1. NRF2 Pathway Activation and Adjuvant Chemotherapy Benefit in Lung Squamous Cell Carcinoma.

    Clinical Cancer Research 21(11):2499 (2015) PMID 25739673

    Genomic profiling of lung squamous cell carcinomas (SCC) has identified NRF2 pathway alterations, which activate oxidative response pathways, in one third of tumors. Preclinical data suggest these tumors may be resistant to platinum-based chemotherapy. We evaluated the clinical relevance of thes...
  2. PIK3CA genotype and treatment decisions in human epidermal growth factor receptor 2-positive breast cancer.

    Journal of Clinical Oncology 33(12):1318 (2015) PMID 25559805

  3. APOBEC3B expression in breast cancer reflects cellular proliferation, while a deletion polymorphism is associated with immune activation.

    PNAS 112(9):2841 (2015) PMID 25730878 PMCID PMC4352793

    Genomic sequencing studies of breast and other cancers have identified patterns of mutations that have been attributed to the endogenous mutator activity of APOBEC3B (A3B), a member of the AID/APOBEC family of cytidine deaminases. A3B gene expression is increased in many cancers, but its upstrea...
  4. APOBEC3B expression in breast cancer reflects cellular proliferation, while a deletion polymorphism is associated with immune activation.

    PNAS 112(9):2841 (2015) PMID 25730878 PMCID PMC4352793

    Genomic sequencing studies of breast and other cancers have identified patterns of mutations that have been attributed to the endogenous mutator activity of APOBEC3B (A3B), a member of the AID/APOBEC family of cytidine deaminases. A3B gene expression is increased in many cancers, but its upstrea...
  5. Glutathione and Thioredoxin Antioxidant Pathways Synergize to Drive Cancer Initiation and Progression

    Cancer Cell 27(2):211 (2015)

    Controversy over the role of antioxidants in cancer has persisted for decades. Here, we demonstrate that synthesis of the antioxidant glutathione (GSH), driven by GCLM, is required for cancer initiation. Genetic loss of Gclm prevents a tumor’s ability to drive malignant transformation....
  6. Glutathione and Thioredoxin Antioxidant Pathways Synergize to Drive Cancer Initiation and Progression

    Cancer Cell 27(2):314 (2015)

  7. Glutathione and thioredoxin antioxidant pathways synergize to drive cancer initiation and progression.

    Cancer Cell 27(2):211 (2015) PMID 25620030

    Controversy over the role of antioxidants in cancer has persisted for decades. Here, we demonstrate that synthesis of the antioxidant glutathione (GSH), driven by GCLM, is required for cancer initiation. Genetic loss of Gclm prevents a tumor's ability to drive malignant transformation. Intriguin...
  8. Breaking up Is Hard to Do: PI3K Isoforms on the Rebound.

    Cancer Cell 27(1):5 (2015) PMID 25584888

    In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a "rebound" of the PI3K activity through different compensation m...
  9. Breaking up is hard to do: PI3K isoforms on the rebound.

    Cancer Cell 27(1):5 (2015) PMID 25584888

    In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a "rebound" of the PI3K activity through different compensation m...
  10. Breaking up Is Hard to Do: PI3K Isoforms on the Rebound

    Cancer Cell (2015)

    In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a “rebound” of the PI3K activity through different comp...
  11. Breaking up Is Hard to Do: PI3K Isoforms on the Rebound

    Cancer Cell (2015)

    In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a “rebound” of the PI3K activity through different comp...
  12. Breaking up Is Hard to Do: PI3K Isoforms on the Rebound

    Cancer Cell (2015)

    In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a “rebound” of the PI3K activity through different comp...
  13. Breaking up Is Hard to Do: PI3K Isoforms on the Rebound

    Cancer Cell (2015)

    In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a “rebound” of the PI3K activity through different comp...
  14. Functional characterization of CFI-400945, a Polo-like kinase 4 inhibitor, as a potential anticancer agent.

    Cancer Cell 26(2):163 (2014) PMID 25043604

    PLK4 was identified as a promising therapeutic target through a systematic approach that combined RNAi screening with gene expression analysis in human breast cancers and cell lines. A drug discovery program culminated in CFI-400945, a potent and selective PLK4 inhibitor. Cancer cells treated wi...
  15. Functional Characterization of CFI-400945, a Polo-like Kinase 4 Inhibitor, as a Potential Anticancer Agent

    Cancer Cell 26(2):163 (2014)

    PLK4 was identified as a promising therapeutic target through a systematic approach that combined RNAi screening with gene expression analysis in human breast cancers and cell lines. A drug discovery program culminated in CFI-400945, a potent and selective PLK4 inhibitor. Cancer cells ...
  16. Estrogen controls the survival of BRCA1-deficient cells via a PI3K-NRF2-regulated pathway.

    PNAS 111(12):4472 (2014) PMID 24567396 PMCID PMC3970526

    Mutations in the tumor suppressor BRCA1 predispose women to breast and ovarian cancers. The mechanism underlying the tissue-specific nature of BRCA1's tumor suppression is obscure. We previously showed that the antioxidant pathway regulated by the transcription factor NRF2 is defective in BRCA1-...
  17. Estrogen controls the survival of BRCA1-deficient cells via a PI3K-NRF2-regulated pathway.

    PNAS 111(12):4472 (2014) PMID 24567396 PMCID PMC3970526

    Mutations in the tumor suppressor BRCA1 predispose women to breast and ovarian cancers. The mechanism underlying the tissue-specific nature of BRCA1's tumor suppression is obscure. We previously showed that the antioxidant pathway regulated by the transcription factor NRF2 is defective in BRCA1-...
  18. Extended adjuvant tamoxifen for early breast cancer: a meta-analysis.

    PLoS ONE 9(2):e88238 (2014) PMID 24586311 PMCID PMC3930532

    Hormone receptor positive breast cancer is characterized by the potential for disease recurrence many years after initial diagnosis. Endocrine therapy has been shown to reduce the risk of such recurrence, but the optimal duration of endocrine therapy remains unclear. We conducted a systematic re...
  19. Extended adjuvant tamoxifen for early breast cancer: a meta-analysis.

    PLoS ONE 9(2):e88238 (2014) PMID 24586311 PMCID PMC3930532

    Hormone receptor positive breast cancer is characterized by the potential for disease recurrence many years after initial diagnosis. Endocrine therapy has been shown to reduce the risk of such recurrence, but the optimal duration of endocrine therapy remains unclear. We conducted a systematic re...
  20. Extended adjuvant tamoxifen for early breast cancer: a meta-analysis.

    PLoS ONE 9(2):e88238 (2014) PMID 24586311 PMCID PMC3930532

    Hormone receptor positive breast cancer is characterized by the potential for disease recurrence many years after initial diagnosis. Endocrine therapy has been shown to reduce the risk of such recurrence, but the optimal duration of endocrine therapy remains unclear. We conducted a systematic re...