Overseas overstatement of "breast cancer breakthrough"

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We don’t always comment on medical research news from overseas. But when we know it might impact US news coverage and news consumers – as when the New York Times drooled over a French artificial heart last week or when the New York Daily News would lead you to believe a cancer cure is right down the pike – then we write about it.

New case in point: A story in The Herald of Scotland headlined, “Breast Cancer Breakthrough.” Excerpt:

“The researchers at Edinburgh University have established that a specific gene plays a key role in causing the spread of an aggressive form of the disease. Dr Elad Katz, who led the study, said that in test-tube experiments they had already managed to halt the spread of tumour cells by targeting drugs at the gene.”

OK, it’s clear that it’s very early interesting research. The story goes on with a researcher’s quote:

“We are at an early stage, but there is now a real possibility there could be a new treatment for women with HER2 positive breast cancer.”

Hmm. That’s letting him get away with a bit of leap. Yes, there’s that possibility. There’s also the huge possibility that there would NOT be a new treatment. But let’s go on.

“Drugs that can potentially kill ¬cancer cells that rely on C35 are already in development. They do this by disabling a protein associated with the gene, which stops it from working.
Katz explained: “The real potential here is not to replace Herceptin, but the fact we can improve on it.”

Semantics is important. It’s not a FACT that they can improve on Herceptin until they, in fact, have done so. Back to the story:

“Professor David Harrison, director of the Breakthrough Breast Cancer Research Unit, said: “It is exciting to know there is a drug out there which could potentially stop this ¬process happening and save the lives of women with breast cancer.
“We now need to do more work in the lab to prove this ¬concept before we can start patient trials.” “

Well, there isn’t a drug “out there” yet. But thanks for the reminder that human trials have not yet begun. Perhaps a bit early to tell a general audience that there’s been a breakthrough.

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Comments (2)

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Gregory D. Pawelski

July 19, 2010 at 3:22 pm

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
Another article: http://www.buxtonadvertiser.co.uk/nhshealth/New-breast-cancer-drug.6421017.jp