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My research seeks to evaluate the molecular factors that promote pancreatic cancer aggression, to develop novel targeted therapeutics that could extend patient survival.
I joined one of Taiwan’s most prestigious universities, the National Chiao Tung University (nationally ranked 2nd) Cancer Biology Laboratory as an undergraduate majoring in Biotechnology. I was trained in team science and clinic-based research that ranged from the collection of patient-derived samples to interacting with scientists, physicians, and patients. I was inspired to pursue research questions that would result in novel therapies to treat patients and therefore designed my research project with the aim to investigate the therapeutic effect of the chromatin remodeling inhibitor, Vorinostat, to overcome platin-based therapeutic resistance. I developed protocols to generate patient-derived xenografts, which we established as an important animal model in the lab to study drug response and resulted in my undergraduate thesis and publication (Pan et al., BMC Cancer, 2016). This led to my acceptance into the five-year combined bachelor-master program in Molecular Medicine and Bioengineering, from which I graduated with the Outstanding Academic Achievement Award for both degrees. This initiated my interest in translational cancer research and precision medicine. I set my next goal on embarking in training in advanced mechanistic-based cancer research that can lead to novel therapeutic interventions.
I am now a PhD candidate in the Pathology Translational Research Lab, led by Drs. Kenneth Shroyer and Luisa Escobar-Hoyos in the Renaissance School of Medicine at SBU. A major skillset I have developed here is the histopathological analysis of patient tumor specimens, providing me with invaluable insight into how to identify and validate diagnostic, prognostic and predictive biomarkers.
As a result, this year I published two manuscripts where we developed an immunohistochemistry-clinical test for K17 to identify the most biologically aggressive and chemoresistant PDACs (Pan, C.H. et al., Mol. Oncol. 2020, and Roa-Peña, L. ... Pan, C.H. et al., Sci Rep. 2019). Currently, this K17 test is being evaluated as a predictive biomarker of cytotoxic-, targeted- and immune-therapies in the largest PDAC trial to date (the “Know Your Tumor” program, Perthera Inc. and PanCAN). We hope this test can guide patient management in the near future.
Pan CH, Otsuka Y, Sridharan B, Woo M, Leiton CV, Babu S, Torrente Gonçalves M, Kawalerski RR, K Bai JD, Chang DK, Biankin AV, Scampavia L, Spicer T, Escobar-Hoyos LF, Shroyer KR. An unbiased high-throughput drug screen reveals a potential therapeutic vulnerability in the most lethal molecular subtype of pancreatic cancer. Mol Oncol. 2020 Aug;14(8):1800-1816. PubMed Central ID: PMC7400780.
Roa-Peña L, Leiton CV, Babu S, Pan CH, Vanner EA, Akalin A, Bandovic J, Moffitt RA, Shroyer KR, Escobar-Hoyos LF. Keratin 17 identifies the most lethal molecular subtype of pancreatic cancer. Sci Rep. 2019 Aug 2;9(1):11239. PubMed Central ID: PMC6677817.
Pan CH, Chang YF, Lee MS, Wen BC, Ko JC, Liang SK, Liang MC. Vorinostat enhances the cisplatin-mediated anticancer effects in small cell lung cancer cells. BMC Cancer. 2016 Nov 7;16(1):857. PubMed Central ID: PMC5100277.
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Identification of K17 as a potential target for developing a biomarker-based personalized treatment for pancreatic cancer: With a strong interest in patient-driven, mechanistic, and therapeutic-discovery research, I aim to identify the mechanisms through which K17 regulates tumor aggression to result in poor survival. We recently reported that K17 is a novel prognostic biomarker in pancreatic cancer. As pancreatic cancer is a disease with a few therapeutic options, new therapeutics are urgently needed. My dissertation project focuses on identifying therapeutic vulnerability. Through an unbiased drug screen, I have reported a drug that showed higher efficacy in targeting K17-expressing PDAC. My ongoing work is addressing what the best mechanism is to shut-off K17’s function by identifying its impact on metabolic rewiring.
Pan CH, Otsuka Y, Sridharan B, Woo M, Leiton CV, Babu S, Torrente Gonçalves M, Kawalerski RR, K Bai JD, Chang DK, Biankin AV, Scampavia L, Spicer T, Escobar-Hoyos LF, Shroyer KR. An unbiased high-throughput drug screen reveals a potential therapeutic vulnerability in the most lethal molecular subtype of pancreatic cancer. Mol Oncol. 2020 Aug;14(8):1800-1816. PubMed Central ID: PMC7400780.
