Nancy Du Lab
Exploring molecular mechanisms of cancer metastasis
Ninety percent of cancer patients do not die of locally confined cancer, but rather from cancer that has spread, leading to diminished function of vital organs. There is an urgent need to better understand drivers of cancer metastasis and to identify novel therapeutic targets.

We want to help patients through our research. The focus in Nancy Du laboratory is to understand the molecular mechanisms underlying metastasis. Our long-term goal is to develop therapeutic strategies to prevent metastatic tumor formation and inhibit metastatic tumor growth. We have developed novel model systems to study the in vivo effects of candidate genes in tumor progression. Major research areas include: identification and functional characterization of metastasis genes and non-coding RNAs, and pre-clinical evaluation of anti-tumor therapeutics.

In many human cancers, the gene that produces RHAMM is over-expressed, leading to too much RHAMM protein. While it is unclear whether RHAMM itself plays a causal role in tumor initiation or progression, we demonstrated that an alternative form of RHAMM, RHAMMB or RHAMMv3, promotes the growth of pancreatic tumors and their spread to lymph nodes and the liver. It was thought that pancreatic cancer metastasizes naturally to the liver simply because the two organs are next to each other in the abdomen. But in a seminal experiment, we identified RHAMMB as the first protein to promote liver-specific metastasis of pancreatic neuroendocrine tumors. In addition, we and others found that overexpression of RHAMM predicts poor survival in cancer patients.

Bcl-xL is another gene that is over-expressed in human cancers, including pancreatic cancer and breast cancer. This protein is normally present in the mitochondrial compartment of a cell, and has been known for its function in preventing a common, programmed form of cell death (apoptosis). When Bcl-xL is overexpressed in cancer, it helps cancer cells to survive. Several drugs have been developed to inhibit the anti-apoptotic function of Bcl-xL. Unfortunately, these drugs have limited therapeutic value in clinical trials by themselves. We demonstrated that in cancer, Bcl-xL travels to the nucleus to promote metastasis independent of its anti-apoptotic function. Our studies suggested a paradigm-shifting insight of Bcl-xL. This unexpected finding provides a possible explanation for why clinical trials using drugs to block anti-apoptosis roles of Bcl-xL have not been effective in halting cancer progression.

Dr. Yi-Chieh Nancy Du is an Associate Professor at the Department of Pathology and Laboratory Medicine at Weill Cornell Medicine. She has been deeply attracted to science since elementary school when she convinced her father to get her a microscope, chemicals, beakers, and test tubes to conduct experiments at home. To pursue her passion for scientific discovery, Dr. Du gave up the opportunity to enter medical school, and instead she joined Department of Life Science at National Tsing Hua University (NTHU), Taiwan. She received mentorship from Dr. Pien-Chien Huang, Dr. Tzong-Hsiung Hseu, and many other professors. She learned how to engineer protein mutations and purify proteins at NTHU and Yale University. Her undergraduate research experience broadened her perspective and had her yearning to remain in the lab day and night. In the lab Dr. Du discovered that the joy of conducting research greatly balances out against the frustration and sometimes the loneliness.

After graduating with a bachelor's degree from NTHU, she entered PhD program of State University of New York at Stony Brook. She was trained by Dr. Bruce Stillman at Cold Spring Harbor Laboratory. Dr. Stillman has made many significant achievements including the biochemical reconstitution with purified proteins of the complete replication of the SV40 DNA genome and the discovery of the Origin Recognition Complex (ORC). In Dr. Du’s graduate studies, she discovered a regulatory mechanism that coordinates cell proliferation with DNA replication and ribosome biogenesis using yeast (Du and Stillman, Cell, 2002).

As a result of Dr. Du’s PhD work, she developed strong interests in cancer research and became a postdoctoral fellow of Nobel Laureate Dr. Harold Varmus at Memorial Sloan Kettering Cancer Center. The most important work from her postdoctoral studies was to develop a mouse model, RIP-Tag; RIP-tva, to study metastasis (Du et al., PLoS Biology, 2007). Using a novel and innovative approach of employing somatic gene transfer system, this mouse model offers a unique opportunity to investigate molecular networks that drive the tumor progression to metastasis.

