Katerina Politi

Summary

Affiliation: Yale University
Country: USA

Publications

  1. doi request reprint Lung cancer in the era of precision medicine
    Katerina Politi
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut Department of Medicine Section of Medical Oncology, Yale University School of Medicine, New Haven, Connecticut Yale Cancer Center, New Haven, Connecticut
    Clin Cancer Res 21:2213-20. 2015
  2. doi request reprint The Next Wave of EGFR Tyrosine Kinase Inhibitors Enter the Clinic
    Katerina Politi
    Department of Pathology, Yale University School of Medicine, New Haven, CT 06510, USA Section of Medical Oncology, Department of Medicine, Yale University School of Medicine, New Haven, CT 06510, USA Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT 06510, USA Electronic address
    Cancer Cell 27:751-3. 2015
  3. pmc Perfect ALKemy: optimizing the use of ALK-directed therapies in lung cancer
    Katerina Politi
    Departments of Pathology and Medicine Section of Medical Oncology, Yale University School of Medicine and Yale Cancer Center, New Haven, Connecticut
    Clin Cancer Res 20:5576-8. 2014
  4. pmc Two sides of the same coin: EGFR exon 19 deletions and insertions in lung cancer
    Katerina Politi
    Yale University School of Medicine, New Haven, CT, USA
    Clin Cancer Res 18:1490-2. 2012
  5. pmc How genetically engineered mouse tumor models provide insights into human cancers
    Katerina Politi
    Memorial Sloan Kettering Cancer Center, New York, NY, USA
    J Clin Oncol 29:2273-81. 2011
  6. pmc Erlotinib resistance in mouse models of epidermal growth factor receptor-induced lung adenocarcinoma
    Katerina Politi
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Dis Model Mech 3:111-9. 2010
  7. pmc Development of new mouse lung tumor models expressing EGFR T790M mutants associated with clinical resistance to kinase inhibitors
    Lucia Regales
    Pao Lab, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 2:e810. 2007
  8. pmc Induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors in mutant EGFR-dependent lung adenocarcinomas
    Yixuan Gong
    Pao Laboratory, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS Med 4:e294. 2007
  9. doi request reprint Afatinib plus Cetuximab Delays Resistance Compared to Single-Agent Erlotinib or Afatinib in Mouse Models of TKI-Naïve EGFR L858R-Induced Lung Adenocarcinoma
    Valentina Pirazzoli
    Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut
    Clin Cancer Res 22:426-35. 2016
  10. pmc HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation
    Ken Takezawa
    Department of Medicine, Division of Hematology Oncology, Vanderbilt Ingram Cancer Center, Nashville, Tennessee 37232, USA
    Cancer Discov 2:922-33. 2012

