|Wayne D. Lancaster, Ph.D.
3230 Scott Hall
540 E. Canfield Avenue
Detroit, MI 48201
|Professor (also with Obstetrics and Gynecology); Ph.D., Wayne State, 1973. Papillomaviruses: molecular biology, evolution, and role in human carcinogenesis; cancer cell genome instability; ovarian carcinogenesis.
The main research interest of the laboratory centers around two gynecologic malignancies: carcinoma of the cervix and epithelial ovarian cancer. Current research into cervical cancer is defining the interactions between independent risk factors associated with the disease (smoking, tetrahydrofolate reductase polymormisms, Chlamydia infection and loss of heterozygosity at the fragile histidine triad gene, and human papillomavirus (HPV) sequences in premalignant lesions. Although HPV is necessary for development of cervical cancer it is not sufficient to cause the disease and other cofactor(s) are thought to play a role in development of the disease. The laboratory has developed human and murine models for ovarian cancer. Growth of ovarian surface epithelial (OSE) cells in culture results, over time, results in the immortalization and eventual malignant transformation of the cells. We have developed assays to monitor growth through organotypic culture in which early invasive cells have been identified. This stage of development may represent either a precursor to ovarian cancer or very early ovarian cancer. The long-range goal of these studies is to identify aberrantly expressed genes in OSE cells at various stages along the path to the malignant phenotype for the purpose of characterizing biochemical pathways whose expression is dysregulated as assayed by microarrays.
Rabah R, Lancaster WD, Thomas R, Gregoire L. 2001. HPV-11 associated recurrent respiratory papillomatosis is more aggressive than HPV-6 associated disease. Ped. Develop. Pathol. 4:68-72.
Tsao SW, Wong N, Wang XH, Liu Y, Cheung YK, Wan TSK, Fung LF, Lancaster WD, Gregoire L, Lo AKF, Wong YC. 2001. Non-random chromosomal imbalances in human ovarian surface epithelial (HOSE) cells immortalized by HPV16-E6E7 viral oncogenes. Cancer Genet. Cytogenet. 130:141-149.
Gregoire L, Rabah R, Schmelz E-M, Munkarah A, Roberts PC, Lancaster WD. 2001. Spontaneous malignant transformation of human ovarian surface epithelial cells in vitro. Clin. Cancer Res. 7:4280-4287.
Rangel LB, Agarwal R, D'Souza T, Pizer ES, Alo PL, Lancaster WD, Gregoire L, Schwartz DR, Cho KR, Morin PJ. 2003. Tight junction proteins claudin-3 and claudin-4 are frequently overexpressed in ovarian cancer but not in ovarian cystadenomas. Clin Cancer Res. 2003 9:2567-2575.
Lancaster WD, Campione-Picarrdo J. 2003. Viral agents. In Bertino JR (ed), Encyclopedia of Cancer, Second Edition. Academic Press, NY (in press).
Gregoire L, Reidy P, Rabah R, Lancaster, WD. 2003. HLA DQ allele associations in Caucasian and African-American juvenile onset laryngeal papilloma patients. Arch. Otol. Head Neck Surg. (in press).