Dr. Shilpa Patil, Ph.D

PhD & Postdoc level expertise in Cancer Research

Vancouver, British Columbia, Canada

Research Interests

Cancer
epigenetics
development
Oncology
Cancer Research
Biophysics
Biochemistry
Molecular Biology
Gastroenterology
Surgery
Hepatology
Endocrinology, Diabetes and Metabolism

About

Dr. Shilpa Patil is a highly experienced cancer researcher with a strong background in Preclinical studies. She received her Ph.D. in Molecular Medicine from the University of Göttingen in 2020, where she focused on developing novel treatments for pancreatic cancer. Prior to that, she completed her MSc in Regenerative Medicine from Manipal University in 2014 and her BSc in Biotechnology from the same institution in 2012. With over 6 years of research experience, Dr. Patil has worked at prestigious institutions such as the University of British Columbia, University of Göttingen and JNCASR. Her expertise lies in the areas of cancer biology, epigenetics, cell and molecular biology, and regenerative medicine. She has published numerous research articles in reputed journals and has presented her work at various international conferences. Dr. Patil is a dedicated and passionate scientist, committed to using her knowledge and skills to contribute to the fight against cancer. She is driven by her curiosity to unravel complex biological processes and her desire to make a positive impact in the field of cancer research. She is also driven to bridge the academia-industry gap.

Publications

EZH2 Regulates Pancreatic Cancer Subtype Identity and Tumor Progression via Transcriptional Repression of GATA6

Cancer Research / Nov 01, 2020

Patil, S., Steuber, B., Kopp, W., Kari, V., Urbach, L., Wang, X., Küffer, S., Bohnenberger, H., Spyropoulou, D., Zhang, Z., Versemann, L., Bösherz, M. S., Brunner, M., Gaedcke, J., Ströbel, P., Zhang, J.-S., Neesse, A., Ellenrieder, V., Singh, S. K., … Hessmann, E. (2020). EZH2 Regulates Pancreatic Cancer Subtype Identity and Tumor Progression via Transcriptional Repression of GATA6. Cancer Research, 80(21), 4620–4632. https://doi.org/10.1158/0008-5472.can-20-0672

Cytosolic 5′-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites

EBioMedicine / Feb 01, 2019

Patzak, M. S., Kari, V., Patil, S., Hamdan, F. H., Goetze, R. G., Brunner, M., Gaedcke, J., Kitz, J., Jodrell, D. I., Richards, F. M., Pilarsky, C., Gruetzmann, R., Rümmele, P., Knösel, T., Hessmann, E., Ellenrieder, V., Johnsen, S. A., & Neesse, A. (2019). Cytosolic 5′-nucleotidase 1A is overexpressed in pancreatic cancer and mediates gemcitabine resistance by reducing intracellular gemcitabine metabolites. EBioMedicine, 40, 394–405. https://doi.org/10.1016/j.ebiom.2019.01.037

Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models

Journal of Visualized Experiments / Apr 07, 2018

Goetze, R.-G., Buchholz, S. M., Patil, S., Petzold, G., Ellenrieder, V., Hessmann, E., & Neesse, A. (2018). Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models. Journal of Visualized Experiments, 134. https://doi.org/10.3791/56979-v

Mutant and Wild-Type Tumor Suppressor p53 Induces p300 Autoacetylation

iScience / Jun 01, 2018

Kaypee, S., Sahadevan, S. A., Patil, S., Ghosh, P., Roy, N. S., Roy, S., & Kundu, T. K. (2018). Mutant and Wild-Type Tumor Suppressor p53 Induces p300 Autoacetylation. IScience, 4, 260–272. https://doi.org/10.1016/j.isci.2018.06.002

TP53-Status-Dependent Oncogenic EZH2 Activity in Pancreatic Cancer

Cancers / Jul 15, 2022

Versemann, L., Patil, S., Steuber, B., Zhang, Z., Kopp, W., Krawczyk, H. E., Kaulfuß, S., Wollnik, B., Ströbel, P., Neesse, A., Singh, S. K., Ellenrieder, V., & Hessmann, E. (2022). TP53-Status-Dependent Oncogenic EZH2 Activity in Pancreatic Cancer. Cancers, 14(14), 3451. https://doi.org/10.3390/cancers14143451

HSP90 Inhibition Synergizes with Cisplatin to Eliminate Basal-like Pancreatic Ductal Adenocarcinoma Cells

