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Photo of Lubomir Turek

Lubomir Turek

Professor,  Pathology

Contact Information

Phone: +1 319 338 0581 X7177
Email: lubomir-turek@uiowa.edu
Web: Research Laboratory

Education

MD, Charles University School of Medicine, Prague, Czech Republic
Fellowship, Tumor Virology, University of Southern California
Residency, Pathology, National Cancer Institute

Appointments

Primary: Pathology

Centers and Program Affiliations

Interdisciplinary Graduate Program in Molecular and Cellular Biology

Research Interests

Genetics of Papillomavirus Infection and Cancer

MeSH Terms from Publications

Papillomaviridae, Papillomavirus Infections, Tumor Virus Infections, DNA, Viral, Oncogene Proteins, Viral, Head and Neck Neoplasms, Humans, Human papillomavirus 16, Female, Papillomavirus E7 Proteins, Cell Transformation, Viral, Risk Factors, Gene Expression Regulation, Viral, DNA Probes, HPV, Uterine Cervical Neoplasms, Prevalence, Middle Aged, Genes, Viral, Carcinoma, Squamous Cell, Alcohol Drinking, Repressor Proteins, Adult, Vaginal Smears, Male, Antibodies, Viral

Research Summary

Molecular Biology and Epidemiology of Human Papillomavirus Infection in Head and Neck Cancer

Oncogenic or "high-risk" (HR) human papillomavirus (HPV) types cause cervical cancer and other anogenital malignancies. Our group was one of the first to provide evidence that HR HPV type 16 also is causally associated with some head and neck cancers (HNC), especially those located in the tonsillar area and oropharynx. We investigate the molecular biology and molecular epidemiology of HPV in HNC carcinogenesis.

HNC represents a unique opportunity to study a cancer that presents clinically as a single disease yet has two distinct etiologies: HPV-associated and HPV-independent, associated with tobacco and alcohol use. Although the HPV-associated HNC often occurs in younger patients and presents as more advanced disease, we and others have shown that patients with HPV-associated HNC have better prognosis and survival. In our epidemiologic studies, we are developing diagnostic and prognostic molecular markers of HPV-associated and HPV-independent HNC.

In our molecular and cell biology projects, we are interested in the progression of the HR HPV-infected cell to cancer. In the infected cell as well as in premalignant clinical lesions, HPV genomes persist as extrachromosomal, supercoiled circular plasmids in the cell nucleus. In many cervical carcinomas and HNCs, however, HPV DNA is integrated in the cellular genome in a way that preserves the viral E6-E7 oncogenes yet disrupts those viral genes that are required for HPV genome replication and gene regulation in plasmid persistence, the E1 and E2 genes. We have developed a colony immortalization assay that allows us to quantitate the ability of HR HPV genomes and mutants to extend the life span of primary human keratinocytes in cell culture. From these experiments, we have isolated and characterized sets of isogenic, immortalized keratinocyte cell clones that maintain HR HPV persistence as unintegrated, plasmid genomes in long-term culture. We are using these cells to study HPV integration and to test treatments that would eliminate HPV plasmid genomes from persistently infected cells, yet would not induce unintended integration that may promote cancer development.

Both approaches use state-of-the-art molecular, genetic and biochemical methods and involve extensive collaborations with colleagues at the local, national and international level.



Recent Publications


Show publications
  1. Rubenstein, L, Smith, E, Pawlita, M, Haugen, T, Hamšíková, E, Turek, L. Human papillomavirus serologic follow-up response and relationship to survival in head and neck cancer: a case-comparison study. Infect Agent Cancer 6:9, 2011. [PubMed]
  2. Lace, M, Anson, J, Klussmann, J, Wang, D, Smith, E, Haugen, T, Turek, L. Human papillomavirus type 16 (HPV-16) genomes integrated in head and neck cancers and in HPV-16-immortalized human keratinocyte clones express chimeric virus-cell mRNAs similar to those found in cervical cancers. J Virol 85(4):1645-54, 2011. [PubMed]
  3. Smith, E, Rubenstein, L, Haugen, T, Hamsikova, E, Turek, L. Tobacco and alcohol use increases the risk of both HPV-associated and HPV-independent head and neck cancers. Cancer Causes Control 21(9):1369-78, 2010. [PubMed]
  4. Smith, E, Parker, M, Rubenstein, L, Haugen, T, Hamsikova, E, Turek, L. Evidence for vertical transmission of HPV from mothers to infants. Infect Dis Obstet Gynecol 2010:326369, 2010. [PubMed]
  5. Smith, E, Rubenstein, L, Hoffman, H, Haugen, T, Turek, L. Human papillomavirus, p16 and p53 expression associated with survival of head and neck cancer. Infect Agent Cancer 5:4, 2010. [PubMed]
  6. Lace, M, Anson, J, Haugen, T, Turek, L. Interferon regulatory factor (IRF)-2 activates the HPV-16 E6-E7 promoter in keratinocytes. Virology 399(2):270-9, 2010. [PubMed]
  7. Smith, E, Pawlita, M, Rubenstein, L, Haugen, T, Hamsikova, E, Turek, L. Risk factors and survival by HPV-16 E6 and E7 antibody status in human papillomavirus positive head and neck cancer. Int J Cancer 127(1):111-7, 2010. [PubMed]
  8. Lace, M, Yamakawa, Y, Ushikai, M, Anson, J, Haugen, T, Turek, L. Cellular factor YY1 downregulates the human papillomavirus 16 E6/E7 promoter, P97, in vivo and in vitro from a negative element overlapping the transcription-initiation site. J Gen Virol 90(Pt 10):2402-12, 2009. [PubMed]
  9. Haugen, T, Lace, M, Ishiji, T, Sameshima, A, Anson, J, Turek, L. Cellular factors are required to activate bovine papillomavirus-1 early gene transcription and to establish viral plasmid persistence but are not required for cellular transformation. Virology 389(1-2):82-90, 2009. [PubMed]
  10. Lace, Michael J, Isacson, Christina, Anson, James R, Lörincz, Attila T, Wilczynski, Sharon P, Haugen, Thomas H, Turek, Lubomír P. Upstream regulatory region alterations found in human papillomavirus type 16 (HPV-16) isolates from cervical carcinomas increase transcription, ori function, and HPV immortalization capacity in culture. J Virol 83(15):7457-66, 2009. [PubMed]