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Hubert
Stöppler, PhD
E-mail:
Research Emphasis:
The limited life span (senescence, aging) of somatic cells can be regarded as
an anti-tumor mechanism, since restricting the life span of cells prevents them
from acquiring the number of mutations necessary to become carcinogenic. We are
interested in analyzing changes in human epithelial cells that allow them to
enter the so-called "extended life span". "Extended life
span" cells may be considered precancerous as they possess an increased
growth potential, enabling them to accumulate the necessary mutations to become
immortalized. Analyzing the molecular changes associated with an "extended
life span" will enable us to identify early markers that signal the onset
of tumorigenesis and might also identify targets for early cancer treatment. Our
model system is the induction of an "extended life span" in primary
human epithelial cells through expression of oncogenes from so-called "high
risk" human papillomavirus (HPV) types (e.g. HPV 16) which influence the
function of various cellular proteins involved in cell proliferation (e.g. p53,
Rb, hDlg, telomerase) and are highly associated with the development of
anogenital cancers, especially cervical cancers. The laboratory is further
analyzing the influence of the effects of HPV oncogene expression on
angiogenesis as well as the cellular mechanisms involved in the control of the
stability of HPV oncoproteins.
Selected Publications:
Kehmeier, E., Rühl, H., Voland, B., Stöppler, M.C., Androphy, E., and
Stöppler, H. (2002) Cellular steady state levels of "high risk" but
not "low risk" human papillomavirus (HPV) E6 proteins are controlled
by proteasome-dependent degradation and independent of their p53 and E6AP
binding capabilities. Virology 299: 72-87
Stöppler, H., Malercyzk, C., Block, K., Aigner, A., and Czubayko, F.(2001) The human papillomaviurs (HPV) 16 E6 oncoprotein leads to an increase in gene expression of the angiogenic switch molecule FGF-BP in non-immortalized human keratinocytes. Oncogene 20: 7430-7436.
Stöppler, H., Hartmann, D.-P., Sherman, L., and Schlegel, R.(1997) The human papillomavirus type 16 E6 and E7 oncoproteins dissociate cellular telomerase activity from the maintenance of telomere length. Journal of Biological Chemistry 20: 13332-13337