Cancers / Dec 07, 2021

Ewers, K. M., Patil, S., Kopp, W., Thomale, J., Quilitz, T., Magerhans, A., Wang, X., Hessmann, E., & Dobbelstein, M. (2021). HSP90 Inhibition Synergizes with Cisplatin to Eliminate Basal-like Pancreatic Ductal Adenocarcinoma Cells. Cancers, 13(24), 6163. https://doi.org/10.3390/cancers13246163

Oligomers of human histone chaperone NPM1 alter p300/KAT3B folding to induce autoacetylation

Biochimica et Biophysica Acta (BBA) - General Subjects / Aug 01, 2018

Kaypee, S., Sahadevan, S. A., Sudarshan, D., Halder Sinha, S., Patil, S., Senapati, P., Kodaganur, G. S., Mohiyuddin, A., Dasgupta, D., & Kundu, T. K. (2018). Oligomers of human histone chaperone NPM1 alter p300/KAT3B folding to induce autoacetylation. Biochimica et Biophysica Acta (BBA) - General Subjects, 1862(8), 1729–1741. https://doi.org/10.1016/j.bbagen.2018.05.003

Preclinical Evaluation of 1,2-Diamino-4,5-Dibromobenzene in Genetically Engineered Mouse Models of Pancreatic Cancer

Cells / Jun 09, 2019

Goetze, R. G., Buchholz, S. M., Ou, N., Zhang, Q., Patil, S., Schirmer, M., Singh, S. K., Ellenrieder, V., Hessmann, E., Lu, Q.-B., & Neesse, A. (2019). Preclinical Evaluation of 1,2-Diamino-4,5-Dibromobenzene in Genetically Engineered Mouse Models of Pancreatic Cancer. Cells, 8(6), 563. https://doi.org/10.3390/cells8060563

Cell Type of Pancreatic Ductal Adenocarcinoma Origin: Implications for Prognosis and Clinical Outcomes

Visceral Medicine / Dec 27, 2021

Patil, S., Dou, Y., & Kopp, J. L. (2021). Cell Type of Pancreatic Ductal Adenocarcinoma Origin: Implications for Prognosis and Clinical Outcomes. Visceral Medicine, 38(1), 4–10. Portico. https://doi.org/10.1159/000520946

Chromatin-Independent Interplay of NFATc1 and EZH2 in Pancreatic Cancer

Cells / Dec 08, 2021

Patil, S., Forster, T., Reutlinger, K., Kopp, W., Versemann, L., Spitalieri, J., Gaedcke, J., Ströbel, P., Singh, S. K., Ellenrieder, V., Neesse, A., & Hessmann, E. (2021). Chromatin-Independent Interplay of NFATc1 and EZH2 in Pancreatic Cancer. Cells, 10(12), 3463. https://doi.org/10.3390/cells10123463

NFATc1 Is a Central Mediator of EGFR-Induced ARID1A Chromatin Dissociation During Acinar Cell Reprogramming

Cellular and Molecular Gastroenterology and Hepatology / Jan 01, 2023

Zhang, Z., Wang, X., Hamdan, F. H., Likhobabina, A., Patil, S., Aperdannier, L., Sen, M., Traub, J., Neesse, A., Fischer, A., Papantonis, A., Singh, S. K., Ellenrieder, V., Johnsen, S. A., & Hessmann, E. (2023). NFATc1 Is a Central Mediator of EGFR-Induced ARID1A Chromatin Dissociation During Acinar Cell Reprogramming. Cellular and Molecular Gastroenterology and Hepatology, 15(5), 1219–1246. https://doi.org/10.1016/j.jcmgh.2023.01.015

Hyperinsulinemia acts via acinar insulin receptors to initiate pancreatic cancer by increasing digestive enzyme production and inflammation

May 06, 2022

Zhang, A. M. Y., Xia, Y. H., Lin, J. S. H., Chu, K. H., Wang, W. C. K., Ruiter, T. J. J., Yang, J. C. C., Chen, N., Chhuor, J., Patil, S., Cen, H. H., Rideout, E. J., Richard, V. R., Schaeffer, D. F., Zahedi, R. P., Borchers, C. H., Johnson, J. D., & Kopp, J. L. (2022). Hyperinsulinemia acts via acinar insulin receptors to initiate pancreatic cancer by increasing digestive enzyme production and inflammation. https://doi.org/10.1101/2022.05.06.490845

Acvr1bloss promotes formation of precancerous lesions from acinar and ductal cells of origin

