Motivated cancer biologist with over 10 years of research experience in multiple human-tumor malignancies with a focus on the identification and validation of oncogenes and on development of alternative therapeutic strategies for the treatment of cancer. Extensive experience with cell-based assays and in vivo models of diseases. Broad technical experience in cell biology, biochemistry, and molecular biology with proven ability to initiate interdisciplinary collaboration. Exceptional problem solving, communication, and multi tasking skills. Lentivirus/adenovirus preparation, transfection and infection Oral gavage, intravenous and intraperitoneal injection, animal dissection, bone marrow collection, tissue collection and processing for RNA and protein extraction, adenovirus delivery to mice by nasal administration Immunohistochemistry staining, immunofluorescence staining Protein expression and purification, immunoprecipitation, RT-PCR Cell proliferation assays, cell apoptosis assays, flow cytometry analysis using Flowjo, lineage depletion assay, colony formation assay in methylcellulose, primary cell culture Strong communication skills, experience in giving poster and oral presentations at international conferences.
Research Associate August 2015 to CurrentFox Chase Cancer Center
Discovered the first link between the unfolded protein response (UPR) and transcription factor X in regulating chemoresistance in acute myeloid leukemia (AML).
This work provides basis for novel therapeutic strategies to overcome chemoresistance in AML.
Identified the differential roles of UPR in normal hematopoietic progenitors and leukemic cell populations.
This study provided important information about the development of leukemia.
Managed laboratory practice and supervised lab members.
August 2012 to July 2015Postdoctoral fellow Fox Chase Cancer Center
Designed and conducted experiments to decipher the molecular mechanism underlying AML progression and chemoresistance.
Successfully characterized the oncogenic role of X that could be a therapeutic target.
Utilized shRNA and CRISPR-cas9 techniques to identify the indispensable role of X in cell growth, cell survival, and cytotoxicity by anti-AML drugs in different subtypes of AML.
Screened target genes/signaling pathways by X using RNA-seq and RT-PCRs.
Studied the phenotypes of X-depleted mice.
Used flow cytometry and complete blood count machine to characterize the features of hematopoiesis with/without X in mice.
Monitored the process of AML development in mice and the life span.
Studied the role of X in coping with stress in AML by measured the protein express levels of UPR components and glycolysis levels by Seahorse machine.
Significantly improved the protocol of glycolysis assays in non-adherent cells performed on Seahorse machine.
Assisted the principal investigator with establishing a new lab, generating animal protocols and inventory list, interviewing candidates for job openings.
Supervised, trained and mentored technicians, undergraduate and graduate students in the lab.
Reviewed manuscripts for: Biochemical Pharmarcology, PLOS One, The Journal of Ovarian Research, Cell Biology and Toxicology.
May 2010 to July 2012Postdoctoral fellow The Wistar Institute
Evaluated the anti-tumor effects of FRAX597, a small molecular inhibitor of PAK1, on neurofibromatosis type 2 (NF2)-associated schwannomas in both cultured cell lines and mice models with NF2.
Determined the IC50 of FRAX597 on PAK1 phosphorylation.
Evaluated the inhibitory effects of FRAX597 on cell proliferation and cell cycle by using Coulter counter and flow cytometry analysis respectively.
Monitored the tumor progression of mice transplanted with schwannoma by bioluminescence imaging on IVIS-200 system.
This work strongly suggested that targeting PAK1 could be an efficient method to treat NF2-associated schwannomas.
Discovered the association of Rac1b up-regulation and tumor progression of non small cell lung cancer.
Extracted RNA and protein from human lung cancer biopsy samples and evaluated protein expressions.
Identified the correlation of Rac1b over-expression and K-ras mutations in the biopsy samples by direct sequencing.
Monitored tumor progression of mice with Rac1b knock-in and evaluated the tumor burden of mice by histological analysis of tumors excised from lungs.
Performed immunohistochemistry analysis on lung tissues and cell proliferation assays in cell lines transduced with retrovirus.
This study characterized the role of Rac1b in promoting lung tumorigenesis.
