Molecular dissection of cancer by differential drug sensitivity
In the clinic, we mainly use anticancer drugs based on outcomes of clinical trials that have been carried out in series of cancer patients based on the site
of the primary tumor, whereas little is known about the molecular mechanisms underlying differential drug sensitivity.
These tumor types include breast cancer, non-small cell lung cancer (NSCLC), stomach cancer, ovarian cancer, and colorectal cancer.
The focus of our research line is to unravel these molecular mechanisms in order to develop tests that may guide treatment decisions in the clinic and ultimately improve survival. For this purpose we use several genome-wide approaches and molecular techniques, in order to dissect the mechanisms that divide clinically well-defined cohorts of breast, colorectal, stomach, ovarian and NSCLC patients into resistant and sensitive to a particular drug. In addition, a second goal is to identify new targets for therapy.
We have a close collaboration with the groups of Jos Jonkers and Piet Borst, who use conditional mouse models for breast cancer, and derived clonal cell lines, to study differential chemosensitivity in a controlled fashion. This collaboration facilitates quick translation from bench to bedside and vice versa.
A second research line focuses on the impact of prognostic molecular classifiers on adjuvant systemic treatment advice in breast cancer.
The research in the Linn lab is supported by grants from the Dutch Cancer Society, A Sister’s Hope, Pink Ribbon, Life Sciences Center Amsterdam (LSCA) Validation Fund, the Seventh Framework Programme (FP7) of the European Commission, generous gifts from individuals, and unrestricted research grants from Sanofi-Aventis, Amgen, Pfizer, Roche and AstraZeneca.
For further information check out our research pages.