Piotr Filipczak, PhD

Piotr Filipczak, PhD

Faculty Titles
Associate Research Scientist
Lovelace Respiratory Research Institute, Albuquerque, NM

UNM Cancer Center Position(s)
Associate Member, Cancer Genetics, Epigenetics & Genomics

Research Program
Cellular and Molecular Oncology

Additional Languages
Polish

Fellowship
Brigham and Women’s Hospital, Harvard Medical School, Boston, MA. Laboratory of Dr. Rebecca M Baron, 2013-2014

Lovelace Respiratory Research Institute, Albuquerque, NM. Laboratory of Dr. Steven A Belinsky, 2015-2016

Expertise, Certifications and Memberships
Member, American Thoracic Society, 2013-2014

Associate Member, American Association for Cancer Research, 2014 – 2016

Active Member, American Association for Cancer Research, 2017 – present

Personal Statement

Personal Statement: My research focuses on molecular mechanisms of oncogenic transcriptome reprogramming that drives malignant phenotype of lung cancer. My recent studies discovered that TET1 gene, originally described as epigenetic eraser demethylatingCpG islands in stem cells is frequently overexpressed in non-small cell lung tumors as a consequence of p53 gene mutation. Elevated TET1 levels alter expression of hundreds of target genes with preference to polycomb regulated genes via a novel demethylation-independent mechanism that in part involves modification of histone 3 at the lysine 9. TET1-regulated reprogramming contributes to cell growth in vitro and in vivo while targeting TET1 expression induces genomic instability followed by irreversible growth arrest. Moreover, TET1 depletion synergizes with standard chemotherapeutics like cisplatin and doxorubicin in therapy-induced senescence. My current ongoing project aims to elucidate if TET1 regulates expression of its gene targets as a methyl-CpG oxidase or a DNA-binding transcription factor to identify direct gene targets of TET1 that prevent lung tumors from senescence thus identifying potential targets for new therapeutic approach, and to describe a potential crosstalk between TET1 and G9a in regulating H3K9 methylation. These studies may provide the basis for testing the TET1 gene as a novel target for treatment of p53-mutated lung tumors.