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Faculty

Paul F. Lambert, Ph.D.

Paul Lambert Photo Professor of Oncology

B.S., 1979, Biochemistry, University of Massachusetts, Amherst
Ph.D., 1985, Biochemistry, University of Wisconsin-Madison
Postdoctoral research: Laboratory of Peter Howley, National Cancer Institute

Office: 220A McArdle Laboratory
Telephone: Office - (608) 262-8533; Lab - (608) 262-6407
Email: lambert@oncology.wisc.edu

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Research Interests: Molecular genetics of papillomaviruses

Research Description: Our research focuses on understanding the biology of human papillomaviruses (HPV) that are implicated in human cancer. A subset of HPVs, most common amongst these HPV16, are now accepted to be the main cause of cervical cancer in women, with greater than 99% of these cancers harboring HPV DNA. In cervical cancers, two viral genes E6 and E7 are selectively expressed. To investigate the role of E6 and E7 in cancer, we have generated transgenic mice in which we targeted expression of HPV16 E6 and E7 to stratified squamous epithelia, the normal tissue site of infection from which cancers arise in humans. These mice are at increased risk of cancers in the skin and the cervix. Using these mice we are investigating the mechanisms of action of E6 and E7, and have found that their interaction with cellular tumor suppressors as well as other cellular factors contribute to their biological activities in vivo. Recently we have also begun studies of a third HPV oncogene, E5, which, while not always expressed in cervical cancers, likely contributes to the progressive disease that leads to the formation of these and other HPV-associated cancers. Recently constructed transgenic mouse models for studying this viral oncogene are providing exciting new insights into its oncogenic properties in vivo.

A second focus of our laboratory is the study of the HPV life cycle. The viral life cycle is intricately tied to the terminal differentiation of the host epithelium infected by the virus. Using an organotypic culturing technique that effectively leads to the formation of synthetic skin in the laboratory, we are investigating the roles of viral and cellular genes in the papillomavirus life cycle. We discovered that E7, one of the two viral genes implicated in cervical cancer, plays a critical role in the reprogramming terminally differentiating epithelial cells to support the amplification of the viral genome, a process that is highly reliant upon the cellular DNA synthetic machinery. This machinery is normally inactive in terminally differentiating cells. We also discovered that E5, another viral oncogene, also contributes to this reprogramming step. Ongoing studies are directed at understanding the role of other viral genes in the life cycle. Recently we discovered that HPV DNA genomes can replicate in yeast and this now provides us a valuable surrogate host in which to identify cellular factors that can contribute to viral DNA replication. Finally, we are interested in how the host modulates the virus. We discovered that methylation of the viral genome by cellular DNA methylases is a dynamic process that can modulate the activity of a viral transcription factor, E2, and likely plays a critical role in modulating levels of viral gene expression during the viral life cycle. These studies provide a foundation for our future interests in understanding the papillomaviral life cycle.

Selected recent publications

Bouvard, V., Baan, R., Straif, K., Grosse, Y., Secretan, B., El Ghissassi, F., Benbrahim-Tallaa, L., Guha, N., Freeman, C., Galichet, L., Cogliano, V., WHO International Agency for Research on Cancer Monograph Working Group (35 collaborators, including Paul F. Lambert). A Review of Human Carcinogens—Part B: Biological Agents. Lancet Oncol., 10: 321-322, 2009.

Chung, S.-H., and Lambert, P. F. Prevention and Treatment of Cervical Cancer in Mice Using Estrogen Receptor Antagonists. Proc. Natl. Acad. Sci. USA, 106: 19467-19472, 2009.

Jabbar, S. F., Abrams, L., Glick, A., and Lambert, P. F. Persistence of High-Grade Cervical Dysplasia and Cervical Cancer Requires the Continuous Expression of the Human Papillomavirus Type 16 E7 Oncogene. Cancer Res., 69: 4407-4414, 2009.

Lambert, P. F. The Interwoven Story of the Small DNA Tumor Viruses. Virology, 384: 255, 2009.

