Department of Obstetrics and Gynecology/Division of Gynecologic Oncology, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A.; Cancer Research Laboratory of the Department of Otolaryngology/Head and Neck Surgery, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A., Department of Pathology, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A., Cancer Research Laboratory of the Department of Otolaryngology/Head and Neck Surgery, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A., Department of Obstetrics and Gynecology, Turku University Hospital, Turku, Finland, Cytogenetics Laboratory, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202, U.S.A., Grenman, Seija E., Worsham, Maria J., Van Dyke, Daniel L., England, Barry G., McClatchey, Kenneth D., Babu, V. Ramesh, Roberts, James A., Maenpaa, Juhani, Carey, Thomas E., Department of Obstetrics and Gynecology/Division of Gynecologic Oncology, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A.; Cancer Research Laboratory of the Department of Otolaryngology/Head and Neck Surgery, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A., Department of Pathology, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A., Cancer Research Laboratory of the Department of Otolaryngology/Head and Neck Surgery, University of Michigan, 1301 East Ann Street, Ann Arbor, Michigan 48109-0506, U.S.A., Department of Obstetrics and Gynecology, Turku University Hospital, Turku, Finland, Cytogenetics Laboratory, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, Michigan 48202, U.S.A., Grenman, Seija E., Worsham, Maria J., Van Dyke, Daniel L., England, Barry G., McClatchey, Kenneth D., Babu, V. Ramesh, Roberts, James A., Maenpaa, Juhani, and Carey, Thomas E.
UM-EC-2 was established from a patient with poorly differentiated stage IB endometrial carcinoma. This cell line produces tumors in nude mice that have the same histological features as the patient's tumor. UM-EC-2 cells express [beta]2-microglobulin, the epidermal growth factor receptor (EGF), and the H blood group antigen. This membrane antigen phenotype is consistent with cells of human endometrial origin. The karyotype of UM-EC-2 is fairly complex, with rearrangements affecting all chromosomes except 3, 10, 14, 19, and 20. There were two populations of cells, a hyperdiploid population with a modal number of 53-55 and a hypertetraploid population with a modal number of 109. A postulated sequence of events before and after tetraploidization is suggested based on the number of copies of individual chromosomes and rearrangements. Comparison of the UM-EC-2 karyotype to that of UM-EC-1 (a previously described line from a different patient with endometrial carcinoma) revealed that the two lines share eight very similar chromosome changes, which include loss of most of chromosome 4, breakpoints affecting proximal bands on 8p, loss of most of 9q, a breakpoint at 12q22, loss of 13q, breakpoints in proximal bands on 18q, and a breakpoint at 22p11. These changes may represent nonrandom chromosome abnormalities in poorly differentiated endometrial cancer. Estrogen (ER) and progesterone (PgR) receptors were not detected in either the primary tumor or the cell line. Nevertheless, UM-EC-2 cells were very sensitive to growth inhibition by tamoxifen (TAM) in vitro. One micromolar TAM caused 50% inhibition of cell growth, 2.5 [mu]M caused cytostasis, and 5 [mu]M TAM was cytotoxic, killing all cells after 5-7 days of exposure to the drug. Paradoxically, 100 nM estradiol (E2) caused a moderate increase in the growth of the cells but it did not prevent or reverse growth inhibitory effects of TAM. These findings support the concept that in some tumors TAM causes growth inhibition by a