Dr. Du was recruited to Weill Cornell Medicine to develop a research laboratory that investigates the molecular mechanisms of cancer metastasis and develops novel therapeutic strategies, with the ultimate goal to save lives. Dr. Du and her team have expanded the scope from mouse models to human tissues and have been collaborating with other scientists and clinicians to better understand cancer metastasis. Dr. Du’s laboratory applies a multidisciplinary approach to analyze the molecular mechanism of metastasis, combining molecular biology and genomics tools with animal models and in vivo imaging technologies. Dr. Du’s laboratory identified several molecular targets of cancer and generated pre-clinical mouse models and cancer-specific nanoparticles as a drug delivery system.

Dr. Du’s achievements have been recognized by Scholar-in-Training Award from the American Association for Cancer Research, Career Development Award from Department of Defense, President's Council of Cornell Women Affinito-Stewart Award, BCRP Breakthrough Award from Department of Defense, and Rasweiler Family Research Scholar in Cancer Research.

Du YC, Stillman B. Yph1p, an ORC-interacting protein: potential links between cell proliferation control, DNA replication, and ribosome biogenesis. Cell. 2002 Jun 28;109(7):835-48. doi: 10.1016/s0092-8674(02)00773-0. PubMed PMID: 12110181; NIHMSID:NIHMS501519.

Varmus H, Pao W, Politi K, Podsypanina K, Du YC. Oncogenes come of age. Cold Spring Harb Symp Quant Biol. 2005;70:1-9. doi: 10.1101/sqb.2005.70.039. Review. PubMed PMID: 16869733; PubMed Central PMCID: PMC1791364.

Du YC, Lewis BC, Hanahan D, Varmus H. Assessing tumor progression factors by somatic gene transfer into a mouse model: Bcl-xL promotes islet tumor cell invasion. PLoS Biol. 2007 Oct 16;5(10):e276. doi: 10.1371/journal.pbio.0050276. PubMed PMID: 17941720; PubMed Central PMCID: PMC2020504.

Podsypanina K, Du YC, Jechlinger M, Beverly LJ, Hambardzumyan D, Varmus H. Seeding and propagation of untransformed mouse mammary cells in the lung. Science. 2008 Sep 26;321(5897):1841-4. doi: 10.1126/science.1161621. Epub 2008 Aug 28. PubMed PMID: 18755941; PubMed Central PMCID: PMC2694414.

Du YC, Klimstra DS, Varmus H. Activation of PyMT in beta cells induces irreversible hyperplasia, but oncogene-dependent acinar cell carcinomas when activated in pancreatic progenitors. PLoS One. 2009 Sep 7;4(9):e6932. doi: 10.1371/journal.pone.0006932. PubMed PMID: 19812721; PubMed Central PMCID: PMC2758666.

Reddy JP, Peddibhotla S, Bu W, Zhao J, Haricharan S, Du YC, Podsypanina K, Rosen JM, Donehower LA, Li Y. Defining the ATM-mediated barrier to tumorigenesis in somatic mammary cells following ErbB2 activation. Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3728-33. doi: 10.1073/pnas.0910665107. Epub 2010 Feb 3. PubMed PMID: 20133707; PubMed Central PMCID: PMC2840493.

Du YC, Chou CK, Klimstra DS, Varmus H. Receptor for hyaluronan-mediated motility isoform B promotes liver metastasis in a mouse model of multistep tumorigenesis and a tail vein assay for metastasis. Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16753-8. doi: 10.1073/pnas.1114022108. Epub 2011 Sep 21. PubMed PMID: 21940500; PubMed Central PMCID: PMC3189086.

Tang LH, Contractor T, Clausen R, Klimstra DS, Du YC, Allen PJ, Brennan MF, Levine AJ, Harris CR. Attenuation of the retinoblastoma pathway in pancreatic neuroendocrine tumors due to increased cdk4/cdk6. Clin Cancer Res. 2012 Sep 1;18(17):4612-20. doi: 10.1158/1078-0432.CCR-11-3264. Epub 2012 Jul 3. PubMed PMID: 22761470.

Choi S, Chen Z, Tang LH, Fang Y, Shin SJ, Panarelli NC, Chen YT, Li Y, Jiang X, Du YN. Bcl-xL promotes metastasis independent of its anti-apoptotic activity. Nat Commun. 2016 Jan 20;7:10384. doi: 10.1038/ncomms10384. PubMed PMID: 26785948; PubMed Central PMCID: PMC4735924.