Pyeon, D., Pearce, S. M., Lank, S. M., Ahlquist, P., and Lambert, P. F. Establishment of Human Papillomavirus Infection Requires Cell Cycle Progression. PLoS Pathog., 5(2):e1000318, 2009.

Shin, M.-K., Balsitis, S., Brake, T., and Lambert, P. F. Human Papillomavirus E7 Oncoprotein Overrides the Tumor Suppressor Activity of p21^Cip1 in Cervical Carcinogenesis. Cancer Res., 69: 5656-5663, 2009.

Wise-Draper, T. M., Morreale, R. J., Morris, T. A., Mintz-Cole, R. A., Hoskins, E. E., Balsitis, S. J., Husseinzadeh, N., Witte, D. P., Wikenheiser-Brokamp, K. A., Lambert, P. F., and Wells, S. I. DEK Proto-Oncogene Expression Interferes with the Normal Epithelial Differentiation Program. Am. J. Pathol., 174: 71-81, 2009.

Zehbe, I., Richard, C., DeCarlo, C. A., Shai, A., Lambert, P. F., Lichtig, H., Tommasino, M., and Sherman, L. Human Papillomavirus 16 E6 Variants Differ in Their Dysregulation of Human Keratinocyte Differentiation and Apoptosis. Virology, 383: 69-77, 2009.

Chung, S.-H., Wiedmeyer, K., Shai, A., Korach, K. S., and Lambert, P. F. Requirement for Estrogen Receptor α in a Mouse Model for Human Papillomavirus-Associated Cervical Cancer. Cancer Res., 68: 9928-9934, 2008.

DeCarlo, C. A., Escott, N. G., Werner, J., Robinson, K., Lambert, P. F., Law, R. D., and Zehbe, I. Gene Expression Analysis of Interferon κ in Laser Capture Microdissected Cervical Epithelium. Anal. Biochem., 381: 59-66, 2008.

Diaz-Chavez, J., Hernandez-Pando, R., Lambert, P. F., and Gariglio, P. Down-regulation of Transforming Growth Factor-β Type II Receptor (TGF-βRII) Protein and mRNA Expression in Cervical Cancer. Mol. Cancer, 7:3, 2008.

Kalantari, M., Lee, D., Calleja-Macias, I. E., Lambert, P. F., and Bernard, H.-U. Effects of Cellular Differentiation, Chromosomal Integration and 5'-Aza-2'-Deoxycytidine Treatment on Human Papillomavirus-16 DNA Methylation in Cultured Cell Lines. Virology, 374: 292-303, 2008.

Lambert, P. F., and Strati, K. Oncogenic Viruses. In: Encyclopedia of Microbiology, 2008.

Massimi, P., Shai, A., Lambert, P., and Banks, L. HPV E6 Degradation of p53 and PDZ Containing Substrates in an E6AP Null Background. Oncogene, 27: 1800-1804, 2008.

Mendoza-Villanueva, D., Diaz-Chavez, J., Uribe-Figueroa, L., Rangel-Escareão, C., Hidalgo-Miranda, A., March-Mifsut, S., Jimenez-Sanchez, G., Lambert, P. F., and Gariglio, P. Gene Expression Profile of Cervical and Skin Tissues from Human Papillomavirus Type 16 E6 Transgenic Mice. BMC Cancer, 8:347, 2008.

Shai, A., Pitot, H. C., and Lambert, P. F. p53 Loss Synergizes with Estrogen and Papillomaviral Oncogenes to Induce Cervical and Breast Cancers. Cancer Res., 68: 2622-2631, 2008.

Strati, K., and Lambert, P. F. Human Papillomavirus Association with Head and Neck Cancers: Understanding Virus Biology and Using It In the Development of Cancer Diagnostics. Expert Opin. Med. Diagn., 2: 11-20, 2008.

Lambert, P. F., and Collins, A. Human Papillomaviruses: Molecular Biology. In: Encyclopedia of Virology, 2007.

