Troy McEachron, Ph.D.

Troy McEachron Assistant Professor of Research Translational Genomics Department of Translational Genomic Health Sciences Campus NRT 1450 Biggy St. Los Angeles +1 323 442 6049 mceachro@usc.edu — Assistant Professor of Research Translational Genomics
Department of Translational Genomic
Health Sciences Campus
NRT 1450 Biggy St. Los Angeles
+1 323 442 6049
mceachro@usc.edu

My research focuses on two separate yet complimentary areas: (1) the utilization of next generation genomic, transcriptomic, and proteomic technologies to profile recurrent and/or refractory pediatric, adolescent, and young adult (AYA) cancer patients for clinical decision making; (2) the use of functional genomics to identify and interrogate the developmental and therapeutic aspects of sarcomas that predominantly arise in the pediatric and AYA populations. My overall research interests are a reflection of my diverse training history. My training background in basic science includes the molecular dissection of autocrine and paracrine signaling mechanisms between tumor and host using in vitro and in vivo models and the characterization of genetically engineered mouse models of pediatric brain tumors. Additionally, my translational science training includes the interpretation and functional validation next generation sequencing data from recurrent/refractory pediatric cancer patients.

Over time I have gained an immense interest in rhabdomyosarcomas (RMS), desmoplastic small round cell tumors (DSRCT), Ewing sarcomas (EWS), and clear cell sarcomas (CCS). The relatively low mutation burden in numerous different types of sarcomas suggests that there are transcriptional and/or epigenetic mechanisms that drive these diseases. This is inline with recent studies suggesting that epigenetic dysregulation and altered developmental programing drive many pediatric malignancies. Moreover, the mechanisms by which sarcoma-specific oncogenic fusion genes initiate and/or sustain disease remains elusive. My laboratory is dedicated to developing new biological tools and approaches to enable a functional genomics inquiry into these mechanisms as to reveal insight into the underlying biology of these sarcomas. Additionally, we will interrogate patient derived material to better define the molecular characteristics of different sarcoma subtypes to enable more precise treatment strategies for these difficult diseases.

PUBLICATIONS

Molecular Genetic Profiling of Adolescent Glassy Cell Carcinoma of the Cervix Reveals Targetable EGFR Amplification with Potential Therapeutic Implications. J Adolesc Young Adult Oncol. 2016 Sep; 5(3):297-302. View in: PubMed

Successful Treatment of Genetically Profiled Pediatric Extranodal NK/T-Cell Lymphoma Targeting Oncogenic STAT3 Mutation. Pediatr Blood Cancer. 2016 Apr; 63(4):727-30. View in: PubMed

Small cell carcinoma of the ovary, hypercalcemic type, displays frequent inactivating germline and somatic mutations in SMARCA4. Nat Genet. 2014 May; 46(5):427-9. View in: PubMed

Histone H3 mutations in pediatric brain tumors. Cold Spring Harb Perspect Biol. 2014 Apr; 6(4):a018689. View in: PubMed

Histone H3 mutations in pediatric brain tumors. Cold Spring Harb Perspect Biol. 2014 Apr 01; 6(4):a018689. View in: PubMed

An integrated approach to identifying clinically relevant targets in pediatric gliomas. CNS Oncol. 2013 Jul; 2(4):303-6. View in: PubMed

PF4/heparin-antibody complex induces monocyte tissue factor expression and release of tissue factor positive microparticles by activation of Fc?RI. PF4/heparin-antibody complex induces monocyte tissue factor expression and release of tissue factor positive microparticles by activation of Fc? RI. Blood. 2012 May 31; 119(22):5285-93. View in: PubMed

Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas. Nat Genet. 2012 Mar; 44(3):251-3. View in: PubMed

Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas. Nat Genet. 2012 Jan 29; 44(3):251-3. View in: PubMed

Regulation of thrombin-induced plasminogen activator inhibitor-1 in 4T1 murine breast cancer cells. Blood Coagul Fibrinolysis. 2011 Oct; 22(7):576-82. View in: PubMed

Protease-activated receptors mediate crosstalk between coagulation and fibrinolysis. Blood. 2010 Dec 02; 116(23):5037-44. View in: PubMed

Protease-activated receptors mediate crosstalk between coagulation and fibrinolysis. Blood. 2010 Dec 2; 116(23):5037-44. View in: PubMed

Tumors, ticks and tissue factor. J Thromb Haemost. 2009 Nov; 7(11):1852-4. View in: PubMed