Yuan Z, Sánchez Claros C, Suzuki M, Maggi EC, Kaner JD, Kinstlinger N, Gorecka J, Quinn TJ, Geha R, Corn A, Pastoriza J, Jing Q, Adem A, Wu H, Alemu G, Du YC, Zheng D, Greally JM, Libutti SK. Loss of MEN1 activates DNMT1 implicating DNA hypermethylation as a driver of MEN1 tumorigenesis. Oncotarget. 2016 Mar 15;7(11):12633-50. doi: 10.18632/oncotarget.7279. PubMed PMID: 26871472; PubMed Central PMCID: PMC4914310.

Wang D, Narula N, Azzopardi S, Smith RS, Nasar A, Altorki NK, Mittal V, Somwar R, Stiles BM, Du YN. Expression of the receptor for hyaluronic acid mediated motility (RHAMM) is associated with poor prognosis and metastasis in non-small cell lung carcinoma. Oncotarget. 2016 Jun 28;7(26):39957-39969. doi: 10.18632/oncotarget.9554. PubMed PMID: 27220886; PubMed Central PMCID: PMC5129984.

Azzopardi S, Pang S, Klimstra DS, Du YN. p53 and p16Ink4a/p19Arf Loss Promotes Different Pancreatic Tumor Types from PyMT-Expressing Progenitor Cells. Neoplasia. 2016 Oct;18(10):610-617. doi: 10.1016/j.neo.2016.08.003. Epub 2016 Sep 21. PubMed PMID: 27664376; PubMed Central PMCID: PMC5035259.

Zhang G, Chi Y, Du YN. Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model. J Vis Exp. 2017 Oct 16;(128). doi: 10.3791/55890. PubMed PMID: 29155705; PubMed Central PMCID: PMC5644377.

Chen YT, Chen Z, Du YN. Immunohistochemical analysis of RHAMM expression in normal and neoplastic human tissues: a cell cycle protein with distinctive expression in mitotic cells and testicular germ cells. Oncotarget. 2018 Apr 20;9(30):20941-20952. doi: 10.18632/oncotarget.24939. eCollection 2018 Apr 20. PubMed PMID: 29765511; PubMed Central PMCID: PMC5940366.

Zhang G, Du YN. Orthotopic Pancreatic Tumor Mouse Models of Liver Metastasis. Methods Mol Biol. 2019;1882:309-320. doi: 10.1007/978-1-4939-8879-2_27. PubMed PMID: 30378065; PubMed Central PMCID: PMC6800204.

Kobayashi S, Contractor T, Vosburgh E, Du YN, Tang LH, Clausen R, Harris CR. Alleles of Insm1 determine whether RIP1-Tag2 mice produce insulinomas or nonfunctioning pancreatic neuroendocrine tumors. Oncogenesis. 2019 Feb 22;8(3):16. doi: 10.1038/s41389-019-0127-1. PubMed PMID: 30796198; PubMed Central PMCID: PMC6386750.

Yuan Z, Gardiner JC, Maggi EC, Adem A, Zhang G, Lee S, Romanienko P, Du YN, Libutti SK. Tissue-specific induced DNA methyltransferase 1 (Dnmt1) in endocrine pancreas by RCAS-TVA-based somatic gene transfer system promotes β-cell proliferation. Cancer Gene Ther. 2019 Mar;26(3-4):94-102. doi: 10.1038/s41417-018-0046-x. Epub 2018 Sep 7. PubMed PMID: 30190513; PubMed Central PMCID: PMC7540611.

Finnerty BM, Moore MD, Verma A, Aronova A, Huang S, Edwards DP, Chen Z, Seandel M, Scognamiglio T, Du YN, Elemento O, Zarnegar R, Min IM, Fahey TJ. UCHL1 loss alters the cell-cycle in metastatic pancreatic neuroendocrine tumors. Endocr Relat Cancer. 2019 Apr 1;26(4):411-423. doi: 10.1530/ERC-18-0507. Epub 2019 Jan 1. PubMed PMID: 30689542.

