[gdpawel]

What they would be looking for is to see if you have the Her2 protein (the wild type verson c35 or Syk). It may be able to tell you whether or not your cells are potentially susceptible to this mechanism of attack. However, they would not be able to tell you if the chemicals BAY61-3606 or piceatannol will work for your individual cancer cells. It is still a "trial-and-error" approach as conventional chemotherapy is.

BAY61-3606 may kill cells containing a normal but overactive Her2 molecule, but piceatannol may have little effect on the mutant signal, because it strikes at a different part of the Her2 molecule. It involves a normal, not mutant, Her2 molecule. Or, vice versa.

While those with Her2 mutations may benefit from BAY61-3606, others without Her2 mutations may benefit from piceatannol. In this setting, to inhibit the mutant receptor, you need to inhibit the domain of the Her2 molecule that lies "within" the cell, as opposed to the domain that lies "outside" the cell.

What is still not understood by purveyors of the Cancer Genome Project is that the original Human Genome Project dealt with a homogeneous population of normal diploid cells. This is different from primary tumors, which are heterogeneous and have a genomic signature unique to each and every patient.

Sequencing the genome of cancer cells is explicitly based upon the assumption that the pathways - network of genes - of tumor cells can be known in sufficient detail to control cancer. Each cancer cell can be different and the cancer cells that are present change and evolve with time.

But the research will hopefully yield a new targeted treatment in the long term. Such knowledge can help to identify targets for new drug treatments.

Source: Cell Function Analysis