1. Reply to Eliezer M. Van Allen, Levi A. Garraway and Jonathan E. Rosenberg's Letter to the Editor re: Floris H. Groenendijk, Jeroen de Jong, Elisabeth E. Fransen van de Putte, et al. ERBB2 Mutations Characterize a Subgroup of Muscle-invasive Bladder Cancers with Excellent Response to Neoadjuvant Chemotherapy. Eur Urol. In press. http://dx.doi.org/10.1016/j.eururo.2015.01.014.

    European Urology 68(2):e33 (2015) PMID 25776733

  2. A price to pay for tumor regression.

    Cell Research 25(7):763 (2015) PMID 25895608 PMCID PMC4493272

    Killing cancer cells can have undesired side effects. Upon drug treatment, drug-sensitive cancer cells secrete an array of growth factors that stimulate the proliferation and dissemination of drug-resistant cells in the population.
  3. Hurdles on the road to personalized medicine.

    Molecular Oncology 9(5):935 (2015) PMID 25226812

    Cancer treatment is slowly shifting from an approach in which the tissue of origin and the histology were the guiding principles for the choice of chemotherapy towards a genotype-centric approach in which the changes in the cancer genome are used to select patients for treatment with highly sele...
  4. PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer.

    Journal of Clinical Oncology 33(12):1334 (2015) PMID 25559818

    We investigated whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) correlates with response to neoadjuvant human epidermal growth factor receptor 2 (HER2) -targeted therapies in patients with breast cancer. Baseline tissue biopsies were ava...
  5. SMARCE1 suppresses EGFR expression and controls responses to MET and ALK inhibitors in lung cancer.

    Cell Research 25(4):445 (2015) PMID 25656847 PMCID PMC4387553

    Recurrent inactivating mutations in components of SWI/SNF chromatin-remodeling complexes have been identified across cancer types, supporting their roles as tumor suppressors in modulating oncogenic signaling pathways. We report here that SMARCE1 loss induces EGFR expression and confers resistan...
  6. Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation.

    International Journal of Cancer 136(6):1434 (2015) PMID 25080865 PMCID PMC4312923

    The multikinase inhibitor sorafenib is under clinical investigation for the treatment of many solid tumors, but in most cases, the molecular target responsible for the clinical effect is unknown. Furthermore, enhancing the effectiveness of sorafenib using combination strategies is a major clinic...
  7. Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation.

    International Journal of Cancer 136(6):1434 (2015) PMID 25080865 PMCID PMC4312923

    The multikinase inhibitor sorafenib is under clinical investigation for the treatment of many solid tumors, but in most cases, the molecular target responsible for the clinical effect is unknown. Furthermore, enhancing the effectiveness of sorafenib using combination strategies is a major clinic...
  8. Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation.

    International Journal of Cancer 136(6):1434 (2015) PMID 25080865

    The multikinase inhibitor sorafenib is under clinical investigation for the treatment of many solid tumors, but in most cases, the molecular target responsible for the clinical effect is unknown. Furthermore, enhancing the effectiveness of sorafenib using combination strategies is a major clinic...
  9. Sorafenib synergizes with metformin in NSCLC through AMPK pathway activation.

    International Journal of Cancer 136(6):1434 (2015) PMID 25080865 PMCID PMC4312923

    The multikinase inhibitor sorafenib is under clinical investigation for the treatment of many solid tumors, but in most cases, the molecular target responsible for the clinical effect is unknown. Furthermore, enhancing the effectiveness of sorafenib using combination strategies is a major clinic...
  10. Resistance to targeted cancer drugs through hepatocyte growth factor signaling.

    Cell Cycle 13(24):3808 (2014) PMID 25426675

    Cancer therapeutics that target a signaling pathway to which the cancer cells are addicted can deliver dramatic initial responses, but resistance is nearly always inevitable. A variety of mechanisms that cancer cells employ to escape from targeted cancer drugs have been described. We review here...
  11. Resistance to targeted cancer drugs through hepatocyte growth factor signaling.