Choi S, Wang D, Chen X, Tang LH, Verma A, Chen Z, Kim BJ, Selesner L, Robzyk K, Zhang G, Pang S, Han T, Chan CS, Fahey TJ 3rd, Elemento O, Du YN. Function and clinical relevance of RHAMM isoforms in pancreatic tumor progression. Mol Cancer. 2019 May 9;18(1):92. doi: 10.1186/s12943-019-1018-y. PubMed PMID: 31072393; PubMed Central PMCID: PMC6506944.

Buicko JL, Finnerty BM, Zhang T, Kim BJ, Fahey TJ 3rd, Nancy Du YC. Insights into the biology and treatment strategies of pancreatic neuroendocrine tumors. Ann Pancreat Cancer. 2019 Jun;2. doi: 10.21037/apc.2019.06.02. Epub 2019 Jun 20. PubMed PMID: 31535089; PubMed Central PMCID: PMC6750261.

Goren L, Zhang G, Kaushik S, Breslin PAS, Du YN, Foster DA. (-)-Oleocanthal and (-)-oleocanthal-rich olive oils induce lysosomal membrane permeabilization in cancer cells. PLoS One. 2019;14(8):e0216024. doi: 10.1371/journal.pone.0216024. eCollection 2019. PubMed PMID: 31412041; PubMed Central PMCID: PMC6693737.

Zhang T, Choi S, Zhang T, Chen Z, Chi Y, Huang S, Xiang JZ, Du YN. miR-431 Promotes Metastasis of Pancreatic Neuroendocrine Tumors by Targeting DAB2 Interacting Protein, a Ras GTPase Activating Protein Tumor Suppressor. Am J Pathol. 2020 Mar;190(3):689-701. doi: 10.1016/j.ajpath.2019.11.007. Epub 2020 Jan 14. PubMed PMID: 31953039; PubMed Central PMCID: PMC7074368.

Schatz-Siemers N, Chen YT, Chen Z, Wang D, Ellenson LH, Du YN. Expression of the Receptor for Hyaluronic Acid-Mediated Motility (RHAMM) in Endometrial Cancer is Associated With Adverse Histologic Parameters and Tumor Progression. Appl Immunohistochem Mol Morphol. 2020 Jul;28(6):453-459. doi: 10.1097/PAI.0000000000000763. PubMed PMID: 30920393; PubMed Central PMCID: PMC7546253.

Zhang T, Na JH, Li S, Chen Z, Zhang G, Pang S, Daniyan AF, Li Y, Shi L, Du YN. Functional impact of cancer patient-associated Bcl-xL mutations. MedComm (2020). 2020 Dec;1(3):328-337. doi: 10.1002/mco2.36. Epub 2020 Oct 29. PubMed PMID: 34308416; PubMed Central PMCID: PMC8302207.

Lin A, Feng J, Chen X, Wang D, Wong M, Zhang G, Na J, Zhang T, Chen Z, Chen YT, Nancy Du YC. High levels of truncated RHAMM cooperate with dysfunctional p53 to accelerate the progression of pancreatic cancer. Cancer Lett. 2021 Aug 28;514:79-89. doi: 10.1016/j.canlet.2021.05.011. Epub 2021 May 24. PubMed PMID: 34044069; PubMed Central PMCID: PMC8235875.

Chen X, Lee SK, Song M, Zhang T, Han MS, Chen YT, Chen Z, Ma X, Tung CH, Du YN. RHAMMB-mediated bifunctional nanotherapy targeting Bcl-xL and mitochondria for pancreatic neuroendocrine tumor treatment. Mol Ther Oncolytics. 2021 Dec 17;23:277-287. doi: 10.1016/j.omto.2021.10.002. eCollection 2021 Dec 17. PubMed PMID: 34761107; PubMed Central PMCID: PMC8560716.

Young A, Bu W, Jiang W, Ku A, Kapali J, Dhamne S, Qin L, Hilsenbeck SG, Du YN, Li Y. Targeting the Pro-survival Protein BCL-2 to Prevent Breast Cancer. Cancer Prev Res (Phila). 2022 Jan;15(1):3-10. doi: 10.1158/1940-6207.CAPR-21-0031. Epub 2021 Oct 19. PubMed PMID: 34667127; PubMed Central PMCID: PMC8741732.
Principal Investigator
Yi-Chieh Nancy Du

