Bio

Bio


I am a Postdoctoral Scholar in the laboratory of Dr. James Brooks, where I perform prostate cancer research. In particular, I am investigating the role of nucleolar and spindle-associated protein (NUSAP1; encoding NuSAP) in prostate cancer progression. NUSAP1 is over-expressed in recurrent prostate cancer, and its expression can predict prostate cancer recurrence. Outside of research, I am actively involved in the Stanford University Postdoctoral Association, where I am Co-Chair, and collaborate with postdocs, faculty, and staff to improve and enrich the postdoctoral experience at Stanford.

Honors & Awards


  • Scholar-in-Training Award, Third AACR International Conference on Frontiers in Basic Cancer Research (2013)
  • Helena Anna Henzl-Gabor Travel Fellowship, Stanford University (2012)
  • Best Poster Award, Gordon Research Conference (2011)
  • Genetics Work-Study Award, UC Davis (2009 - 2010)
  • UCD & Humanities Graduate Research Award, UC Davis (2008 - 2009)
  • Genetics Work-Study Award, UC Davis (2008 - 2009)
  • UCD & Humanities Graduate Research Award, UC Davis (2007 - 2008)
  • Member, Phi Sigma Honor Society (2007)
  • George Lee Fellowship in Genetics, UC Davis (2007)
  • Floyd and Mary Schwall Fellowship in Medical Research in Genetics, UC Davis (2005 - 2008)
  • Member, Golden Key Honor Society (2001)
  • Member, Phi Beta Kappa Honor Society (2001)
  • Member, Phi Kappa Phi Honor Society (2001)

Boards, Advisory Committees, Professional Organizations


  • Co-Chair, Stanford University Postdoctoral Association (2012 - Present)
  • Member, Association for Women in Science (2012 - Present)
  • Member, Women in Science and Engineering (2012 - Present)
  • Ex Officio Member, Provost Advisory Committee on Postdoctoral Affairs (2012 - Present)
  • Member, National Postdoctoral Association (2012 - Present)
  • Editor-In-Chief, Postdoc Journal (2013 - 2013)
  • Postdoctoral Representative, Committee on Academic Computing and Information Systems (2012 - 2013)
  • Council member, Stanford University Postdoctoral Assocaition (2011 - Present)
  • Member, American Association for Cancer Research (2008 - Present)
  • Representative, Graduate Student Association (2008 - 2009)

Professional Education


  • Bachelor of Science, University of California Davis (2001)
  • Doctor of Philosophy, University of California Davis (2011)

Stanford Advisors


Research & Scholarship

Current Research and Scholarly Interests


Prostate cancer is a major health problem in the United States. The American Cancer Society estimates that one out of six men will be diagnosed with prostate cancer during his lifetime, while one out of thirty-six men will die from it. Since most men will not acquire an aggressive and potentially lethal form of the disease, the challenge is being able to distinguish between aggressive and indolent forms of prostate cancer, and properly treating the aggressive forms.

We have recently identified nucleolar and spindle-associated protein (NUSAP1; encoding NuSAP) as a prognosticator for prostate cancer. We found that NUSAP1 is over-expressed in recurrent prostate cancer tumors, and validated this correlation in independent prostate cancer datasets. Although NuSAP is known to be essential for cell cycle progression, faithfully binding to and stabilizing microtubules during mitosis, little is known about its role in prostate cancer progression. Hence, we are performing an extensive analysis to understand the role of NuSAP in aggressive prostate cancer. In particular, we are investigating the regulation and role of NuSAP in mechanisms of proliferation, invasion, apoptosis, cellular movement, cell cycle progression, metastasis, tumor growth, and responses to chemotherapy. Understanding the role of NuSAP in prostate cancer progression will provide insights into the inner workings of aggressive cancer cells, and may lead to new ways to prognosticate and treat aggressive forms of prostate cancer.

Projects


  • Role of NuSAP in Prostate Cancer Progression, Stanford University

    We have recently shown that nucleolar and spindle-associated protein (NUSAP1; encoding NuSAP) is overexpressed in recurrent prostate cancer tumors. Correlation between NUSAP1 transcript levels and prognosis has been seen in melanomas, glioblastomas, and breast cancers, indicating that NuSAP plays an important role in cancer aggressiveness. Although NuSAP is known to be essential for cell cycle progression, faithfully binding to and stabilizing microtubules during mitosis, little is known about its role in cancer progression. Hence, in this study we are performing an extensive analysis to understand the role of NuSAP in aggressive prostate cancer. We are investigating the regulation and role of NuSAP in mechanisms of proliferation, invasion, apoptosis, cellular movement, cell cycle progression, metastasis, tumor growth, and antitubulin chemotherapy. Understanding the role of NuSAP in prostate cancer progression will provide insights into the inner workings of aggressive cancer cells, and may lead to new ways to prognosticate and treat aggressive forms of prostate cancer.

