Global

Genetics Experts

John Brognard


Investigator
The Center for Cancer Research
United States of America

Biography

John received a BSc degree in chemistry from James Madison University (Harrisonburg, Virginia), followed by a MSc degree in biotechnology from Johns Hopkins University (Baltimore, Maryland). He then joined Dr. Phillip Dennis’s laboratory at the National Cancer Institute in Bethesda, Maryland, where they discovered signaling pathways that promote resistance to chemotherapy, elucidated mechanisms implicated in the initial stages of lung tumorigenesis, and developed small molecule inhibitors targeting constitutively active Akt in lung cancer. John obtained his PhD from University of California, San Diego in Dr. Alexandra Newton’s laboratory, where he discovered a novel class of phosphatases (PHLPP1 and PHLPP2) that act directly on Akt and PKC to decrease signalling through these pathways. Lastly, John trained as a postdoctoral fellow in Dr. Tony Hunter’s laboratory at the Salk Institute. Utilizing bioinformatic tools they screened cancer genomes to identify novel kinases implicated in cancer by the presence of functional somatic mutations. He joined the CRUK Manchester Institute as a group leader in September of 2010 and the lab was focused on identifying mechanisms to promote lung tumorigenesis. John then moved to the Laboratory of Cell and Developmental Signaling at the NCI as a Earl Stadtman Investigator in the summer of 2016. His research will be focused on defining novel enzymes that act to suppress or promote tumorigenesis and in some cases can serve as novel targets for therapeutic intervention. The lab has several ongoing collaborations with pharmaceutical companies including Genentech and AstraZeneca to investigate novel inhibitors targeting newly identified kinases implicated in cancer. 

Research Interest

Cancer Biology, Cell Biology, Genetics and Genomics 

Publications

  • Shameem F, Eleanor WT, Yaoyong L, Natalie LS, Franziska H, et al. (2013) Targeted genetic dependency screen facilitates identification of actionable mutations in FGFR4, MAP3K9, and PAK5 in lung cancer. Proc Natl Acad Sci USA 110: 12426-12431

  • Anna AM, Natalie LS, Hayeon B, Eleanor WT, Matthew Collier, et al. (2016) Recurrent MLK4 Loss-of-Function Mutations Suppress JNK Signaling to Promote Colon Tumorigenesis. Cancer Res. 76: 724-735

  • Ewelina Testoni, Natalie L. Stephenson, Pedro Torres‐Ayuso, Anna A. Marusiak,et al. (2016) Somatically mutated ABL1 is an actionable and essential NSCLC survival gene. EMBO Mol Med. 8: 105-116

Global Experts from United States of America

Global Experts in Subject

Share This Profile
Recent Expert Updates
  • Matthew L Stone
    Matthew L Stone
    pediatrics
    University of Virginia Health System; Charlottesville, VA
    United States of America
  • Dr.   Matthew
    Dr. Matthew
    pediatrics
    University of Virginia Health System; Charlottesville, VA
    United States of America
  • Dr.  L Stone Matthew
    Dr. L Stone Matthew
    pediatrics
    University of Virginia Health System; Charlottesville, VA
    United States of America
  • Dr.  L Stone
    Dr. L Stone
    pediatrics
    University of Virginia Health System; Charlottesville, VA
    United States of America
  • Dr. Matthew L Stone
    Dr. Matthew L Stone
    pediatrics
    University of Virginia Health System; Charlottesville, VA
    United States of America
  • Dr.  R Sameh
    Dr. R Sameh
    pediatrics
    King Abdul Aziz University
    United Arab Emirates
  • Dr.   R Ismail,
    Dr. R Ismail,
    pediatrics
    King Abdul Aziz University
    United Arab Emirates
  • Sameh R Ismail,
    Sameh R Ismail,
    pediatrics
    King Abdul Aziz University
    United Arab Emirates
  • Dr.   Sameh R Ismail,
    Dr. Sameh R Ismail,
    pediatrics
    King Abdul Aziz University
    United Arab Emirates
  • Dr.   William
    Dr. William
    pediatrics
    Maimonides Medical Center
    United States of America