Dr. Testa’s research focuses on genetic and signaling alterations in malignant mesothelioma and on AKT function and oncogenic activity. His group cloned the AKT2 protooncogene and provided the first evidence for its recurrent involvement in human cancers. He also discovered inherited and somatic mutations of critical drivers of mesothelioma pathogenesis, including the tumor suppressor genes NF2, CDKN2A and BAP1. His team has reported extensively on genetically engineered mouse models of cancer, particularly with regard to mesothelioma and thymic lymphoma. In 2011, he and his colleagues reported a novel BAP1-tumor predisposition syndrome characterized by inherited susceptibility to mesothelioma, uveal melanoma, and several other tumor types. He has published extensively on the use of mesothelioma mouse models for preclinical studies of novel molecularly targeted therapeutics, such as inhibitors or the Akt/mTOR, FAK, and JAK/STAT3 pathways.

He is author on more than 440 articles and reviews and is an editorial board member for four scientific journals. Dr. Testa is an elected Fellow of the AAAS, has served as a member of the NCI Board of Scientific Counselors (Basic Sciences), and has received several awards for his work in mesothelioma and leukemia research.

Molecular biology of mesothelioma; role of AKT in oncogenesis

• The BAP1 tumor predisposition syndrome and other genetic factors that may predispose to mesothelioma
• Molecular genetic basis of malignant mesothelioma susceptibility and progression.
• Role of the AKT1/2 oncogenes in tumorigenesis and resistance to anti-cancer therapies.
• Characterization of genes that interact with and/or cooperate with AKT kinase activation in tumor development.
• Use of genetically engineered mice to assess gene–environment interactions, the role of asbestos-induced inflammation in tumor development, and as preclinical models for selective drug targeting of cellular pathways underpinning human tumorigenesis

Dr. Testa's webpage on the Fox Chase Cancer Center website