The lab experience should be a positive one. As a member of my lab each student should achieve mastery of new biological lab techniques, an intellectual understanding of research questions and literature, and a feeling of collaboration and camaraderie through active learning. The lab team experience promotes success of both the students and the projects. Graduate and undergraduate students in my lab are expected to participate in research projects as part of a team. No student is singularly responsible for her/his own personal project. Students help each other get experiments finished, troubleshoot problems, and analyze results for posters and publications. New students get to learn from the more senior students; senior students in turn test their understanding of concepts and protocols by teaching the new.  Publications include all members of the team further promoting collaboration as well as a sense of accomplishment by everyone. Students are expected to participate in weekly lab research progress meetings, journal clubs, and joint meetings with other University lab collaborators.





DNA repair and genome stability in mitotic cells using a mouse model 

Although the role of homologous recombination (HR) to repair DNA damage is well appreciated in meiosis of prokaryotes, yeast, and metazoans. However the role of interchromosomal HR (between TWO different chromosomes) to occur in vivo in many different types of cells of mammals is only minimally understood. It is important to understand when interchromosomal HR can occur because it has the potential maintain genome stability, and also drive genetic diversity and evolution, or even genome rearrangements leading to cancer.

Our laboratory established unique mouse models using green fluorescent protein reporters (GFP) to determine the potential of DNA damage to promote HR in vivo. These models were the first to demonstrate that interchromosomal HR occurs in vivo in multiple organ systems, and provide an ideal platform to further elucidate which cells at specific developmental stages of development or differentiation may be most likely to undergo this type of DSB repair. Our research will lead to an understanding of the fundamental mechanisms of DSB rejoining at the chromosomal level, and also provide insight on genome stability and genetic evolution.

DNA damage-induced chromosomal rearrangements in leukemia

The long-term objective of this research is to understand the mechanisms used by hematopoietic (blood) cells to repair of one type of DNA damage — the double-strand break (DSB)– and the initial molecular events that lead to genomic rearrangements such as translocations, which are a hallmark of leukemias. DNA damaging agents are common therapy in the treatment of human cancers, but they also produce chromosomal rearrangements and oncogenic transformation and tumor formation. Recent data from my lab indicates that chromosomal rearrangements analogous to those observed in hematopoietic malignancies are readily formed during DSB repair in both human and mouse hematopoietic stem cell-enriched populations. My lab uses multiple genetic approaches in cultured cell lines and genetically engineered mice to identify the initial events that promote the formation of DNA damage-induced chromosomal rearrangements, and the cooperative mutations or predisposing factors that can promote (or suppress) transformation of cells that acquire them.

There is a growing list of compounds in our daily life that promote or stabilize chromosomal DSBs and may lead to these chromosomal rearrangements. These include dietary supplements and environmental toxins including estrogens used as hormone supplements, bioflavonoids such as genistein and quercetin found in foods, soy products energy drinks and dietary supplements, quinones or benzenes found in paints and flame retardants used in homes and furniture. Our research will provide an understanding of which of these can produce genome changes that may lead to leukemia and also determine if exposure in utero through maternal exposure may promote infant leukemia. tWe hope this research may lead to new approaches to prevention or therapy.

Targeted Nanoparticle-Aptamer Therapy of Ovarian Cancer

Epithelial ovarian cancer (EOC) is responsible for an estimated 21,800 new cases and 14,000 deaths each year. Overall, patients have a five-year survival rate of 30%-40%. The primary option of treatment is often invasive surgery and adjuvant chemotherapy with cisplatin and taxane (Paclitaxel) that lead to multiple systemic side effects and toxicity, limiting the doses physicians can use. Up to 80% of patients will eventually relapse and become platinum-taxane resistant.

We identified single-stranded DNA aptamers a Cell-SELEX screen that we hypothesize will selectively associate with and internalize into ovarian cancer cells but not other cells both in cultured cell lines and in a xenograft mouse model. Conjugation of the aptamers to polymer nanoparticles loaded with paclitaxel will be assessed for potential to promote in vivo targeting of platinum-based chemotherapeutics directly to tumor cells. In addition to potential translational outcomes, our studies will increase our understanding of the basic biologic characteristics of individual epithelial ovarian tumor cell membranes, aptamer association and internalization, and cellular response to aptamers and nanoparticles. This research will provide a significant new effective therapeutic approach to epithelial ovarian cancer treatment.

