Molecular Gynaecology

Cancer cells originate from a former individual healthy cell. During the process of becoming a neoplastic disease the genetic material has undergone several changes in the form of mutations. These mutations occurring in a highly diverse multi-step process providing new biological capabilities. They include sustained proliferation, unrestricted growth, evasion of apoptosis, enabling replicative immortality, inducing angiogenesis, and activating invasion and metastasis. These capabilities which are termed the "The Hallmarks of Cancer" were recently extended by two additional ones: "reprogramming of energy metabolism and evading immune destruction". In contrast to cancer cells, a third layer of complexity: "the tumor microenvironment" has been added as a hallmark of human tumors only. The unrestricted growth and sustained proliferation of cancer cells and tumors which lead to an contiguously cell division focusses our work at the key players of the mamalian cell cycle, especially of cell cycle kinases. By using pioneering molecular tools like RNA Interference or the CRISPR/Cas9 Genome Editing Technology in cell-based and preclinical models (breast and ovarian cancer) we are defining critical drivers of the cell cycle and aim to provide startegies for improved cancer intervention. We hope that these new approaches will improve our understanding and treatment of neoplastic diseases.

Publications

2015

Stamping out RAF and MEK1/2 to inhibit the ERK1/2 pathway: an emerging threat to anticancer therapy.

Mandal R, Becker S, Strebhardt K. Oncogene. 2015 Sep 14.

 

Drugging Plk1: An attractive approach to inhibit androgen receptor signaling.

Strebhardt K. Cell Cycle. 2015;14(14):2193-4.

 

The role of Plk3 in oncogenesis.

Helmke C, Becker S, Strebhardt K. Oncogene. Apr 27 (2015).

 

Thoughts on the current assessment of Polo-like kinase inhibitor drug discovery.

Strebhardt K, Becker S, Matthess Y. Expert Opinion Drug Discovovery. Jan;10(1):1-8 (2015).

 

Mitotic arrest and slippage induced by pharmacological inhibition of Polo-like kinase 1.

Raab M, Krämer A, Hehlgans S, Sanhaji M, Kurunci-Csacsko E, Dötsch C, Bug G, Ottmann O, Becker S, Pachl F, Kuster B, Strebhardt K. Molecular Oncology. Jan;9(1):140-54 (2015).

 

1987 - 2014

Publication List on Pubmed