Postdoctoral Fellow
Tiantian Zhang

Postdoctoral Fellow
Xiang Chen

Research Technician
Anthony Lin

Research Assistant
Sandi Bajrami

Research Assistant
Cheryl Zhang

Anthony (Tony) Daniyan, Resident 2010-2012
Co-author on 1 Publication; National Heart, Lung, and Blood Institute (NHLBI) Cardiovascular Training Grant Recipient; NIH Division of Loan Repayment Award
Current Position
Assistant Attending, Memorial Sloan Kettering Cancer Center

Leigh Selesner, Research Technician 2010-2014
Co-author on 1 Publication
Current Position
Resident, Oregon Health and Sciences University in Portland

Soyoung Choi, Postdoctoral Fellow 2012-2016
First author on 2 Publications; co-author on 1 Publication
Current Position
Principal investigator, Samsung Bioepis, South Korean

Stephanie Azzopardi, Undergraduate Student 2012-2016
First author on 1 Publication; co-author on 1 Publication; 2015 Barry Goldwater Scholarship and Excellence in Education Foundation, Honorable Mention.
Current Position
WCM MD/PhD student

Sharon Pang, Undergraduate Student 2014-2017
Best medical science poster at 2016 Undergraduate Research Conference; Co-author on 3 Publications
Current Position
MD student, Johns Hopkins University

Bu Jung Kim, Research Technician 2014-2015, 2019
Co-author on 2 Publications
Current Position
Resident, Geisinger Health Center

Samantha Li, High School Student 2014-2017
Co-author on 1 Publication
Current Position
Graduate student, Columbia University

Megan Wong, Undergraduate Student 2015-2018
Co-author on 1 Publication
Current Position
Graduate student, Case Western University

George Zhang, Research Technician 2016-2019
First author on 2 Publications; co-author on 5 Publications
Current Position
MD student, University of Vermont Larner College of Medicine

Joseph HyungJoon Na, Research Technician 2017-2019
co-author on 2 Publications
Current Position
MD student, University of Buffalo

Shihui Wang, Undergraduate Student 2017-2018
2017 NYU Dean's Undergraduate Research Fund Grant
Current Position
DDS student, NYU College of Dentistry

Makheni Jean-Pierre, Tri-Institutional Gateways to the Laboratory Summer Student 2018
2018/2019 Undergraduate Research & Creative Activities (URECA) Travel grant; 2019 NIH Undergraduate Scholarship (UGSP)
Current Position
NIH UGSP Postbac

Sha Li, Postdoctoral Fellow 2017-2018
2019 Presidential Postdoctoral Research Fellowship, Princeton University
Current Position
Postdoctoral Fellow

Jennifer Feng, Undergraduate Student 2018-2021
Co-first author on 1 Publication
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Nature Reviews Molecular Biology
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Trends in Cell Biology
RIP-Tag; RIP-tva preclinical mouse model
The use of a powerful mouse model, RIP-Tag, has provided significant insights for the molecular mechanism of tumorigenesis in general, far beyond pancreatic neuroendocrine tumors (panNETs). In this model, the rat insulin promoter (RIP) drives the expression of the SV40 T antigen (Tag) in pancreatic β cells. The mice develop tumors through well-defined stages that are similar to human tumorigenesis, including hyperplasia, angiogenesis, adenoma, and invasive carcinoma in four months. However, this valuable preclinical mouse model does not develop metastatic disease.

To investigate molecular networks that drive the progression from primary cancer to metastasis, we have developed a bitransgenic mouse model, RIP-Tag; RIP-tva, in which the receptor for subgroup A avian leukosis virus (RIP-tva) is also expressed in pancreatic β cells. As such, genetic alterations can be introduced in vivo into pancreatic β cells by infection with avian retroviral vectors harboring desired genetic alteration (Figure 1). This approach has the advantage of introducing somatic genetic changes specifically into premalignant lesions of pancreatic β cells in a time-control manner, thus more faithfully mimicing sporadic tumor development. This approach also avoids any potential perturbation of normal tissue formation often observed in conventional transgenic models due to the ectopic expression of the gene of interest during development. In parallel, using cell lines derived from pancreatic neuroendocrine cell tumors in RIP-Tag; RIP-tva mice, further biochemical and cellular analysis can be easily performed in vitro.

