1. Vulnerabilities of PTEN-TP53-deficient prostate cancers to compound PARP-PI3K inhibition.

    Cancer Discovery 4(8):896 (2014) PMID 24866151 PMCID PMC4125493

    Prostate cancer is the most prevalent cancer in males, and treatment options are limited for advanced forms of the disease. Loss of the PTEN and TP53 tumor suppressor genes is commonly observed in prostate cancer, whereas their compound loss is often observed in advanced prostate cancer. Here, w...
  2. Vulnerabilities of PTEN-TP53-deficient prostate cancers to compound PARP-PI3K inhibition.

    Cancer Discovery 4(8):896 (2014) PMID 24866151 PMCID PMC4125493

    Prostate cancer is the most prevalent cancer in males, and treatment options are limited for advanced forms of the disease. Loss of the PTEN and TP53 tumor suppressor genes is commonly observed in prostate cancer, whereas their compound loss is often observed in advanced prostate cancer. Here, w...
  3. Vulnerabilities of PTEN-TP53-deficient prostate cancers to compound PARP-PI3K inhibition.

    Cancer Discovery 4(8):896 (2014) PMID 24866151 PMCID PMC4125493

    Prostate cancer is the most prevalent cancer in males, and treatment options are limited for advanced forms of the disease. Loss of the PTEN and TP53 tumor suppressor genes is commonly observed in prostate cancer, whereas their compound loss is often observed in advanced prostate cancer. Here, w...
  4. Vulnerabilities of PTEN-TP53-deficient prostate cancers to compound PARP-PI3K inhibition.

    Cancer Discovery 4(8):896 (2014) PMID 24866151 PMCID PMC4125493

    Prostate cancer is the most prevalent cancer in males, and treatment options are limited for advanced forms of the disease. Loss of the PTEN and TP53 tumor suppressor genes is commonly observed in prostate cancer, whereas their compound loss is often observed in advanced prostate cancer. Here, w...
  5. A co-clinical approach identifies mechanisms and potential therapies for androgen deprivation resistance in prostate cancer.

    Nature Genetics 45(7):747 (2013) PMID 23727860 PMCID PMC3787876

    Here we report an integrated analysis that leverages data from treatment of genetic mouse models of prostate cancer along with clinical data from patients to elucidate new mechanisms of castration resistance. We show that castration counteracts tumor progression in a Pten loss-driven mouse model...
  6. A co-clinical approach identifies mechanisms and potential therapies for androgen deprivation resistance in prostate cancer.

    Nature Genetics 45(7):747 (2013) PMID 23727860 PMCID PMC3787876

    Here we report an integrated analysis that leverages data from treatment of genetic mouse models of prostate cancer along with clinical data from patients to elucidate new mechanisms of castration resistance. We show that castration counteracts tumor progression in a Pten loss-driven mouse model...
  7. Vorinostat combined with bexarotene for treatment of cutaneous T-cell lymphoma: in vitro and phase I clinical evidence supporting augmentation of retinoic acid receptor/retinoid X receptor activation by histone deacetylase inhibition.

    Leukemia & Lymphoma 53(8):1501 (2012) PMID 22239668

    The retinoid X receptor (RXR)-agonist bexarotene and the histone deacetylase inhibitor (HDACI) vorinostat are each established monotherapies for cutaneous T-cell lymphomas (CTCLs). We investigated the combination of HDACI and retinoic acid receptor (RAR)/RXR agonists in vitro and in a phase I, m...
  8. Vorinostat combined with bexarotene for treatment of cutaneous T-cell lymphoma: in vitro and phase I clinical evidence supporting augmentation of retinoic acid receptor/retinoid X receptor activation by histone deacetylase inhibition.

    Leukemia & Lymphoma 53(8):1501 (2012) PMID 22239668

    The retinoid X receptor (RXR)-agonist bexarotene and the histone deacetylase inhibitor (HDACI) vorinostat are each established monotherapies for cutaneous T-cell lymphomas (CTCLs). We investigated the combination of HDACI and retinoic acid receptor (RAR)/RXR agonists in vitro and in a phase I, m...
  9. TSPYL5 suppresses p53 levels and function by physical interaction with USP7.

    Nature Cell Biology 13(1):102 (2011) PMID 21170034

    We have previously reported a gene expression signature that is a powerful predictor of poor clinical outcome in breast cancer. Among the seventy genes in this expression profile is a gene of unknown function: TSPYL5 (TSPY-like 5, also known as KIAA1750). TSPYL5 is located within a small region ...
  10. TSPYL5 suppresses p53 levels and function by physical interaction with USP7.

