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Casey Langdon PhD

Casey G Langdon PhD

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  • Assistant Professor
  • College of Medicine
  • Pediatrics
Academic Focus
  • Sarcoma
  • Cancer cell biology
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Office Location


Education & Training:

Campbell University, 2008, B.S. in Biochemistry and Biology (double major)
Yale University, 2015, PhD in Experimental Pathology (PI – David F. Stern)
St. Jude Children’s Research Hospital, 2015-2022, Postdoctoral Research Associate (PI – Mark Hatley)



Research Interests:


The Langdon Laboratory’s mission is to elucidate the intricacies and mechanisms underlying how different oncogenic events shape cancer cell fate decisions in pediatric sarcomas with the goal to better tailor pharmacological interventions for these devastating tumors. We are initially focused on Ewing sarcoma. Ewing sarcoma is a devastating pediatric bone cancer with no new advancements in therapeutic options for these patients in decades. The Laboratory uses a combination of molecular biology techniques and pharmacological intervention strategies to assess different cooperating drivers that facilitate sarcomagenesis. The overarching goal of the Laboratory is two-fold: to perform high impact basic science to investigate the mechanistic determinants of Ewing sarcoma development and to translate that work into transformative care for these patients.


Highlight Publications:


1. Langdon, CG. Nuclear PTEN’s functions in suppressing tumorigenesis: Implications for rare cancers.(2023) Biomolecules 13(2):259. DOI: 10.3390/biom13020259. Review
Hanna, JA, Langdon CG, Garcia MR, Benton, A, Lanman NA, Finkelstein D, Rehg JE, and Hatley ME. Genetic context of oncogenic drivers dictates vascular sarcoma development in aP2-Cre mice. (2022) JPathol 257(1):109-24. DOI: 10.1002/path.5873


2. Langdon, CG, Gadek KE, Garcia MR, Evans MK, Reed KB, Bush M, Hanna JA, Drummond CJ, Maguire MC, Leavey PJ, Finkelstein D, Jin H, Schreiner PA, Rehg JE, and Hatley ME. Synthetic essentiality between PTEN and core dependency factor PAX7 dictates rhabdomyosarcoma identity. 


3. Theodosakis, N*, Langdon CG*, Micevic G, Krykbaeva I, Means RE, Stern DF, and Bosenberg MW. Inhibition of isoprenylation synergizes with MAPK blockade to prevent growth in treatment-resistant melanoma, colorectal, and lung cancer. (2019) Pigment Cell Melanoma Res 32:292-302. DOI:10.1111/pcmr.12742 * indicates these authors contributed equally


4. Langdon, CG, Platt JT, Means RE, Iyidogan P, Mamillapalli R, Klein M, Held MA, Lee JW, Koo, JS,Hatzis, C, Hochster, HS, and Stern, DF. Combinatorial screening of pancreatic adenocarcinoma reveals sensitivity to drug combinations including bromodomain inhibitor plus neddylation inhibitor. (2017) MolCancer Ther 16:1041-53. DOI: 10.1158/1535-7163.MCT-16-0794


5. Langdon, CG*, Wiedemann N*, Held MA, Mamillapalli R, Iyidogan P, Theodosakis N, Platt JT, Levy F, Vuagniaux G, Wang S, Bosenberg MW, and Stern DF. SMAC mimetic Debio 1143 synergizes with taxanes, topoisomerase inhibitors and bromodomain inhibitors to impede growth of lung adenocarcinoma cells. (2015) Oncotarget 6:37410-25 DOI: 10.18632/oncotarget.6138 * indicates these authors contributed equally


6. Langdon, CG, Held MA, Platt JT, Iyidogan P, Mamillapalli R, Koo AB, Klein MI, Liu Z, Bosenberg MW,and Stern DF. The broad spectrum tyrosine kinase inhibitor dovitinib suppresses growth of BRAF mutant melanoma cells in combination with other signaling pathway inhibitors. (2015) Pigment Cell Melanoma Res 28:417-30 DOI: 10.1111/pcmr.12376


7. Held, MA, Langdon CG, Platt JT, Graham-Steed T, Liu Z, Chakraborty A, Bacchiocchi A, Koo A, Haskins JW, Bosenberg MW, and Stern DF. Genotype-selective combination therapies for melanoma identified by high-throughput drug screening. (2013) Cancer Discov 3:52-67. DOI: 10.1158/2159-8290.CD-12-0408