The RCAS-tva system

Doxycycline-inducible PyMT mouse model
The cellular origins of the various forms of pancreatic cancer have not been resolved. It is not known whether different pancreatic tumor types arise from transformation or transdifferentiation of different target cells or whether they arise from a common precursor, with tumor types determined by the specific genetic alterations. The pancreas is composed of ductal, acinar, and endocrine cells, which are morphologically and functionally distinct. Resembling the physiologic and cellular diversity of the pancreas is a spectrum of pancreatic malignancies that possess histological and molecular features that recapitulate to some degree the properties of their normal cellular counterparts. In addition, pancreatic tumors with mixed differentiation have been found.

Previous studies suggested that experimental pancreatic ductal carcinomas might be induced by polyoma middle T antigen (PyMT) expressed in non-ductal cells (Yoshida and Hanahan, Am J Pathol, 1994; Lewis et al., Genes Dev, 2003). To ask whether PyMT transforms and transdifferentiates endocrine cells toward exocrine tumor phenotypes, we have generated a transgenic mouse line that inducibly expresses the PyMT oncogene and the linked Luciferase reporter (tet-o-PyMT-IRES-Luciferase) in different cell types. Luciferase bioluminescence emission facilitates monitoring transgene expression in living mice. We found that the ability of PyMT to induce tumorigenesis is dependent upon cell lineages. Conditional activation of PyMT in pancreatic β cells of transgenic mice led to irreversible expansion of the β cell population regardless of the developmental stage at which it was expressed (Figure 2). However, activation of PyMT starting from pancreatic precursor cells induced either lethal acinar cell carcinomas or β-cell hyperplasia. Although continued expression of PyMT was required for maintenance of acinar cell carcinomas, it was not required to maintain the survival of the expanded β cell population, in contrast with all other studies on acquired dependence of hyperplastic/tumor cells on an activated oncogene for their survival.

While losses of functional p53 and p16Ink4a/p19Arf have been identified in human pancreatic acinar cell carcinoma (PACC) and pancreatic neuroendocrine tumors (PanNETs), their roles in promoting tumorigenesis of the two pancreatic tumors types has not been previously investigated. We demonstrate that p53 loss in pancreatic progenitor cells results in aggressive PACC, whereas p16Ink4a/p19Arf loss results in PanNETs in the context of PyMT induction. In a model of β-cell hyperplasia, p53 and p16Ink4a/p19Arf play cooperative roles in constraining the progression of PanNETs.

Postdoctoral Fellows
We welcome highly motivated candidates with a recent Ph.D. degree in the field of molecular biology, cancer biology, developmental biology, genomics, or genetics. Ph.D. candidates expected graduation are also encouraged to apply. Applicant must be fluent in English, collegial and able to work independently, with at least one recent first author publication in a high-impact journal. High levels of critical thinking and strong troubleshooting ability are expected.

To apply for a postdoctoral fellowship in the laboratory, please send the following information to Dr. Nancy Du:
  • A detailed curriculum vitae
  • Names and contact information of 3 references
  • Why you are interested in our lab and your post-doctoral training goals

Graduate Students
Our laboratory does not admit graduate students directly. Please apply Weill Cornell Graduate School programs in Biochemistry & Structural Biology, Cell & Developmental Biology, and Molecular Biology ( or Tri-Institutional MD-PhD Program ( We welcome graduate students interested in rotating in the lab and conducting PhD thesis research.

Medical Students
We welcome highly motivated medical students. To apply, please send a cover letter with available hours, CV, contact information for 2 references in one PDF file to Dr. Du.

Undergraduate Students
We accept undergraduate students from Macaulay Honors at Hunter College. Undergraduate students who make significant contributions to research projects can become co-authors of research papers. If you are interested in joining our lab, please contact Dr. Nancy Du by email and include your resume, a transcript, your hours for lab research, and names and contact information of at least 2 references. Priority will be given to students with genuine interest, a strong commitment in research, and excellent grade in relevant science courses.
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TEL: +1.646.962.9574
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Dr. Nancy Du
413 E. 69 th Street, C440B
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USPS Mailing Address
Dr. Nancy Du
Department of Pathology and Laboratory Medicine
Weill Cornell Medical College
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New York, NY 10065
Email Address
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Cancer Search, Molecular Mechanisms, Cancer Metastasis, Mouse Model, Pancreatic Cancer, TVA, Tag, PyMT, RHAMM, Bcl-xL