Personalised Cancer Therapy

We stand at the threshold of a paradigm shift in cancer therapy. The progress of genome and proteomic technologies (TAP), in particular, the development of new generations of DNA and protein chips, have opened up new options regarding molecular differentiation of tumours.

It has been learned that the molecular signature of a tumour, i.e. the genes and proteins involved in the disease process, vary from tumour type to tumour type. And what's more: within a given tumour type, there are marked differences from patient to patient. It has likewise come to light that in one patient, multiple proteins were involved in the onset of cancer and its further progression. These proteins are in most cases integrated in various mechanisms of the disease process. If just one of these proteins is inhibited, then that is insufficient to combat the disease effectively. These discoveries, especially those stemming from protein and receptor analyses of tumours, permit the conception of "target-oriented therapies" to be implemented for improved treatment success. Target-oriented active agents include the following: Gleevec (cAbl, cKit, PDGF receptors); Iressa and Tarceva (EGF receptor, the EGF receptor mutation in non-small cell lung cancer correlates with the tumour response achieved via Iressa); Avastin (VEGF); Erbitux, Vectibix (EGF receptor, the KRAS wild-type in colon cancer correlates with the tumour response achieved via antibody therapy); Herceptin, Tyverb (ErbB2 receptor and EGF receptor); Nexavar (cKit, FLT-3, PDGF receptors); Sutent (VEGF-1,2, cKit, PDGF receptors). Moreover, p53 mutation analyses enable a targeted treatment. In approximately 50% of all tumours, p53 mutates – this is linked with a poor prognosis (e.g. ovarian, bladder cancer) and/or a poor response to therapy (e.g. breast cancer). The personalised cancer therapy is not a "tailor-made" therapy, but it is an increasingly better-fitting therapy.

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Personalised cancer therapy, Centre for Cancer Medicine

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