Faculty Summaries
Joseph R Testa, PhD, FACMG
Joseph R. Testa, PhD
  • Carol & Kenneth E. Weg Chair in Human Genetics
  • Scientific Leader, Kidney Cancer Working Group
  • Director, Clinical Cytogenomics Laboratory
  • Co-Leader, Cancer Biology
  • Director, Genomics Facility
Office Phone: 215-728-2610
Fax: 215-214-1623
Office: P3037
Molecular biology of mesothelioma; AKT oncogenic activity


  • The BAP1 tumor predisposition syndrome.
  • 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.
Description of research projects
Selected Publications

Fox Chase Programs

Extramural Affiliations

    1. A retroviral oncogene, akt, encoding a serine-threonine kinase containing an SH2-like region. Bellacosa A, Testa JR, Staal SP, Tsichlis PN. Science. 1991; 254: 274-7. PubMed
    2. AKT2, a putative oncogene encoding a member of a subfamily of protein-serine/threonine kinases, is amplified in human ovarian carcinomas. Cheng JQ, Godwin AK, Bellacosa A, Taguchi T, Franke TF, et al. Proc Natl Acad Sci U S A. 1992; 89:9267-71. PMID: 1409633 PMCID: PMC50107. PMCID: PMC50107.
    3. p16 alterations and deletion mapping of 9p21-p22 in malignant mesothelioma. Cheng JQ, Jhanwar SC, Klein WM, Bell DW, Lee WC, et al. Cancer Res. 1994; 54:5547-51. PMID: 7923195.
    4. High frequency of inactivating mutations in the neurofibromatosis type 2 gene (NF2) in primary malignant mesotheliomas. Bianchi AB, Mitsunaga SI, Cheng JQ, Klein WM, Jhanwar SC, et al. Proc Natl Acad Sci U S A. 1995; 92:10854-8. PMCID: PMC40529.
    5. p21-activated kinase links Rac/Cdc42 signaling to merlin. Xiao GH, Beeser A, Chernoff J, Testa JR. J Biol Chem. 2002; 277:883-6. PMID: 11719502.
    6. A mouse model recapitulating molecular features of human mesothelioma. Altomare DA, Vaslet CA, Skele KL, De Rienzo A, Devarajan K, et al. Cancer Res. 2005; 65:8090-5. PMID: 16166281.
    7. Re-expression of the tumor suppressor NF2/merlin inhibits invasiveness in mesothelioma cells and negatively regulates FAK. Poulikakos PI, Xiao GH, Gallagher R, Jablonski S, Jhanwar SC, et al. Oncogene. 2006; 25:5960-8. PubMed PMID: 16652148.
    8. A novel recurrent chromosomal inversion implicates the homeobox gene Dlx5 in T-cell lymphomas from Lck-Akt2 transgenic mice. Tan Y, Timakhov RA, Rao M, Altomare DA, Xu J, et al. Cancer Res. 2008; 68:1296-302. PMID: 18316591.
    9. Testa JR, Cheung M, Pei J, Below JE, Tan Y, et al. Germline BAP1 mutations predispose to malignant mesothelioma. Nat Genet. 2011; 43:1022-5. PMCID: PMC3184199.
    10. Losses of both products of the Cdkn2a/Arf locus contribute to asbestos-induced mesothelioma development and cooperate to accelerate tumorigenesis. Altomare DA, Menges CW, Xu J, Pei J, Zhang L, et al. PLoS One. 2011; 6:e18828. PMCID: PMC3079727.
    11. BAP1 and cancer. Carbone M, Yang H, Pass HI, Krausz T, Testa JR, et al. Nat Rev Cancer. 2013; 13:153-9. PMCID: PMC3792854.
    12. Tumor suppressor alterations cooperate to drive aggressive mesotheliomas with enriched cancer stem cells via a p53-miR-34a-c-Met axis. Menges CW, Kadariya Y, Altomare D, Talarchek J, Neumann-Domer E, et al. Cancer Res. 2014; 74:1261-71. PMCID: PMC3945416.
    13. Germline mutation of Bap1 accelerates development of asbestos-induced malignant mesothelioma. Xu J, Kadariya Y, Cheung M, Pei J, Talarchek J, et al. Cancer Res. 2014; 74:4388-97. PMCID: PMC4165574.
    14. Merlin deficiency predicts FAK inhibitor sensitivity: a synthetic lethal relationship. Shapiro IM, Kolev VN, Vidal CM, Kadariya Y, Ring JE, et al. Sci Transl Med. 2014; 6:237ra68. PMCID: PMC4165339
    15. Germline BAP1 mutation in a family with high incidence of multiple primary cancers and a potential gene-environment interaction. Cheung M, Kadariya Y, Talarchek J, Pei J, et al. Cancer Lett. (in press)
All publications