Jun 08, 2023

Saeki, K., Patil, S., Sun, Y., Su, G. H., & Kopp, J. L. (2023). Acvr1bloss promotes formation of precancerous lesions from acinar and ductal cells of origin. https://doi.org/10.1101/2023.06.08.544226

EZH2-GATA6 axis in Pancreatic ductal adenocarcinoma

Patil, S. (n.d.). EZH2-GATA6 axis in Pancreatic ductal adenocarcinoma [University Goettingen Repository]. https://doi.org/10.53846/goediss-8223

Kombinierte Radiochemotherapeutika zur Behandlung von endogenen Pankreaskarzinomen im KPC-Modell – eine feasibility Studie

Zeitschrift für Gastroenterologie / Aug 13, 2019

Goetze, R., Buchholz, S., Patil, S., Schirmer, M., Hessmann, E., & Neeße, A. (2019, August 13). Kombinierte Radiochemotherapeutika zur Behandlung von endogenen Pankreaskarzinomen im KPC-Modell – eine feasibility Studie. 74. Jahrestagung Der Deutschen Gesellschaft Für Gastroenterologie, Verdauungs- Und Stoffwechselkrankheiten Mit Sektion Endoskopie – 13. Herbsttagung Der Deutschen Gesellschaft Für Allgemein- Und Viszeralchirurgie Gemeinsam Mit Den Arbeitsgemeinschaften Der DGAV. https://doi.org/10.1055/s-0039-1695456

EZH2 controls PDAC plasticity by regulating differentiation genes

Pancreatology / Jun 01, 2019

Patil, S., Najafova, Z., Kari, V., Wang, X., Bohnenberger, H., Kopp, W., Spitalieri, J., Neesse, A., Ellenrieder, V., Johnsen, S., & Hessmann, E. (2019). EZH2 controls PDAC plasticity by regulating differentiation genes. Pancreatology, 19, S11. https://doi.org/10.1016/j.pan.2019.05.021

Impact of cytosolic 5'-nucleotidase 1A on chemotherapeutic resistance in pancreatic cancer

Pancreatology / Jun 01, 2018

Patzak, M. S., Hessmann, E., Kari, V., Kitz, J., Patil, S., Richards, F. M., Jodrell, D. I., Johnsen, S. A., Ellenrieder, V., & Neesse, A. (2018). Impact of cytosolic 5’-nucleotidase 1A on chemotherapeutic resistance in pancreatic cancer. Pancreatology, 18(4), S91. https://doi.org/10.1016/j.pan.2018.05.247

The Wild-type and Gain-of-function Mutant p53 Enhance p300 Autoacetylation through Conformational Switching

Sep 27, 2017

Kaypee, S., Ghosh, R., Sahadevan, S. A., Patil, S., Shasmal, M., Ghosh, P., Roy, N., Sengupta, J., Roy, S., & Kundu, T. K. (2017). The Wild-type and Gain-of-function Mutant p53 Enhance p300 Autoacetylation through Conformational Switching. https://doi.org/10.1101/194704

Role of oncogenic EZH2 histone methyltransferase activity in PDAC cellular plasticity

Pancreatology / Jul 01, 2017

Patil, S., Witte, H., Neesse, A., Johnsen, S., Ellenrieder, V., & Hessmann, E. (2017). Role of oncogenic EZH2 histone methyltransferase activity in PDAC cellular plasticity. Pancreatology, 17(3), S41. https://doi.org/10.1016/j.pan.2017.05.128

Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models

Journal of Visualized Experiments / Apr 07, 2018

Goetze, R.-G., Buchholz, S. M., Patil, S., Petzold, G., Ellenrieder, V., Hessmann, E., & Neesse, A. (2018). Utilizing High Resolution Ultrasound to Monitor Tumor Onset and Growth in Genetically Engineered Pancreatic Cancer Models. Journal of Visualized Experiments, 134. https://doi.org/10.3791/56979

Education

University of Göttingen

Ph.D, Cancer Research / June, 2020

Göttingen

Manipal Academy of Higher Education

MSc, Regenerative Medicine / August, 2014

Manipal

Manipal Academy of Higher Education

BSc, Biotechnology / August, 2012

Manipal

Experience

University of British Columbia

Postdoctoral Research Fellow / January, 2021July, 2023

University of Gottingen

Postdoctoral Researcher / July, 2020December, 2020

JNCASR

Research Assistant / September, 2014February, 2016

Links & Social Media

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