Lambert, P. F., and Griep, A. E. In Vivo Models for the Study of Animal and Human Papillomaviruses. In: R. Garcea and D. DiMaio (Eds.), The Papillomaviruses, pp. 253-276. The Netherlands: Springer Scientific (Kluwer Academic), 2007.

Maufort, J. P., Genther Williams, S. M., Pitot, H. C., and Lambert, P. F. Human Papillomavirus 16 E5 Oncogene Contributes to Two Stages of Skin Carcinogenesis. Cancer Res., 67: 6106-6112, 2007.

Nakahara, T., and Lambert, P. F. Induction of Promyelocytic Leukemia (PML) Oncogenic Domains (PODs) by Papillomavirus. Virology, 366: 316-329, 2007.

Pyeon, D., Newton, M. A., Lambert, P. F., den Boon, J. A., Sengupta, S., Marsit, C. J., Woodworth, C. D., Connor, J. P., Haugen, T. H., Smith, E. M., Kelsey, K. T., Turek, L. P., and Ahlquist, P. Fundamental Differences in Cell Cycle Deregulation in Human Papillomavirus-Positive and Human Papillomavirus-Negative Head/Neck and Cervical Cancers. Cancer Res., 67: 4605-4619, 2007.

Shai, A., Brake, T., Somoza, C., and Lambert, P. F. The Human Papillomavirus E6 Oncogene Dysregulates the Cell Cycle and Contributes to Cervical Carcinogenesis through Two Independent Activities. Cancer Res., 67: 1626-1635, 2007. Erratum in: Cancer Res., 67: 3492, 2007.

Shai, A., Nguyen, M. L., Wagstaff, J., Jiang, Y.-h., and Lambert, P. F. HPV16 E6 Confers p53-dependent and p53-independent Phenotypes in the Epidermis of Mice Deficient for E6AP. Oncogene, 26: 3321-3328, 2007.

Spardy, N., Duensing, A., Charles, D., Haines, N., Nakahara, T., Lambert, P. F., and Duensing, S. The Human Papillomavirus Type 16 E7 Oncoprotein Activates the Fanconi Anemia (FA) Pathway and Causes Accelerated Chromosomal Instability in FA Cells. J. Virol., 81: 13265-13270, 2007.

Strati, K., and Lambert, P. F. Role of Rb-Dependent and Rb-Independent Functions of Papillomavirus E7 Oncogene in Head and Neck Cancer. Cancer Res., 67: 11585-11593, 2007.

Balsitis, S., Dick, F., Dyson, N., and Lambert, P. F. Critical Roles for Non-pRb Targets of Human Papillomavirus Type 16 E7 in Cervical Carcinogenesis. Cancer Res., 66: 9393-9400, 2006.

Lambert, P. F., Balsitis, S. J., Shai, A., Simonson, S. J. S., and Williams, S. M. G. Transgenic Mouse Models for the In Vivo Analysis of Papillomavirus Oncogene Function. In: M. Saveria Campo (Ed.), Papillomavirus Research: From Natural History to Vaccines and Beyond, pp. 213-228. Caister Academic Press, 2006.

Strati, K., Pitot, H. C., and Lambert, P. F. Identification of Biomarkers That Distinguish Human Papillomavirus (HPV)-positive Versus HPV-negative Head and Neck Cancers in a Mouse Model. Proc. Natl. Acad. Sci. USA, 103: 14152-14157, 2006.

Balsitis, S., Dick, F., Lee, D., Farrell, L., Hyde, R. K., Griep, A. E., Dyson, N., and Lambert, P. F. Examination of the pRb-Dependent and pRb-Independent Functions of E7 in Vivo. J. Virol., 79: 11392-11402, 2005.

Brake, T., and Lambert, P. F. Estrogen Contributes to the Onset, Persistence, and Malignant Progression of Cervical Cancer in a Human Papillomavirus-transgenic Mouse Model. Proc. Natl. Acad. Sci. USA, 102: 2490-2495, 2005.

