesions, thus far and can serve as a powerful molecular or immunohistochemical test in difficult cases (Figures 3d-f).…”

Post-radiation Atypical Vascular Lesion/Angiosarcoma Arising in the Larynx

“…C-myc amplification has been reported in the majority of post-radiation AS arising in the breast [4,6,8]. Although it was negative in our case, several cases of post-radiation AS with negative C-myc amplification have been reported [1,12].…”

“…In our case, C-myc amplification was negative and did not support a diagnosis of AS. Several cases of C-myc amplification negative post-radiation AS have been reported [1,12], and thus its possibility could not be completely excluded. In addition, C-myc amplification has not been specifically investigated in the laryngeal region and may not play a role in post-radiation AS that arise in this region.…”

“…Atypical vascular lesions (AVL) and angiosarcomas (AS) are lesions known to arise after radiation therapy [1][2][3][4][5][6][7][8][9][10][11][12]. They are most commonly described in the breast region status post radiation for breast carcinoma.…”

Active TGF-β signaling and decreased expression of PTEN separates angiosarcoma of bone from its soft tissue counterpart

“…[22][23][24] In that perspective, high levels of MYC amplification are found in 55-100% of angiosarcomas secondary to radiation exposure or chronic lymphedema after breast surgery and radiation, which is in 25% associated with FLT4 (FMSlike tyrosine kinase-4 encoding for VEGFR3) amplification. [22][23][24] In addition, KDR (kinase insert domain receptor, VEGFR2) mutations are present in 10% of angiosarcoma of the breast, either primary or secondary to radiation exposure. 22,23 These findings implicate that, based on tumor-specific alterations, angiosarcoma of soft tissue is highly heterogeneous.…”