    Nature Cell Biology 13(1):102 (2011) PMID 21170034

    We have previously reported a gene expression signature that is a powerful predictor of poor clinical outcome in breast cancer. Among the seventy genes in this expression profile is a gene of unknown function: TSPYL5 (TSPY-like 5, also known as KIAA1750). TSPYL5 is located within a small region ...
  11. UNC45A confers resistance to histone deacetylase inhibitors and retinoic acid.

    Molecular Cancer Research 7(11):1861 (2009) PMID 19843631

    To identify potential biomarkers of therapy response, we have previously done a large-scale gain-of-function genetic screen to identify genes whose expression confers resistance to histone deacetylase inhibitors (HDACI). This genetic screen identified two genes with a role in retinoic acid signa...
  12. UNC45A confers resistance to histone deacetylase inhibitors and retinoic acid.

    Molecular Cancer Research 7(11):1861 (2009) PMID 19843631

    To identify potential biomarkers of therapy response, we have previously done a large-scale gain-of-function genetic screen to identify genes whose expression confers resistance to histone deacetylase inhibitors (HDACI). This genetic screen identified two genes with a role in retinoic acid signa...
  13. The preferentially expressed antigen in melanoma (PRAME) inhibits myeloid differentiation in normal hematopoietic and leukemic progenitor cells.

    Blood 114(15):3299 (2009) PMID 19625708 PMCID PMC2759652

    The preferentially expressed antigen in melanoma (PRAME) is expressed in several hematologic malignancies, but either is not expressed or is expressed at only low levels in normal hematopoietic cells, making it a target for cancer therapy. PRAME is a tumor-associated antigen and has been describ...
  14. The preferentially expressed antigen in melanoma (PRAME) inhibits myeloid differentiation in normal hematopoietic and leukemic progenitor cells.

    Blood 114(15):3299 (2009) PMID 19625708 PMCID PMC2759652

    The preferentially expressed antigen in melanoma (PRAME) is expressed in several hematologic malignancies, but either is not expressed or is expressed at only low levels in normal hematopoietic cells, making it a target for cancer therapy. PRAME is a tumor-associated antigen and has been describ...
  15. ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome.

    Cancer Cell 15(4):328 (2009) PMID 19345331 PMCID PMC2693316

    Retinoids play key roles in differentiation, growth arrest, and apoptosis and are increasingly being used in the clinic for the treatment of a variety of cancers, including neuroblastoma. Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OA...
  16. ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome.

    Cancer Cell 15(4):328 (2009) PMID 19345331 PMCID PMC2693316

    Retinoids play key roles in differentiation, growth arrest, and apoptosis and are increasingly being used in the clinic for the treatment of a variety of cancers, including neuroblastoma. Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OA...
  17. ZNF423 is critically required for retinoic acid-induced differentiation and is a marker of neuroblastoma outcome.

    Cancer Cell 15(4):328 (2009) PMID 19345331 PMCID PMC2693316

    Retinoids play key roles in differentiation, growth arrest, and apoptosis and are increasingly being used in the clinic for the treatment of a variety of cancers, including neuroblastoma. Here, using a large-scale RNA interference-based genetic screen, we identify ZNF423 (also known as Ebfaz, OA...
  18. Genome-wide loss-of-function screen reveals an important role for the proteasome in HDAC inhibitor-induced apoptosis.

    Cancer Cell 15(1):57 (2009) PMID 19111881

    Aberrant acetylation has been strongly linked to tumorigenesis, and the modulation of acetylation through targeting histone deacetylases (HDACs) is gathering increasing pace as a viable therapeutic strategy. A genome-wide loss-of-function screen identified HR23B, which shuttles ubiquitinated car...
  19. Genome-wide loss-of-function screen reveals an important role for the proteasome in HDAC inhibitor-induced apoptosis.

    Cancer Cell 15(1):57 (2009) PMID 19111881

    Aberrant acetylation has been strongly linked to tumorigenesis, and the modulation of acetylation through targeting histone deacetylases (HDACs) is gathering increasing pace as a viable therapeutic strategy. A genome-wide loss-of-function screen identified HR23B, which shuttles ubiquitinated car...
  20. Genome-wide loss-of-function screen reveals an important role for the proteasome in HDAC inhibitor-induced apoptosis.

    Cancer Cell 15(1):57 (2009) PMID 19111881

    Aberrant acetylation has been strongly linked to tumorigenesis, and the modulation of acetylation through targeting histone deacetylases (HDACs) is gathering increasing pace as a viable therapeutic strategy. A genome-wide loss-of-function screen identified HR23B, which shuttles ubiquitinated car...