Collins, A. S., Nakahara, T., Do, A., and Lambert, P. F. Interactions with Pocket Proteins Contribute to the Role of Human Papillomavirus Type 16 E7 in the Papillomavirus Life Cycle. J. Virol., 79: 14769-14780, 2005.

Davy, C. E., Jackson, D. J., Raj, K., Peh, W. L., Southern, S. A., Das, P., Sorathia, R., Laskey, P., Middleton, K., Nakahara, T., Wang, Q., Masterson, P. J., Lambert, P. F., Cuthill, S., Millar, J. B. A., and Doorbar, J. Human Papillomavirus Type 16 E1^E4-Induced G₂ Arrest Is Associated with Cytoplasmic Retention of Active Cdk1/Cyclin B1 Complexes. J. Virol., 79: 3998-4011, 2005.

Genther Williams, S. M., Disbrow, G. L., Schlegel, R., Lee, D., Threadgill, D. W., and Lambert, P. F. Requirement of Epidermal Growth Factor Receptor for Hyperplasia Induced by E5, a High-Risk Human Papillomavirus Oncogene. Cancer Res., 65: 6534-6542, 2005.

Holmgren, S. C., Patterson, N. A., Ozbun, M. A., and Lambert, P. F. The Minor Capsid Protein L2 Contributes to Two Steps in the Human Papillomavirus Type 31 Life Cycle. J. Virol., 79: 3938-3948, 2005.

Kim, K., Angeletti, P. C., Hassebroek, E. C., and Lambert, P. F. Identification of cis-Acting Elements That Mediate the Replication and Maintenance of Human Papillomavirus Type 16 Genomes in Saccharomyces cerevisiae. J. Virol., 79: 5933-5942, 2005.

Lambert, P. F., and Brake, T. Models for Human Cervical Cancer. In: Drug Discov. Today: Dis. Models, 2: 15 -20, 2005.

Lambert, P. F., Ozbun, M. A., Collins, A., Holmgren, S., Lee, D., and Nakahara, T. Using an Immortalized Cell Line to Study the HPV Life Cycle in Organotypic “Raft” Cultures. Methods Mol. Med., 119: 141-156, 2005.

Nakahara, T., Peh, W. L., Doorbar, J., Lee, D., and Lambert, P. F. Human Papillomavirus Type 16 E1^E4 Contributes to Multiple Facets of the Papillomavirus Life Cycle. J. Virol., 79: 13150-13165, 2005.

Pyeon, D., Lambert, P. F., and Ahlquist, P. Production of Infectious Human Papillomavirus Independently of Viral Replication and Epithelial Cell Differentiation. Proc. Natl. Acad. Sci. USA, 102: 9311-9316, 2005.

Simonson, S. J. S., Difilippantonio, M. J., and Lambert, P. F. Two Distinct Activities Contribute to Human Papillomavirus 16 E6’s Oncogenic Potential. Cancer Res., 65: 8266-8273, 2005.

Matsumoto, K., Leggatt, G. R., Zhong, J., Liu, X., de Kluyver, R. L., Peters, T., Fernando, G. J. P., Liem, A., Lambert, P. F., and Frazer, I. H. Impaired Antigen Presentation and Effectiveness of Combined Active/Passive Immunotherapy for Epithelial Tumors. J. Natl. Cancer Inst., 96: 1611-1619, 2004.

Schaeffer, A. J., Nguyen, M., Liem, A., Lee, D., Montagna, C., Lambert, P. F., Ried, T., and Difilippantonio, M. J. E6 and E7 Oncoproteins Induce Distinct Patterns of Chromosomal Aneuploidy in Skin Tumors from Transgenic Mice. Cancer Res., 64: 538-546, 2004.

Balsitis, S. J., Sage, J., Duensing, S., Münger, K., Jacks, T., and Lambert, P. F. Recapitulation of the Effects of the Human Papillomavirus Type 16 E7 Oncogene on Mouse Epithelium by Somatic Rb Deletion and Detection of pRb-Independent Effects of E7 In Vivo. Mol. Cell. Biol., 23: 9094-9103, 2003.

