Rhabdomyosarcoma (RMS) is a high-risk pediatric sarcoma that resembles developing skeletal muscle. Transcriptional dysregulation drives RMS pathogenesis in tumors carrying chimeric transcription factors (“fusion-positive (FP)”), and those without (“fusion-negative” (FN)). Here, we develop a novel approach against RMS...
Brian J. Abraham, Annika L. Gustafson, S. Nance et al.· Cancer Research· 0 citations
Sequential changes in transcriptional cell state are essential for normal development and are coopted in cancer. Controlling these changes for therapeutic benefit has been challenged by a lack of tools reflecting distinct states in live cells. Here, using the pediatric solid tumor high-risk neuroblastoma, which displ...
Noha A. M. Shendy, Yang E. Zhang, Brian J. Abraham et al.· Cancer Research· 0 citations
Resistance to conventional chemotherapies is a major cause of cancer patient relapse and subsequent death. The fundamental biological properties of tumor cells are not only driven by acquired genetic mutations, but also by aberrant epigenetic regulation leading to corresponding changes in the expressed transcriptome....
G. McKay-Corkum, Noha A. M. Shendy, S. Nance et al.· Cancer Research· 0 citations
Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma. Alveolar RMS (ARMS) has a poor prognosis and is driven by either t(2;13)(q35;q14) or t(1;13)(p36;q14) translocations resulting in the PAX3::FOXO1 (P3F) and PAX7::FOXO1 (P7F) fusion oncoproteins, respectively. Current in vivo model systems fail t...
Bradley T. Stevens, Yang E. Zhang, Matthew R. Garcia et al.· Cancer Research· 0 citations
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