%A Spraker,Holly %A Price,Shawn %A Chaturvedi,Aashi %A Schiffman,Joshua %A Jones,Kevin %A Lessnick,Stephen %A Beckerle,Mary %A Randall,R. Lor %D 2012 %J Frontiers in Oncology %C %F %G English %K Clones,Ewing sarcoma,Metastatic %Q %R 10.3389/fonc.2012.00002 %W %L %M %P %7 %8 2012-January-16 %9 Perspective %+ Dr Holly Spraker,Primary Children's Medical Center, University of Utah,Pediatric Hematology-Oncology,100 North Mario Capecchi Drive,PCMC - 4th Floor Oncology,Salt Lake City,84113,UT,United States,holly.spraker@imail.org %+ Dr Holly Spraker,Huntsman Cancer Institute - Unversity of Utah,2000 Circle of Hope Drive,Salt Lake City,84112,UT,United States,holly.spraker@imail.org %# %! Ewing sarcoma metastatic clones %* %< %T The Clone Wars – Revenge of the Metastatic Rogue State: The Sarcoma Paradigm %U https://www.frontiersin.org/articles/10.3389/fonc.2012.00002 %V 2 %0 JOURNAL ARTICLE %@ 2234-943X %X Ewing sarcoma (ES) is the second most common bone tumor affecting primarily adolescents and young adults. Despite recent advances in biological understanding, intensification of chemotherapeutic treatments, and progress in local control with surgery and/or radiation therapy, patients with metastatic or recurrent ES continue to have a dismal prognosis with less than 20% overall survival. All ES is likely metastatic at diagnosis although our methods of detection and classification may not account for this. Progressive disease may arise via a combination of: (1) selection of chemotherapy-resistant clones in primary tumor, (2) signaling from bone or lung microenvironments that may attract tumor cells to distant locations, and/or (3) genetic changes within the ES cells themselves due to DNA-damaging chemotherapeutic agents or other “hits.” These possibilities and the evidence base to support them are explored.