Brake, T., Connor, J. P., Petereit, D. G., and Lambert, P. F. Comparative Analysis of Cervical Cancer in Women and in a Human Papillomavirus-Transgenic Mouse Model: Identification of Minichromosome Maintenance Protein 7 as an Informative Biomarker for Human Cervical Cancer. Cancer Res., 63: 8173-8180, 2003.

Genther, S. M., Sterling, S., Duensing, S., Münger, K., Sattler, C., and Lambert, P. F. Quantitative Role of the Human Papillomavirus Type 16 E5 Gene during the Productive Stage of the Viral Life Cycle. J. Virol., 77: 2832-2842, 2003.

Kim, K., Garner-Hamrick, P. A., Fisher, C., Lee, D., and Lambert, P. F. Methylation Patterns of Papillomavirus DNA, Its Influence on E2 Function, and Implications in Viral Infection. J. Virol., 77: 12450-12459, 2003.

Middleton, K., Peh, W., Southern, S., Griffin, H., Sotlar, K., Nakahara, T., El-Sherif, A., Morris, L., Seth, R., Hibma, M., Jenkins, D., Lambert, P., Coleman, N., and Doorbar, J. Organization of Human Papillomavirus Productive Cycle during Neoplastic Progression Provides a Basis for Selection of Diagnostic Markers. J. Virol., 77: 10186-10201, 2003.

Nguyen, M. L., Nguyen, M. M., Lee, D., Griep, A. E., and Lambert, P. F. The PDZ Ligand Domain of the Human Papillomavirus Type 16 E6 Protein Is Required for E6's Induction of Epithelial Hyperplasia In Vivo. J. Virol., 77: 6957-6964, 2003.

Nguyen, M. M., Nguyen, M. L., Caruana, G., Bernstein, A., Lambert, P. F., and Griep, A. E. Requirement of PDZ-Containing Proteins for Cell Cycle Regulation and Differentiation in the Mouse Lens Epithelium. Mol. Cell. Biol., 23: 8970-8981, 2003.

Riley, R. R., Duensing, S., Brake, T., Münger, K., Lambert, P. F., and Arbeit, J. M. Dissection of Human Papillomavirus E6 and E7 Function in Transgenic Mouse Models of Cervical Carcinogenesis. Cancer Res., 63: 4862-4871, 2003.

Angeletti, P. C., Kim, K., Fernandes, F. J., and Lambert, P. F. Stable Replication of Papillomavirus Genomes in Saccharomyces cerevisiae. J. Virol., 76: 3350-3358, 2002.

Kim, K., and Lambert, P. F. E1 Protein of Bovine Papillomavirus 1 Is Not Required for the Maintenance of Viral Plasmid DNA Replication. Virology, 293: 10-14, 2002.

Nguyen, M., Song, S., Liem, A., Androphy, E., Liu, Y., and Lambert, P. F. A Mutant of Human Papillomavirus Type 16 E6 Deficient in Binding a-Helix Partners Displays Reduced Oncogenic Potential In Vivo. J. Virol., 76: 13039-13048, 2002.

Young, M. R., Farrell, L., Lambert, P., Awasthi, P., and Colburn, N. H. Protection Against Human Papillomavirus Type 16-E7 Oncogene-Induced Tumorigenesis by In Vivo Expression of Dominant-Negative c-jun. Mol. Carcinog., 34: 72-77, 2002.

Azoury-Ziadeh, R., Herd, K., Fernando, G. J. P., Lambert, P., Frazer, I. H., and Tindle, R. W. Low Level Expression of Human Papillomavirus Type 16 (HPV16) E6 in Squamous Epithelium Does Not Elicit E6 Specific B- or T-Helper Immunological Responses, or Influence the Outcome of Immunisation with E6 Protein. Virus Res., 73: 189-199, 2001.

