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Creek, Kim
Kim Creek
Chair, Professor
Office Location
USC Campus
CLS 609C

715 Sumter Street

Columbia
, SC29208
Phone: (803) 777-0952

Fax: (803) 777-8356

creekk@sccp.sc.edu
Links
Home Page / Laboratory Page
Direct Link to Profile
 
  • University of Puget Sound, Tacoma, Washington B.S. 1976 Biology
  • Purdue University, West Lafayette, Indiana Ph.D. 1980 Cell Biology/Biochemistry
  • Washington Univ. School of Medicine, St. Louis, MO Postdoctoral 1983 Cell Biology
  • National Cancer Institute, NIH, Bethesda, Maryland Staff Fellow 1987 Carcinogenesis
  1. Khan, M.A., Canhoto, A.J., Housley, P.R., Creek, K.E., and Pirisi, L: Glucocorticoids stimulate growth of human papillomavirus type 16 (HPV16)-immortalized human keratinocytes and support HPV16-mediated immortalization without affecting the levels of HPV16 E6/E7 mRNA. Exp. Cell Res. 236: 304-310, 1997.
  2. Hodam, J.R. and Creek, K.E.: Comparison of the metabolism of retinol delivered to human keratinocytes either bound to serum retinol-binding protein or added directly to the culture medium. Exp. Cell Res. 238: 257-264, 1998.
  3. Xu, X., Liao, J., Creek, K.E., and Pirisi, L.: Human keratinocytes and tumor-derived cell lines express alternatively spliced forms of transforming growth factor-??mRNA, encoding precursors lacking carboxyl-terminal valine residues. Oncogene 18: 5554-5562, 1999.
  4. Asbill, C., Kim, N., El-Kattan, A., Creek, K.E., Wertz, P. and Michniak, B.: Evaluation of a human bio-engineered skin equivalent for drug permeation studies. Pharm. Res. 17: 1092-1097, 2000
  5. Xie, D., Shu, O.-X., Deng, Z., Wen, W.-Q., Creek, K.E., Dai, Q., Gao, Y.-T., Jin, F., and Zheng, W.: A population-based case-control study of HER2 genetic polymorphism and breast cancer risk. J. Natl. Cancer Instit. 92: 412-417, 2000.
  6. Borger, D.R., Mi, Y., Geslani, G., Zyzak, L.L., Batova, A., Engin, T.S.W., Pirisi, L., and Creek, K.E.: Retinoic acid resistance at late stages of human papillomavirus type 16-mediated transformation of human keratinocytes arises despite intact retinoid signaling and is due to a loss of sensitivity to transforming growth factor-beta. Virol. 270: 397-407, 2000.
  7. Mi, Y., Borger, D.R., Fernandes, P.R., Pirisi, L., and Creek, K.E.: Loss of transforming growth factor-beta (TGF-?) receptor type I mediates TGF-? resistance in human papillomavirus type 16 transformed human keratinocytes at late stages of in vitro progression Virol. 270: 408-416, 2000.
  8. Xu, X., Kelleher, K.F., Liao, J., Creek, K.E., and Pirisi, L.: Unique carboxyl terminal sequences of wild-type and alternatively spliced variant forms of transforming growth factor-? precursors mediate specific interactions with ErbB4 and ErbB2.Oncogene 19: 3172-3181, 2000.
  9. Krahmer, M.T., Walters, J.J., Fox, K.F., Fox, A. Creek, K.E., Pirisi, L., Wunschel, D.S., Smith, R.D., Tabb, D.L., and Yates, J.R.: MS for identification of single nucleotide polymorphisms and MS/MS for discrimination of isomeric PCR products. Anal. Chem. 72: 4033-4040, 2000.
  10. Akerman, G.S., Tolleson, W.H., Brown, K.L., Zyzak, L.L., Mourateva, E., Engin, T.S.W., Basaraba, A., Coker, A.L., Creek, K.E., and Pirisi, L.: Human papillomavirus type 16 E6 and E7 cooperate to increase epidermal growth factor receptor (EGFR) mRNA levels, overcoming mechanisms by which excessive EGFR signaling shortens the life span of normal human keratinocytes. Cancer Res. 61: 3837-3843, 2001.
  11. Walters, J.J., Muhammad, W., Fox, K.F., Fox, A., Xie, D., Creek, K.E., and Pirisi, L.: Genotyping single nucleotide polymorphisms using intact polymerase chain reaction products by electrospray quadrupole mass spectrometry. Rapid Commun. Mass Spectrom. 15: 1752-1759, 2001.
  12. Baldwin, A., Pirisi, L., and Creek, K.E.: NFI/Ski interactions mediate transforming growth factor-beta modulation of human papillomavirus type 16 early gene expression. J. Virol, 78: 3953-3964, 2004.
  13. Ohashi, Y., Creek, K.E., Pirisi, L., Kalus, R., and Young, S.R.: RNA degradation in human breast tissue after surgical removal: a time-course study. Exp. Mol. Path. 77: 98-103, 2004.
  14. Bagasra O, Stir, A.E., Pirisi-Creek L., Creek K.E., Bagasra A.U., Glenn, N. and Lee J.S. Role of microRNAs in the regulation of lentiviral latency and persistence. Applied Immunohistochemistry and Molecular Morphology, 14: 276-290, 2006.
  15. Gillison, M.L., Chen, R., Goshu, E., Rushlow, D., Chen, N., Banister, C. Creek, K.E., and Gallie, B.L.: Human retinoblastoma is not caused by known pRb-inactivating human DNA tumor viruses. Int. J. Cancer 120: 1482-1490, 2007.
  16. Baldwin, A., Hypes, M.K., Pirisi, L., and Creek K.E.: NFI is an essential positive transcription factor for human Papillomavirus type 16 early gene expression. The Open Virology Journal 1: 33-38, 2007.
  17. Wan, F., Miao, X., Quraishi, I., Kennedy, V., Creek, K.E., and Pirisi, L.: Gene expression changes during HPV-mediated carcinogenesis: A comparison between an in vitro cell model and cervical cancer. Int. J. Cancer 123: 32-40, 2008.
  18. Bheda, A., Creek, K.E., and Pirisi, L.: Loss of p53 induces epidermal growth factor receptor promoter activity in normal human keratinocytes. Oncogene 27: 4315-4323, 2008.
  19. Hypes, M.K., Pirisi, L., and Creek, K.: Mechanisms of decreased expression of transforming growth factor-      beta receptor type I at late stages of HPV16-mediated transformation. Cancer Letters 282: 177-186, 2009.