Physicians

Departments / Divisions

• Pediatrics / Pediatrics-Hematology/Oncology
• Pharmacology & Cancer Biology

Address
DUMC 102382
Durham, NC 27710

Appointment Telephone
919-684-3401

Office Telephone
919-684-3401

Fax Telephone
919-681-7950

Training

• MD, Duke University School of Medicine, 1995

Residency

• Pediatrics, Children's Hospital of Philadelphia (Pennsylvania), 1995-1998

Fellowship

• Pediatric Hematology-Oncology, Children's Hospital of Philadelphia (Pennsylvania), 1998-1999
• Pediatric Hematology-Oncology, Duke University Medical Center, 1999-2001

Other Training

• PhD, Cell Biology, Duke University, 1993

Clinical Interests
Pediatric hematology-oncology with emphasis on caring for children, adolescents, young adults with sarcomas

Research Interests
Pediatric Sarcomas: Sarcomas are among the most difficult-to-treat cancers in pediatric oncology, with metastatic forms having the highest mortality. We have established genetically defined human cell-based models for the pediatric skeletal muscle cancer known as rhabdomyosarcoma. Current therapies are based on xenograft models in immunocompromised mice, using established patient-derived patient cell lines, but because of the genetic variability of these cell lines, a true understanding of the causative role of certain genetic changes (e.g. chromosomal translocations) in rhabdomyosarcoma formation is not understood. Specific goals of this research program include the identification of signaling pathways corrupted in rhabdomyosarcoma, with focus on the PAX3-FOXO1 mutation and its downstream effectors, and identification of new therapeutic targets for treatment of this childhood cancer.

Industry Relationships and Collaborations (What's this?)

This faculty member has no reported relationships with industry.

Representative Publications
Belyea, B; Kephart, JG; Blum, J; Kirsch, DG; Linardic, CM. Embryonic signaling pathways and rhabdomyosarcoma: contributions to cancer development and opportunities for therapeutic targeting. Sarcoma. 2012;2012:406239. (2012) Abstract

Crose, LE; Etheridge, KT; Chen, C; Belyea, B; Talbot, LJ; Bentley, RC; Linardic, CM. FGFR4 blockade exerts distinct antitumorigenic effects in human embryonal versus alveolar rhabdomyosarcoma. Clinical Cancer Research. 2012;18:3780-3790. (2012) Abstract

Ignatius, MS; Chen, E; Elpek, NM; Fuller, AZ; Tenente, IM; Clagg, R; Liu, S; Blackburn, JS; Linardic, CM; Rosenberg, AE; Nielsen, PG; Mempel, TR; Langenau, DM. In vivo imaging of tumor-propagating cells, regional tumor heterogeneity, and dynamic cell movements in embryonal rhabdomyosarcoma. Cancer Cell. 2012;21:680-693. (2012) Abstract

Belyea, BC; Naini, S; Bentley, RC; Linardic, CM. Inhibition of the Notch-Hey1 axis blocks embryonal rhabdomyosarcoma tumorigenesis. Clinical Cancer Research. 2011;17:7324-7336. (2011) Abstract

Crose, LE; Linardic, CM. Receptor tyrosine kinases as therapeutic targets in rhabdomyosarcoma. Sarcoma. 2011;2011:756982. (2011) Abstract

Linardic, CM. PAX3-FOXO1 fusion gene in rhabdomyosarcoma. Cancer Letters. 2008;270:10-18. (2008) Abstract

Linardic, CM; Counter, CM. Genetic modeling of Ras-induced human rhabdomyosarcoma. Methods in Enzymology. 2008;438:419-427. (2008) Abstract

Naini, S; Etheridge, KT; Adam, SJ; Qualman, SJ; Bentley, RC; Counter, CM; Linardic, CM. Defining the cooperative genetic changes that temporally drive alveolar rhabdomyosarcoma. Cancer Research. 2008;68:9583-9588. (2008) Abstract

Linardic, CM; Naini, S; Herndon, JE; Kesserwan, C; Qualman, SJ; Counter, CM. The PAX3-FKHR fusion gene of rhabdomyosarcoma cooperates with loss of p16INK4A to promote bypass of cellular senescence. Cancer Research. 2007;67:6691-6699. (2007) Abstract

Kendall, SD; Linardic, CM; Adam, SJ; Counter, CM. A network of genetic events sufficient to convert normal human cells to a tumorigenic state. Cancer Research. 2005;65:9824-9828. (2005) Abstract

Linardic, CM; Downie, DL; Qualman, S; Bentley, RC; Counter, CM. Genetic modeling of human rhabdomyosarcoma. Cancer Research. 2005;65:4490-4495. (2005) Abstract