Duensing, S., Duensing, A., Flores, E. R., Do, A., Lambert, P. F., and Münger, K. Centrosome Abnormalities and Genomic Instability by Episomal Expression of Human Papillomavirus Type 16 in Raft Cultures of Human Keratinocytes. J. Virol., 75: 7712-7716, 2001.

Frazer, I. H., De Kluyver, R., Leggatt, G. R., Guo, H. Y., Dunn, L., White, O., Harris, C., Liem, A., and Lambert, P. Tolerance or Immunity to a Tumor Antigen Expressed in Somatic Cells Can Be Determined by Systemic Proinflammatory Signals at the Time of First Antigen Exposure. J. Immunol., 167: 6180-6187, 2001.

Tindle, R. W., Herd, K., Doan, T., Bryson, G., Leggatt, G. R., Lambert, P., Frazer, I. H., and Street, M. Nonspecific Down-Regulation of CD8⁺ T-Cell Responses in Mice Expressing Human Papillomavirus Type 16 E7 Oncoprotein from the Keratin-14 Promoter. J. Virol., 75: 5985-5997, 2001.

Verma, M., Lambert, P. F., and Srivastava, S. K. Meeting highlights: National Cancer Institute workshop on Molecular Signatures of Infectious Agents. Dis. Markers, 17: 191-201, 2001.

Do, A. N. D., Farrell, L., Kim, K., Nguyen, M. L., and Lambert, P. F. Oncogenic Viruses. In: Encyclopedia of Microbiology, Volume 3, Seco^nd Edition, pp. O-8-O-17. San Diego: Academic Press, 2000.

Doan, T., Herd, K. A., Lambert, P. F., Fernando, G. J. P., Street, M. D., and Tindle, R. W. Peripheral Tolerance to Human Papillomavirus E7 Oncoprotein Occurs by Cross-Tolerization, Is Largely Th-2-independent, and Is Broken by Dendritic Cell Immunization. Cancer Res., 60: 2810-2815, 2000.

Flores, E. R., Allen-Hoffmann, B. L., Lee, D., and Lambert, P. F. The Human Papillomavirus Type 16 E7 Oncogene Is Required for the Productive Stage of the Viral Life Cycle. J. Virol., 74: 6622-6631, 2000.

Heino, P., Zhou, J., and Lambert, P. F. Interaction of the Papillomavirus Transcription/Replication Factor, E2, and the Viral Capsid Protein, L2. Virology, 276: 304-314, 2000.

Nelson, J. H., Hawkins, G. A., Edlund, K., Evander, M., Kjellberg, L., Wadell, G., Dillner, J., Gerasimova, T., Coker, A. L., Pirisi, L., Petereit, D., and Lambert, P. F. A Novel and Rapid PCR-Based Method for Genotyping Human Papillomaviruses in Clinical Samples. J. Clin. Microbiol., 38: 688-695, 2000.

Song, S., Liem, A., Miller, J. A., and Lambert, P. F. Human Papillomavirus Types 16 E6 and E7 Contribute Differently to Carcinogenesis. Virology, 267: 141-150, 2000.

Doan, T., Herd, K., Street, M., Bryson, G., Fernando, G., Lambert, P., and Tindle, R. Human Papillomavirus Type 16 E7 Oncoprotein Expressed in Peripheral Epithelium Tolerizes E7-Directed Cytotoxic T-Lymphocyte Precursors Restricted through Human (and Mouse) Major Histocompatibility Complex Class I Alleles. J. Virol., 73: 6166-6170, 1999.

Flores, E. R., Allen-Hoffmann, B. L., Lee, D., Sattler, C. A., and Lambert, P. F. Establishment of the Human Papillomavirus Type 16 (HPV-16) Life Cycle in an Immortalized Human Foreskin Keratinocyte Cell Line. Virology, 262: 344-354, 1999.

Hilditch-Maguire, P. A., (Lieppe[sic]) Leippe, D. M., West, D., Lambert, P. F., and Frazer, I. H. T Cell-Mediated and Non-Specific Inflammatory Mechanisms Contribute to the Skin Pathology of HPV 16 E6E7 Transgenic Mice. Intervirology, 42: 43-50, 1999.