Collaborators

Detail Information

Publications19

  1. doi request reprint Lung cancer in the era of precision medicine
    Katerina Politi
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut Department of Medicine Section of Medical Oncology, Yale University School of Medicine, New Haven, Connecticut Yale Cancer Center, New Haven, Connecticut
    Clin Cancer Res 21:2213-20. 2015
    ....
  2. doi request reprint The Next Wave of EGFR Tyrosine Kinase Inhibitors Enter the Clinic
    Katerina Politi
    Department of Pathology, Yale University School of Medicine, New Haven, CT 06510, USA Section of Medical Oncology, Department of Medicine, Yale University School of Medicine, New Haven, CT 06510, USA Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT 06510, USA Electronic address
    Cancer Cell 27:751-3. 2015
    ..In tyrosine kinase inhibitor-resistant lung tumors, rociletinib and AZD9291 are highly active when T790M is present and modestly active when T790M is absent. ..
  3. pmc Perfect ALKemy: optimizing the use of ALK-directed therapies in lung cancer
    Katerina Politi
    Departments of Pathology and Medicine Section of Medical Oncology, Yale University School of Medicine and Yale Cancer Center, New Haven, Connecticut
    Clin Cancer Res 20:5576-8. 2014
    ..Different mutants exhibit differential sensitivity to ALK inhibitors. Matching the mutational profile of the tumor with the appropriate ALK inhibitor is likely to be important to maximize benefit for patients...
  4. pmc Two sides of the same coin: EGFR exon 19 deletions and insertions in lung cancer
    Katerina Politi
    Yale University School of Medicine, New Haven, CT, USA
    Clin Cancer Res 18:1490-2. 2012
    ..The finding that exon 19 insertion mutations are also sensitive to this class of drugs suggests that testing for these mutations should be done and that these patients will benefit from treatment with tyrosine kinase inhibitors...
  5. pmc How genetically engineered mouse tumor models provide insights into human cancers
    Katerina Politi
    Memorial Sloan Kettering Cancer Center, New York, NY, USA
    J Clin Oncol 29:2273-81. 2011
    ..Alternatives to GEMMs, such as chemically induced or spontaneous tumor models, are not discussed in this review...
  6. pmc Erlotinib resistance in mouse models of epidermal growth factor receptor-induced lung adenocarcinoma
    Katerina Politi
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA
    Dis Model Mech 3:111-9. 2010
    ..This preclinical mouse model, therefore, recapitulates the molecular changes responsible for resistance to TKIs in human tumors and holds promise for the discovery of additional mechanisms of drug resistance in lung cancer...
  7. pmc Development of new mouse lung tumor models expressing EGFR T790M mutants associated with clinical resistance to kinase inhibitors
    Lucia Regales
    Pao Lab, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS ONE 2:e810. 2007
    ..The EGFR T790M mutation confers acquired resistance to kinase inhibitors in human EGFR mutant lung adenocarcinoma, is occasionally detected before treatment, and may confer genetic susceptibility to lung cancer...
  8. pmc Induction of BIM is essential for apoptosis triggered by EGFR kinase inhibitors in mutant EGFR-dependent lung adenocarcinomas
    Yixuan Gong
    Pao Laboratory, Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, New York, United States of America
    PLoS Med 4:e294. 2007
    ..We sought to improve understanding of this process in order to provide insight into mechanisms of sensitivity and/or resistance to tyrosine kinase inhibitors and to uncover new targets for therapy...
  9. doi request reprint Afatinib plus Cetuximab Delays Resistance Compared to Single-Agent Erlotinib or Afatinib in Mouse Models of TKI-Naïve EGFR L858R-Induced Lung Adenocarcinoma
    Valentina Pirazzoli
    Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut
    Clin Cancer Res 22:426-35. 2016
    ..This combination has shown a 29% response rate in a clinical trial in patients with acquired resistance to first-generation TKIs. An outstanding question is whether this regimen is beneficial when used as first-line therapy...
  10. pmc HER2 amplification: a potential mechanism of acquired resistance to EGFR inhibition in EGFR-mutant lung cancers that lack the second-site EGFRT790M mutation
    Ken Takezawa
    Department of Medicine, Division of Hematology Oncology, Vanderbilt Ingram Cancer Center, Nashville, Tennessee 37232, USA
    Cancer Discov 2:922-33. 2012
    ..Collectively, these results reveal a previously unrecognized mechanism of resistance to EGFR-TKIs and provide a rationale to assess the status and possibly target HER2 in EGFR-mutant tumors with acquired resistance to EGFR-TKIs...
  11. pmc Targeting the FOXO1/KLF6 axis regulates EGFR signaling and treatment response
    Jaya Sangodkar
    Department of Genetics and Genomic Sciences, Mount Sinai School of Medicine, New York, NY, USA
    J Clin Invest 122:2637-51. 2012
    ....
  12. pmc Acquired resistance of EGFR-mutant lung adenocarcinomas to afatinib plus cetuximab is associated with activation of mTORC1
    Valentina Pirazzoli
    Yale Cancer Center, Yale University School of Medicine, New Haven, CT 06510, USA
    Cell Rep 7:999-1008. 2014
    ....
  13. pmc ERBB3-independent activation of the PI3K pathway in EGFR-mutant lung adenocarcinomas
    Xiaoling Song
    Department of Pathology and Yale Cancer Center, Yale University School of Medicine, New Haven, Connecticut
    Cancer Res 75:1035-45. 2015
    ....
  14. pmc Lung adenocarcinomas induced in mice by mutant EGF receptors found in human lung cancers respond to a tyrosine kinase inhibitor or to down-regulation of the receptors
    Katerina Politi
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, New York 10021, USA
    Genes Dev 20:1496-510. 2006
    ..These models may be useful for developing improved therapies for patients with lung cancers bearing EGFR mutations...
  15. pmc EGF receptor gene mutations are common in lung cancers from "never smokers" and are associated with sensitivity of tumors to gefitinib and erlotinib
    William Pao
    Program in Cancer Biology and Genetics and Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 101:13306-11. 2004
    ..Collectively, these data show that adenocarcinomas from never smokers comprise a distinct subset of lung cancers, frequently containing mutations within the TK domain of EGFR that are associated with gefitinib and erlotinib sensitivity...
  16. doi request reprint Emerging Agents and New Mutations in EGFR-Mutant Lung Cancer
    Deborah Ayeni
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut
    Clin Cancer Res 21:3818-20. 2015
    ..Additional mutations in EGFR can confer resistance that, depending on their genomic context, could determine new drug sensitivities of the cancer cells...
  17. doi request reprint Generation of drug-resistant tumors using intermittent dosing of tyrosine kinase inhibitors in mouse
    Valentina Pirazzoli
    Department of Pathology, Yale University School of Medicine, New Haven, Connecticut 06510
    Cold Spring Harb Protoc 2014:178-81. 2014
    ..Although this protocol is specific for this experimental system, the concepts and general design can be adapted for use with GEMMs of other cancers. ..
  18. pmc Reduced NF1 expression confers resistance to EGFR inhibition in lung cancer
    Elza C de Bruin
    1Signal Transduction and 2High Throughput Screening Laboratories, Cancer Research UK London Research Institute 3The Institute of Cancer Research, London, United Kingdom 4Yale Cancer Center, Departments of 5Medicine Medical Oncology, and 6Pathology, Yale University School of Medicine, New Haven, Connecticut 7Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York 8Cancer Genetics Branch, National Human Genome Research Institute, Bethesda, Maryland 9Division of Molecular Carcinogenesis, The Netherlands Cancer Institute Departments of 10Pathology and 11Pulmonary Diseases, VU University Medical Center, Amsterdam, the Netherlands 12Pathology Service, and 13Oncology Service Hospital Universitario Marques de Valdecilla, IFIMAV, Santander, Spain
    Cancer Discov 4:606-19. 2014
    ..These findings identify a subgroup of patients with EGFR-mutant lung adenocarcinoma who might benefit from combination therapy with EGFR and MEK inhibitors...
  19. pmc Oncogene cooperation in tumor maintenance and tumor recurrence in mouse mammary tumors induced by Myc and mutant Kras
    Katrina Podsypanina
    Program in Cancer Biology and Genetics, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
    Proc Natl Acad Sci U S A 105:5242-7. 2008
    ..These results demonstrate that tumor viability is maintained by each gene in a combination of oncogenes and that targeted approaches will also benefit from combination therapies...