Biomarkers of Ovarian Cancer 

Epithelial ovarian cancer (EOC) is responsible for an estimated 21,800 new cases and 14,000 deaths each year. Overall, patients have a five-year survival rate of 30%-40%. The primary option of treatment is often invasive surgery and adjuvant chemotherapy with cisplatin and taxane (Paclitaxel) that lead to multiple systemic side effects and toxicity, limiting the doses physicians can use. Up to 80% of patients will eventually relapse and become platinum-taxane resistant.

The overall goals of this research are to (1) use genetic, genomic, and proteomic approaches to understand how altered proteins promote ovarian cancer and may act as biomarkers of susceptibility and disease, and (2) use knowledge about tumor specific characteristics or biomarkers to develop new targeted therapies. Our research used both bioinformatic approaches and proteomic approaches to identify significant loss of HOXC6 in epithelial ovarian cancer in both the tumor itself and in the serum of patients with this cancer type.




I am director of an NSF-sponsored REU Site, Biology and Biotechnology that supports 10 undergraduate students during the summer in the department to perform independent research. In addition students have the opportunity to learn about several biotechnology approaches and equipment as well as hear about turning ideas into commercial enterprise. The University provides a professional development program.



Professional Experience

  • Post-doctoral Fellow; Department of Cell Biology and Genetics, Sloan-Kettering Institute, NY (1995-1999)
  • Research Associate; Department of Cell Biology and Genetics, Sloan-Kettering Institute, NY (1999-2001)
  • Assistant Professor; Institute for Cancer Genetics, Department of Pathology, Columbia University, NY (2001-2005)
  • Associate Professor; Department of Biological Sciences, Bioinformatics Research Center, Center for Biomedical Engineering and Science, UNC Charlotte, NC (2006- present)
  • Graduate Programs Coordinator, Department of Biological Sciences, UNC Charlotte, NC (20013- present)


  • A.B., Department of Molecular Biology, Princeton University (1990)
  • Ph.D., Department of Genetics & Development, Columbia University (1995)

Courses Taught

  • Cancer Genetics (6000/8000)
  • Molecular Biology (4199/5199)
  • Cell Biology (3111)




My BIBLIOGRAPHY maintained by the US National Library of Medicine.