    Location

    Stanford, CA

Lab Affiliations


Publications

Journal Articles


  • Inactive DNMT3B Splice Variants Modulate De Novo DNA Methylation PLOS ONE Gordon, C. A., Hartono, S. R., Chedin, F. 2013; 8 (7)

    Abstract

    Inactive DNA methyltransferase (DNMT) 3B splice isoforms are associated with changes in DNA methylation, yet the mechanisms by which they act remain largely unknown. Using biochemical and cell culture assays, we show here that the inactive DNMT3B3 and DNMT3B4 isoforms bind to and regulate the activity of catalytically competent DNMT3A or DNMT3B molecules. DNMT3B3 modestly stimulated the de novo methylation activity of DNMT3A and also counteracted the stimulatory effects of DNMT3L, therefore leading to subtle and contrasting effects on activity. DNMT3B4, by contrast, significantly inhibited de novo DNA methylation by active DNMT3 molecules, most likely due to its ability to reduce the DNA binding affinity of co-complexes, thereby sequestering them away from their substrate. Immunocytochemistry experiments revealed that in addition to their effects on the intrinsic catalytic function of active DNMT3 enzymes, DNMT3B3 and DNMT34 drive distinct types of chromatin compaction and patterns of histone 3 lysine 9 tri-methylation (H3K9me3) deposition. Our findings suggest that regulation of active DNMT3 members through the formation of co-complexes with inactive DNMT3 variants is a general mechanism by which DNMT3 variants function. This may account for some of the changes in DNA methylation patterns observed during development and disease.

    View details for DOI 10.1371/journal.pone.0069486

    View details for Web of Science ID 000322391400061

    View details for PubMedID 23894490

  • Mini-grants Mobilize the Stanford Postdoctoral Community The POSTDOCket Levesque, I. R., Yan, J., Gordon, C. A., de Morree, A. 2013; 11 (3): 3-4
  • Regulation of de novo DNA Methylation by Inactive DNMT3B Splice Variants ProQuest/UMI Gordon, C. A. 2011
  • DNMT3L Modulates Significant and Distinct Flanking Sequence Preference for DNA Methylation by DNMT3A and DNMT3B In Vivo PLOS GENETICS Wienholz, B. L., Kareta, M. S., Moarefi, A. H., Gordon, C. A., Ginno, P. A., Chedin, F. 2010; 6 (9)

    Abstract

    The DNTM3A and DNMT3B de novo DNA methyltransferases (DNMTs) are responsible for setting genomic DNA methylation patterns, a key layer of epigenetic information. Here, using an in vivo episomal methylation assay and extensive bisulfite methylation sequencing, we show that human DNMT3A and DNMT3B possess significant and distinct flanking sequence preferences for target CpG sites. Selection for high or low efficiency sites is mediated by the base composition at the -2 and +2 positions flanking the CpG site for DNMT3A, and at the -1 and +1 positions for DNMT3B. This intrinsic preference reproducibly leads to the formation of specific de novo methylation patterns characterized by up to 34-fold variations in the efficiency of DNA methylation at individual sites. Furthermore, analysis of the distribution of signature methylation hotspot and coldspot motifs suggests that DNMT flanking sequence preference has contributed to shaping the composition of CpG islands in the human genome. Our results also show that the DNMT3L stimulatory factor modulates the formation of de novo methylation patterns in two ways. First, DNMT3L selectively focuses the DNA methylation machinery on properly chromatinized DNA templates. Second, DNMT3L attenuates the impact of the intrinsic DNMT flanking sequence preference by providing a much greater boost to the methylation of poorly methylated sites, thus promoting the formation of broader and more uniform methylation patterns. This study offers insights into the manner by which DNA methylation patterns are deposited and reveals a new level of interplay between members of the de novo DNMT family.

    View details for DOI 10.1371/journal.pgen.1001106

    View details for Web of Science ID 000282369200044

    View details for PubMedID 20838592

  • DNA (cytosine-5)-methyltransferase 3B - [Isoform 1] DNM3B Targeted Proteins Database 1 Moarefi , A. H., Gordon, C. A., Chedin, F. 2008

    View details for DOI 10.2970/tpdb.2008.211

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