Ph.D : 2010Oncology University College － London, UK
M.S : Cancer Biology, 2005The University of － HK, Hong KongCancer Biology
B.S : Biology, 2003Hong Kong Baptist University － HKBiology
Oral Zhou C, Martinez E, Di Marcantonio D, Aghayev T, Syeks SM (2015). X regulates ER stress signaling to promote chemoresistance in myeloid leukemia. In: 20th Annual Research Symposium at Fox Chase Cancer Center; Jun 2015; Philadelphia. Zhou C, Wong OG, Masters J, Williamson M (2009). Prostate cancer related mutations in Plexin-B1 affect RhoD signaling and cell function. In: Minisymposium in Cellular and Molecular Biology Session, 100th Annual Meeting of the American Association for Cancer Research; April 2009; Colorado. Poster Zhou C, Di Marcantonio D, Martinez E, Solanki-Tatel N, Peri S, Scholl C, Frohling S, Wiest DL, Sykes, SM (2015). X regulates ER stress signaling to promote chemotherapy resistance in acute myeloid leukemia. In: 57th ASH Annual Meeting and Exposition; December 2015; Florida (accepted). Zhou C, Ling MT, Lee TK, Man K, Wang X, Wong YC (2005). FTY720, a fungus metabolite, inhibits invasion ability of androgen independent prostate cancer cells through inactivation of RhoA-GTPase. In: 96th Annual Meeting of the American Association for Cancer Research; April 2005; California. ACADEMIC PUBLICATIONS Zhou C, Di Marcantonio D, Martinez E, Solanki-Tatel N, Peri S, Scholl C, Frohling S, Wiest DL, Sykes, SM. X regulates ER stress signaling to promote chemotherapy resistance in acute myeloid leukemia. Manuscript in preparation. Frax597, a small molecule inhibitor of the p21-activated kinases, inhibits tumorigenesis of neurofibromatosis type 2 (NF2)-associated Schwannomas. Licciulli S, Maksimoska J, Zhou C, Troutman S, Kota S, Liu Q, Duron S, Campbell D, Chernoff J, Field J, Marmorstein R, Kissil JL. J Biol Chem. 2013 Oct 4;288(40): 29105-14. The Rac1 splice form Rac1b promotes K-ras-induced lung tumorigenesis. Zhou C, Licciulli S, Avila JL, Cho M, Troutman S, Jiang P, Kossenkov AV, Shoe LC, Liu Q, Vachiani A, Albelda SM, Kissil JL. Oncogene. 2013 Feb 14;32(7):903-9. Effects of cancer-associated mutations in the PlexinB1 gene. Zhou C, Wong OG, Masters J, Williamson M. Mol Cancer. 2012 Mar 9;11(1):11. Plexin-B1 mutations in prosate cancer. Wong OG, Nitkunan T, Oinuma I, Zhou C, Blanc V, Brown RS, Bott SR, Nariculam J, Box G, Munson P, Constantinou J, Feneley MR, Klocker H, Eccles SA, Negishi M, Freeman A, Masters JR, Williamson M. Proc Natl Acad Sci USA. 2007 Nov 27;104(48): 19040-5. FTY720, a fungus metabolite, inhibits invasion ability of androgen-independent prostate cancer cells through inactivation of RhoA-GTPase. Zhou C, Ling MT, Lee TK, Man K, Wang X, Wong YC. Cancer Lett. 2006 Feb 20;233(1):36-47. Overexpression of Id-1 in prostate cancer cells promotes angiogenesis through activation of vascular endothelial growth factor (VEGF). Ling MT, Lau TC, Zhou C, Chua CW, Kwok WK, Wang X, Wong YC. Carcinogenesis. 2005 Oct 26;(10):1668-76. Up-regulation of TWIST in prostate cancer and its implication as a therapeutic target Kwok WK, Ling MT, Lee TW, Lau TC, Zhou C, Zhang X, Chua CW, Chan KW, Chan FL, Glackin C, Wong YC, Wang X. Cancer Res. 2005 Jun 15;65(12):5153-62. FTY720, a fungus metabolite, inhibits in vivo growth of androgen-independent prostate cancer. Chua CW, Lee DT, Ling MT, Zhou C, Man K, Ho J, Chan FL, Wang X, Wong YC. Int J Cancer. 2005 Dec 20;117(6):1039-48.
AWARDS ASH Abstract Achievement Award, American Society of Hematology 2015 The Greenwald Fellowship, Fox Chase Cancer Center 2015 Dorothy Hodgkin Postgraduate Awards, University College London 2005-2008 Outstanding Presentation, Annual Postgraduate Seminars, The University of Hong Kong 2005
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