I trained both as a scientist and as a physician and, throughout my career, I have focused on the treatment and biology of ovarian cancer (OvCa). My Ph.D. thesis was on the role of proteases in ovarian cancer and my clinical fellowship involved a special emphasis on the treatment of patients with this disease. As a surgeon and clinician, I am familiar with the presentation of ovarian cancer in patients, and experience the incredible obstacles we face in its treatment. In the laboratory, I have built the research infrastructure necessary for effective ovarian cancer research.
The Lengyel lab has elucidated, at least in part, the first critical steps of ovarian cancer metastasis by paying close attention to the host microenvironment. We have collected the 25 most commonly used ovarian cancer cell lines from all over the world, including those which are chemotherapy resistant. We have established several mouse models for OvCa, and using a genetic mouse model (K-rasG12D/+/Pten-/- -- established by Dr. Tyler Jacks), a syngeneic orthotopic mouse model using mouse OvCa cells (ID8 -- established by K. Roby), and several xenograft ip models using primary and cultured human OvCa cells. I have also established a prospective OvCa tissue bank and, together with 2 gynecologic pathologists, we have assembled 13 tissue arrays including normal tissue, borderline tumor and primary tumor, & corresponding metastasis. As a surgeon, the main focus of my practice is patients with OvCa; therefore, I will be able to enroll a substantial number of patients on the proposed clinical trial and have the infrastructure in place to collect the tissue required for the translational studies.
My clinical experience treating ovarian cancer, together with my laboratory, which focuses on OvCa biology, gives me a unique opportunity and obligation to find new treatments that can benefit patients with ovarian cancer.
University of Munich
Munich
M.D. - M.D.
1992
Adipocyte-induced FABP4 expression in ovarian cancer cells promotes metastasis and mediates carboplatin resistance.
Mukherjee A, Chiang CY, Daifotis HA, Nieman KM, Fahrmann JF, Lastra RR, Romero IL, Fiehn O, Lengyel E. Adipocyte-induced FABP4 expression in ovarian cancer cells promotes metastasis and mediates carboplatin resistance. Cancer Res. 2020 Feb 13.
PMID: 32054768
RADAR: differential analysis of MeRIP-seq data with a random effect model.
Zhang Z, Zhan Q, Eckert M, Zhu A, Chryplewicz A, De Jesus DF, Ren D, Kulkarni RN, Lengyel E, He C, Chen M. RADAR: differential analysis of MeRIP-seq data with a random effect model. Genome Biol. 2019 12 23; 20(1):294.
PMID: 31870409
Mesothelial Cell HIF1a Expression Is Metabolically Downregulated by Metformin to Prevent Oncogenic Tumor-Stromal Crosstalk.
Hart PC, Kenny HA, Grassl N, Watters KM, Litchfield LM, Coscia F, Blaženovic I, Ploetzky L, Fiehn O, Mann M, Lengyel E, Romero IL. Mesothelial Cell HIF1a Expression Is Metabolically Downregulated by Metformin to Prevent Oncogenic Tumor-Stromal Crosstalk. Cell Rep. 2019 Dec 17; 29(12):4086-4098.e6.
PMID: 31851935
Cancer-derived small extracellular vesicles promote angiogenesis by heparin-bound, bevacizumab-insensitive VEGF, independent of vesicle uptake.
Ko SY, Lee W, Kenny HA, Dang LH, Ellis LM, Jonasch E, Lengyel E, Naora H. Cancer-derived small extracellular vesicles promote angiogenesis by heparin-bound, bevacizumab-insensitive VEGF, independent of vesicle uptake. Commun Biol. 2019; 2:386.
PMID: 31646189
Cancer-derived small extracellular vesicles promote angiogenesis by heparin-bound, bevacizumab-insensitive VEGF, independent of vesicle uptake.
Ko SY, Lee W, Kenny HA, Dang LH, Ellis LM, Jonasch E, Lengyel E, Naora H. Cancer-derived small extracellular vesicles promote angiogenesis by heparin-bound, bevacizumab-insensitive VEGF, independent of vesicle uptake. Commun Biol. 2019 Oct 18; 2(1):386.
PMID: 31925178
Ultrasensitive, multiplexed chemoproteomic profiling with soluble activity-dependent proximity ligation.
Li G, Eckert MA, Chang JW, Montgomery JE, Chryplewicz A, Lengyel E, Moellering RE. Ultrasensitive, multiplexed chemoproteomic profiling with soluble activity-dependent proximity ligation. Proc Natl Acad Sci U S A. 2019 Oct 22; 116(43):21493-21500.
PMID: 31591248
Quantitative High-Throughput Screening Using an Organotypic Model Identifies Compounds that Inhibit Ovarian Cancer Metastasis.
Kenny HA, Lal-Nag M, Shen M, Kara B, Nahotko DA, Wroblewski K, Fazal S, Chen S, Chiang CY, Chen YJ, Brimacombe KR, Marugan J, Ferrer M, Lengyel E. Quantitative High-Throughput Screening Using an Organotypic Model Identifies Compounds that Inhibit Ovarian Cancer Metastasis. Mol Cancer Ther. 2020 Jan; 19(1):52-62.
PMID: 31562255
New Roles for Glycogen in Tumor Progression.
Dauer P, Lengyel E. New Roles for Glycogen in Tumor Progression. Trends Cancer. 2019 Jul; 5(7):396-399.
PMID: 31311654
Proteomics reveals NNMT as a master metabolic regulator of cancer-associated fibroblasts.
Eckert MA, Coscia F, Chryplewicz A, Chang JW, Hernandez KM, Pan S, Tienda SM, Nahotko DA, Li G, Blaženovic I, Lastra RR, Curtis M, Yamada SD, Perets R, McGregor SM, Andrade J, Fiehn O, Moellering RE, Mann M, Lengyel E. Proteomics reveals NNMT as a master metabolic regulator of cancer-associated fibroblasts. Nature. 2019 05; 569(7758):723-728.
PMID: 31043742
Mutant p53 regulates LPA signaling through lysophosphatidic acid phosphatase type 6.
Chryplewicz A, Tienda SM, Nahotko DA, Peters PN, Lengyel E, Eckert MA. Mutant p53 regulates LPA signaling through lysophosphatidic acid phosphatase type 6. Sci Rep. 2019 Mar 26; 9(1):5195.
PMID: 30914657