  • Richardson, C., Moynahan, M., Jasin, M. Double-strand break repair by interchromosomal recombination: Suppression of chromosomal translocations. Genes & Dev. 12:3831-3842, 1998.
  • Richardson, C., and Jasin, M. Frequent chromosomal translocations induced by DNA double-strand breaks. Nature 405: 697-700, 2000.
  • Richardson, C., and Jasin, M. Coupled homologous and nonhomologous repair of a double-strand break preserves genomic integrity in mammalian cells. Mol. Cell. Biol. 20: 9068-9075, 2000.
  • Elliott, B., Richardson, C., Jasin, M. Chromosomal translocation mechanisms at intronic alu elements in mammalian cells. Mol. Cell 17: 885-894, 2005.
  • Richardson, C. , Stark, J., Ommundsen, M., Jasin, M. Over-expression of Rad51 promotes alternative DSB repair and genome instability. Oncogene 23: 546-553, 2004.
  • Richardson, C., Horikoshi, N., and Pandita, T. The DSB response network in meiosis. DNA Repair 3: 1149-1164, 2004.
  • Richardson, C. Rad51, genomic stability, and tumorigenesis. Cancer Letters 218: 127-139, 2005.
  • Libura, J., Slater, D.J., Felix, C.A., Richardson, C. t-AML-like MLL Rearrangements are induced by etoposide in primary human CD34+ cells and remain stable after clonal expansion. Blood 105: 2124-2131, 2005.
  • Pulte, D., Lopez, R.A., Baker, S.T., Ward, M., Ritchie, E., Richardson, C., O’Neill, D.W., Bank, A. Ikaros increases normal apoptosis of adult erythroid cells. Amer J Hem 81: 12-17, 2006.
  • Weinstock, D., Elliott, B., Richardson, C., Jasin, M. Modeling oncogenic translocations: Distinct roles for double-strand break repair pathways in translocation formation in mammalian cells. DNA Repair, 5: 1065-1074, 2006.
  • Sung, P.A., Libura, J., Richardson, C. Etoposide and illegitimate DNA double-strand break repair in the generation of MLL chromosomal translocations. DNA Repair, 5: 1109-1118, 2006.
  • Felix, C., Robinson, B., Germano, G., Kolaris, C., Raffini, L., Nigro, L., Roumm,. E., Megonigal, M., Slater, D., Whitmarsh, R., Saginario, C., Lovett, B., Libura, J., Pegram, L., Zheng, N., Pang, S., Zhou, X., Rappaport, E., Richardson, C., Cheung, N., Blair, I., Osheroff, N. Translocation mechanism in secondary leukemias following topoisomerase II poison. In Proceedings of the Third International Symposium on Secondary Leukemias. Rome, Italy: 2006.
  • Angevine A., McCafferty, J, Bhagat, G, Friedman, R, Vogel, S, Bank, A, Richardson, C., Mears, J. Differential Gene Expression in Nodular Sclerosis Hodgkin s Lymphoma: Revealing the role of cells in the microenvironment in disease pathogenesis. Blood, 11(108A), 2006 .
  • Mantha, S., Ward, M., McCafferty, J., Herron, A., Palomero, T., Ferrando, A., Bank, A., Richardson, C. Activating Notch1 mutations are an early event in T-cell malignancy of Ikaros point mutant Plastic /+ mice. Leuk Res, 31(3): 321-327, 2007.
  • Francis, R. and Richardson, C. Hematopoietic multipotent progenitor cells highly susceptible to alternative double-strand break repair pathways that promote genome rearrangements. Genes & Dev, 2007.
  • Koptyra, M., Cramer, K., Richardson, C., Skorski, T. BCR/ABL promotes accumulation of chromosomal aberrations after oxidative and genotoxic stress. Leukemia, 22(10): 1969-1972, 2008.
  • Libura, J., Ward, M., Solecka, J., Richardson, C. Etoposide initiated MLL rearrangements detected at high frequency in primitive hematopoietic stem cells with in vitro and in vivo long term repopulating potential. Eur J Hem, 81(3): 185-195, 2008.
  •  Pandita, T.K. and Richardson, C. Chromatin remodeling finds its place in the DNA double-strand break response. Nucleic Acid Res, Jan 12 2009.
  • Mouzannar, R., McCafferty, J., Benedetto, G., Richardson, C. Low dose and high dose oxidative stress elicit early genomic and phospho-proteomic cellular responses that provide insight into cellular transformation. Int J Genomics Proteomics, 2(1): 2011. PMID: 21743783.
  • White, R, Sung, P, Vestal, CG, Benedetto, G., Cornelio, N., and Richardson, C. Double-strand break repair by interchromosomal recombination: an in vivo repair mechanism utilized by multiple somatic tissues in mammals.       PlosONE, 8(12): 1-16, 2013. e84379. PMID: 24349572 PMCID: PMC3862804
  • Bariar, B, Vestal, CG, Richardson, C. Long-term impact of chromatin remodeling and DNA damage in stem cells induced by environmental toxins and dietary agents. J Environ Pathology, Toxicology, and Oncology, 32(4): 305-25, 2013.
  • Richardson, C. Yan, S., Vestal, C.V. Oxidative stress, bone marrow failure, and genome instability in hematopoietic stem cells. Int J Mol Sci, 16(2): 2366-85, 2015.
  • Benedetto, G. Hamp, T.J., Wesselman, P.J., Richardson, C. Identification of epithelial ovarian tumor specific aptamers. Nucleic Acid Therapeutics, 25(3): 162-172, 2015.
  • Benedetto, G., Vestal, CG, Richardson, C. Aptamer-functionalized nanoparticles as “smart bombs”:  The unrealized potential for personalized medicine and targeted cancer treatment. Targeted Oncology, 2015,
  • Tait, D.L., Bahrani-Mostafavi, Z., Vestal, C.G., Richardson, C., Mostafavi, M.T. Down-regulation of HOXC6 in serous ovarian cancer. Cancer Investigation, 2015.

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