Roa-Peña L, Leiton CV, Babu S, Pan CH, Vanner EA, Akalin A, Bandovic J, Moffitt RA, Shroyer KR, Escobar-Hoyos LF. Keratin 17 identifies the most lethal molecular subtype of pancreatic cancer. Sci Rep. 2019 Aug 2;9(1):11239. PubMed Central ID: PMC6677817.
Identification of a novel therapeutic vulnerability in pancreatic cancer with mutated p53 and altered RNA splicing: Working with my co-mentor, Dr. Luisa Escobar-Hoyos, we identified a novel function of neomorphic mutant p53. We have shown that this key driver of pancreatic cancer effectively rewires the
spliceosome in a manner that allows pancreatic cancer cells to maximally respond to oncogenic KRAS and other small GTPases. This finding is of considerable significance, as it represents a previously unrecognized point of synergy between the most commonly altered oncogene (Kras) and the most commonly altered tumor suppressor gene (Tp53) in pancreatic cancer. These findings are also significant from a therapeutic perspective as we have identified that mutant p53-induced spliceosome rewiring induces a novel therapeutic vulnerability in pancreatic cancer cells, namely, dramatically enhanced sensitivity to pharmacologic inhibition of spliceosome function.
Escobar-Hoyos LF, Penson A, Kannan R, Cho H, Pan CH, Singh RK, Apken LH, Hobbs GA, Luo R, Lecomte N, Babu S, Pan FC, Alonso-Curbelo D, Morris JP 4th, Askan G, Grbovic-Huezo O, Ogrodowski P, Bermeo J, Saglimbeni J, Cruz CD, Ho YJ, Lawrence SA, Melchor JP, Goda GA, Bai K, Pastore A, Hogg SJ, Raghavan S, Bailey P, Chang DK, Biankin A, Shroyer KR, Wolpin BM, Aguirre AJ, Ventura A, Taylor B, Der CJ, Dominguez D, Kümmel D, Oeckinghaus A, Lowe SW, Bradley RK, Abdel-Wahab O, Leach SD. Altered RNA Splicing by Mutant p53 Activates Oncogenic RAS Signaling in Pancreatic Cancer. Cancer Cell. 2020 Aug 10;38(2):198-211.e8. PubMed Central ID: PMC8028848.
Development of a novel therapeutic regimen in treating small cell lung cancer: I joined one of Taiwan’s most prestigious universities, the National Chiao Tung University (nationally ranked 2nd) Cancer Biology Laboratory as an undergraduate majoring in Biotechnology. I was trained in team science and clinic-based research that ranged from the collection of patient-derived samples to interacting with scientists, physicians, and patients. I was inspired to pursue research questions that would result in novel therapies to treat patients and therefore designed my research project with the aim to investigate the therapeutic effect of the chromatin remodeling inhibitor, Vorinostat, to overcome platin-based therapeutic resistance. I developed protocols to generate patient-derived xenografts, which we established as an important animal model in the lab to study drug response. The results demonstrate that combination effects significantly inhibited cancer development and a clinical trial is warranted. This led to my acceptance into the five-year combined bachelor-master program in Molecular Medicine and Bioengineering, from which I graduated with the Outstanding Academic Achievement Award for both degrees.
Pan CH, Chang YF, Lee MS, Wen BC, Ko JC, Liang SK, Liang MC. Vorinostat enhances the cisplatin-mediated anticancer effects in small cell lung cancer cells. BMC Cancer. 2016 Nov 7;16(1):857. PubMed Central ID: PMC5100277.
Identification of druggable targets for prostate cancer: This is a lab rotation project I did in the Cold Spring harbor Laboratory. We found that an enzyme PHLPP2 could be a viable target for treating prostate cancer. I was in the team generating CRISPR-Cas 9 PHLPP2 knockout cell lines and testing novel compounds in inhibiting PHLPP2 in vitro.
Nowak DG, Katsenelson KC, Watrud KE, Chen M, Mathew G, D'Andrea VD, Lee MF, Swamynathan MM, Casanova-Salas I, Jibilian MC, Buckholtz CL, Ambrico AJ, Pan CH, Wilkinson JE, Newton AC, Trotman LC. The PHLPP2 phosphatase is a druggable driver of prostate cancer progression. J Cell Biol. 2019 Jun 3;218(6):1943-1957. PubMed Central ID: PMC6548123.
National Chiao Tung University:
TR: Transfer Credit, P: Pass. For undergraduate C- is the passing grade. For graduate B- is the passing grade.
Stony Brook University:
S: Satisfactory. Students must achieve a B or better in all required courses* and must maintain a B average in elective courses.