    Cell Cycle 13(24):3808 (2014) PMID 25426675

    Cancer therapeutics that target a signaling pathway to which the cancer cells are addicted can deliver dramatic initial responses, but resistance is nearly always inevitable. A variety of mechanisms that cancer cells employ to escape from targeted cancer drugs have been described. We review here...
  12. Loss of p53 induces cell proliferation via Ras-independent activation of the Raf/Mek/Erk signaling pathway.

    PNAS 111(42):15155 (2014) PMID 25288756 PMCID PMC4210339

    The Ras family of small GTPases constitutes a central node in the transmission of mitogenic stimuli to the cell cycle machinery. The ultimate receptor of these mitogenic signals is the retinoblastoma (Rb) family of pocket proteins, whose inactivation is a required step to license cell proliferat...
  13. Loss of p53 induces cell proliferation via Ras-independent activation of the Raf/Mek/Erk signaling pathway.

    PNAS 111(42):15155 (2014) PMID 25288756 PMCID PMC4210339

    The Ras family of small GTPases constitutes a central node in the transmission of mitogenic stimuli to the cell cycle machinery. The ultimate receptor of these mitogenic signals is the retinoblastoma (Rb) family of pocket proteins, whose inactivation is a required step to license cell proliferat...
  14. Feedback and redundancy in receptor tyrosine kinase signaling: relevance to cancer therapies.

    Trends in Biochemical Sciences 39(10):465 (2014) PMID 25239057

    Mammalian cells have multiple regulatory mechanisms to deal with perturbations in cellular homeostasis, including feedback loops and crosstalk between the major signaling pathways. While these mechanisms are critically required to help cells survive under dynamic physiological circumstances, the...
  15. Feedback and redundancy in receptor tyrosine kinase signaling: relevance to cancer therapies.

    Trends in Biochemical Sciences 39(10):465 (2014) PMID 25239057

    Mammalian cells have multiple regulatory mechanisms to deal with perturbations in cellular homeostasis, including feedback loops and crosstalk between the major signaling pathways. While these mechanisms are critically required to help cells survive under dynamic physiological circumstances, the...
  16. Drug resistance to targeted therapies: déjà vu all over again.

    Molecular Oncology 8(6):1067 (2014) PMID 24910388

    A major limitation of targeted anticancer therapies is intrinsic or acquired resistance. This review emphasizes similarities in the mechanisms of resistance to endocrine therapies in breast cancer and those seen with the new generation of targeted cancer therapeutics. Resistance to single-agent ...
  17. Drug resistance to targeted therapies: Déjà vu all over again

    Molecular Oncology 8(6):1067 (2014) PMID 24910388

    A major limitation of targeted anticancer therapies is intrinsic or acquired resistance. This review emphasizes similarities in the mechanisms of resistance to endocrine therapies in breast cancer and those seen with the new generation of targeted cancer therapeutics. Resistance to sin...
  18. RAF suppression synergizes with MEK inhibition in KRAS mutant cancer cells.

    Cell Reports 8(5):1475 (2014) PMID 25199829

    KRAS is the most frequently mutated oncogene in human cancer, yet no therapies are available to treat KRAS mutant cancers. We used two independent reverse genetic approaches to identify components of the RAS-signaling pathways required for growth of KRAS mutant tumors. Small interfering RNA (siR...
  19. RAF Suppression Synergizes with MEK Inhibition in KRAS Mutant Cancer Cells

    Cell Reports 8(5):1475 (2014)

    KRAS is the most frequently mutated oncogene in human cancer, yet no therapies are available to treat KRAS mutant cancers. We used two independent reverse genetic approaches to identify components of the RAS-signaling pathways required for growth of KRAS mutant tumors. Small interferin...
  20. RAF suppression synergizes with MEK inhibition in KRAS mutant cancer cells.

    Cell Reports 8(5):1475 (2014) PMID 25199829

    KRAS is the most frequently mutated oncogene in human cancer, yet no therapies are available to treat KRAS mutant cancers. We used two independent reverse genetic approaches to identify components of the RAS-signaling pathways required for growth of KRAS mutant tumors. Small interfering RNA (siR...