Sporadic versus Radiation-Associated Angiosarcoma: A Comparative Clinicopathologic and Molecular Analysis of 48 Cases

Abstract

Angiosarcomas are aggressive tumors of vascular endothelial origin, occurring sporadically or in association with prior radiotherapy. We compared clinicopathologic and biologic features of sporadic angiosarcomas (SA) and radiation-associated angiosarcomas (RAA). Methods. From a University of Michigan institutional database, 37 SA and 11 RAA were identified. Tissue microarrays were stained for p53, Ki-67, and hTERT. DNA was evaluated for TP53 and ATM mutations. Results. Mean latency between radiotherapy and diagnosis of RAA was 11.9 years: 6.7 years for breast RAA versus 20.9 years for nonbreast RAA (P = 0.148). Survival after diagnosis did not significantly differ between SA and RAA (P = 0.590). Patients with nonbreast RAA had shorter overall survival than patients with breast RAA (P = 0.03). The majority of SA (86.5%) and RAA (77.8%) were classified as high-grade sarcomas (P = 0.609). RAA were more likely to have well-defined vasoformative areas (55.6% versus 27%, P = 0.127). Most breast SA were parenchymal in origin (80%), while most breast RAA were cutaneous in origin (80%). TMA analysis showed p53 overexpression in 25.7% of SA and 0% RAA, high Ki-67 in 35.3% of SA and 44.4% RAA, and hTERT expression in 100% of SA and RAA. TP53 mutations were detected in 13.5% of SA and 11.1% RAA. ATM mutations were not detected in either SA or RAA. Conclusions. SA and RAA are similar in histology, immunohistochemical markers, and DNA mutation profiles and share similar prognosis. Breast RAA have a shorter latency period compared to nonbreast RAA and a significantly longer survival.

Hepatic small vessel neoplasm, a rare infiltrative vascular neoplasm of uncertain malignant potential

“…We did not find any specific toxin or drug exposure in review of HSVN patient history. MYC amplification has been established in some primary (non–radiation-associated) cutaneous ASs [1], and a subset of nonhepatic, sporadic ASs has abnormal p53/ TP53 [26]; we found IHC evidence to support similar changes in hepatic AS but no IHC or molecular evidence of a MYC or TP53 abnormality in HSVN.…”

Cutaneous angiosarcoma: a current update

“…Vorburger et al demonstrated a shorter mean latency period (between initiation of radiation therapy and development of AS) of 7.6 years for breast RAA, compared with 20.9 years for RAA arising in other anatomic sites 7. A study by Hung et al comparing RAA and sporadic AS of the breast showed that 80% of RAA were cutaneous in origin, compared with sporadic AS, of which 80% demonstrated parenchymal origin 8. Interestingly, there appears to be no difference in survival between sporadic AS and RAA of the breast 7 9…”

Combined hepatocellular‐cholangiocarcinoma with angiosarcomatoid change: A case report with immunohistochemical study

“…Mutations of the TP53 gene in angiosarcomas were examined in some studies. Although their results varied, TP53 gene mutations were found in 4–52% of cases, and overexpression of p53 was immunohistochemically detected in 20–49% of cases …”

“…Although their results varied, TP53 gene mutations were found in 4-52% of cases, and overexpression of p53 was immunohistochemically detected in 20-49% of cases. [16][17][18] In this case, undifferentiated sarcomatoid cells expressing pan-cytokeratin were detected in the transitional zone between HCC and mesenchymal cells, indicating that the sarcomatoid cells might have been derived from carcinoma cells via a metaplastic or dedifferentiation process. The tumor showed strong and diffuse expression of p53 protein in the nucleus of angiosarcomatoid cells in contrast to lower levels of expression in undifferentiated sarcomatoid and carcinoma cells.…”