[Lani]

Debbie, you sound like an oncologist (in fact your points are those I hear/read again and again in journals and meetings of oncologist, but not in meetings of cancer researchers seeking to understand the disease to better treat it)

There are tests that phenotype single cells, whether ctcs or dtcs, to determine what pathways are driving these cells and they should be much more indicative of what kills individual patients, the mets, rather than the primaries.

What is left over after a PCR (or failure to reach pCR) can be very different from what is in the bone marrow. For one thing the cell usually left the tumor early, long before the tumor was even biopsied and the tumor may have had different characteristics or clones with different characteristics may have developed since. The primary tumor may also be heterogeneous and the area sampled for hr, her2 testing may not indicate all areas of the tumor, let alone the ones which survive the chemo.

Let's say for example that the primary is heterogeneous and has clonal areas which are HR+her2- and HR+her2+ for example. The micromet may be different than that portion of the primary tumor they characterized and so the primary treatment would not work on it. If they are in fact bc cancer stem cells and rarely divide the same chemo which killed the bulk of cells in the primary tumor may not affect them as chemos affect dividing cells.

Knowing what cells are there and what they represent can only IMPROVE treatment. If people keep hiding your head in the sand and saying it won't change treatment how will ever get to a point where treatment CAN BE improved?

I think that the ability to phenotype individual cancer cells eg DTC as the ultimate ability to help an individual cancer patient with their individual cancer--true personalized treatment. Whether society will say personalized treatment is too expensive in the future is another thing altogether.

Until someone tries we will not know and right now few clinical trials even ask for bone marrows, not even the I-Spy trial.

As for the papers, just put K Pantel into PubMed--there are lots of them including those specifically discussing her2+ DTC

Just like her2 testing was not widely performed in an acceptable and reproducible manner at first, bone marrow testing for DTC needs to be improved. But saying not to do it because it is not well tested for and won't change treatment is throwing in the towel without trying. The recent Swiss article posted here was an example of that thinking. How about trying to improve the testing, learn what can be learned and then deciding whether it pans out that we can change the natural history of the disease?

Will get off my soapbox now.