Primary and secondary cutaneous angiosarcoma: Distinctive clinical, pathological and molecular features

Differences in potential key genes and pathways between primary and radiation-associated angiosarcoma of the breast

“…Angiosarcoma of the breast can be divided into primary and secondary malignancies. Primary angiosarcoma of the breast is a rare malignant tumor that occurs without a history of cancer or identifiable risk factors and usually occurs in women between the ages of 30 and 50 years [30] . Recently, multiple reports highlighted the increasing incidence in secondary breast angiosarcoma with the rise in the number of women with breast cancer treated with breast conservation therapy (BCT) and postoperative radiotherapy [ 22 , 30 , 31 ].…”

“…Primary angiosarcoma of the breast is a rare malignant tumor that occurs without a history of cancer or identifiable risk factors and usually occurs in women between the ages of 30 and 50 years [30] . Recently, multiple reports highlighted the increasing incidence in secondary breast angiosarcoma with the rise in the number of women with breast cancer treated with breast conservation therapy (BCT) and postoperative radiotherapy [ 22 , 30 , 31 ]. However, most current studies on primary and secondary angiosarcomas are case reports and little is known about the genetic abnormalities due to the lack of large-scale genomic studies, which seriously hinders the progress of diagnosis and treatment of angiosarcoma.…”

Hemoptoe, thin-walled lung cysts, and spontaneous pneumothorax are features of metastatic cutaneous angiosarcoma

“…Cutaneous angiosarcoma is a rare neoplasm that originates from endothelial cells of blood vessels. It accounts for less than 1% of all soft tissue sarcomas and typically develops on the face or scalp [ 1 ]. Elderly men are the most affected group.…”

“…Elderly men are the most affected group. cAS is often associated with either chronic lymphedema or previous irradiation [ 1 , 2 ].…”

Kutane Angiosarkome: molekulare Pathogenese und neue therapeutische Ansätze

“…Während sich bei sCAS Mutationen in KIT, FLT4, RET, UNC5A, CTLA4, ISRL2, ICOS, RAB17 und RASGRP3 finden, zeichnet sich pCAS durch Mutationen in TP53 sowie in mehreren Proteinen des MAP-Kinase-Signalwegs wie KRAS, HRAS, NRAS, BRAF, MAPK1 und NF1 aus. Darüber hinaus weist pCAS Mutationen in PTPRB/VE-PTP, PLCG1, NTSR-1, ANKRD1 und CDKN2A sowie in dem Fusionsgen NUP160-SCL43A3 auf[16][17][18][19]. Bemerkenswert ist, dass der Funktionsverlust von TP53 und die Amplifikation/Überexpression von Myc fast ausschließlich bei pCAS beziehungsweise sCAS auftreten.…”