Lambert, P., Flores, E., Heino, P., and Song, S. Papillomaviruses-Human: Molecular Biology. In: Encyclopedia of Virology, pp. 1-7. San Diego: Academic Press, 1999.

Song, S., and Lambert, P. F. Different Responses of Epidermal and Hair Follicular Cells to Radiation Correlate with Distinct Patterns of p53 and p21 Induction. Am. J. Pathol., 155: 1121-1127, 1999.

Song, S., Pitot, H. C., and Lambert, P. F. The Human Papillomavirus Peripheral Type 16 E6 Gene Alone Is Sufficient to Induce Carcinomas in Transgenic Animals. J. Virol., 73: 5887-5893, 1999.

Doan, T., Chambers, M., Street, M., Fernando, G. J. P., Herd, K., Lambert, P., and Tindle, R. Mice Expressing the E7 Oncogene of HPV16 in Epithelium Show Central Tolerance, and Evidence of Peripheral Anergising Tolerance, to E7-Encoded Cytotoxic T-Lymphocyte Epitopes. Virology, 244: 352-364, 1998.

Frazer, I. H., Fernando, G. J. P., Fowler, N., Leggatt, G. R., Lambert, P. F., Liem, A., Malcolm, K., and Tindle, R. W. Split Tolerance to a Viral Antigen Expressed in Thymic Epithelium and Keratinocytes. Eur. J. Immunol., 28: 2791-2800, 1998.

Griep, A. E., Krawcek, J., Lee, D., Liem, A., Albert, D. M., Carabeo, R., Drinkwater, N., McCall, M., Sattler, C., Lasudry, J. G. H., and Lambert, P. F. Multiple Genetic Loci Modify Risk for Retinoblastoma in Transgenic Mice. Invest. Ophthalmol. Vis. Sci., 39: 2723-2732, 1998.

Song, S., Gulliver, G. A., and Lambert, P. F. Human Papillomavirus Type 16 E6 and E7 Oncogenes Abrogate Radiation-induced DNA Damage Responses in Vivo Through p53-dependent and p53-independent Pathways. Proc. Natl. Acad. Sci. USA, 95: 2290-2295, 1998.

Flores, E. R., and Lambert, P. F. Evidence for a Switch in the Mode of Human Papillomavirus Type 16 DNA Replication during the Viral Life Cycle. J. Virol., 71: 7167-7179, 1997.

Gulliver, G. A., Herber, R. L., Liem, A., and Lambert, P. F. Both Conserved Region 1 (CR1) and CR2 of the Human Papillomavirus Type 16 E7 Oncogene Are Required for Induction of Epidermal Hyperplasia and Tumor Formation in Transgenic Mice. J. Virol., 71: 5905-5914, 1997.

Mansky, K. C., Batiza, A., and Lambert, P. F. Bovine Papillomavirus Type 1 E1 and Simian Virus 40 Large T Antigen Share Regions of Sequence Similarity Required for Multiple Functions. J. Virol., 71: 7600-7608, 1997.

Herber, R., Liem, A., Pitot, H., and Lambert, P. F. Squamous Epithelial Hyperplasia and Carcinoma in Mice Transgenic for the Human Papillomavirus Type 16 E7 Oncogene. J. Virol., 70: 1873-1881, 1996.

Jeon, S., and Lambert, P. F. Integration of Human Papillomavirus Type 16 DNA into the Human Genome Leads to Increased Stability of E6 and E7 mRNAs: Implications of Cervical Carcinogenesis. Proc. Natl. Acad. Sci. USA, 92: 1654-1658, 1995.

Rank, N. M., and Lambert, P. F. Bovine Papillomavirus Type 1 E2 Transcriptional Regulators Directly Bind Two Cellular Transcription Factors, TFIID and TFIIB. J. Virol., 69: 6323-6334, 1995.