NET is not, as many of you know, my only interest when it comes to cancer. I have called myself a cancer magnet more than once because I know so many people whose lives have been–and are being–affected by this foul disease.

Nor is cancer in general my only interest–though it seems that way both to some readers and to myself at times. One of those other interests collided with my interest in cancer today–and maybe not in a good way.

First the high

It began innocently enough with a post on Facebook from the Case Western Reserve School of Medicine. The press release was titled, “Researchers discover gene that permanently stops cancer cell proliferation” and told the story of a mutated gene that shuts down the growth of

cancer cells in vitro. If the mutated gene could be introduced to human cancer cells in the body, the thinking is we would have a non-radiation, non-chemo means of stopping a tumor from growing. There would be none of the side effects cytotoxic methods induce.

Further, it might even prove the long-sought-after-perhaps-mythical magic bullet that would end cancer as a serious health problem.

Because the piece is a press release there was not a lot of evidence presented.There have been no Phase I trials–just a series of experiments done in a lab in a petri dish. But the news was not something I wanted to sit on, so I posted it to our Walking with Jane Facebook page and to the local Relay for Life site.

Then the low

Then I got a note from a friend–a 4.5 year survivor of cancer with an obvious reason for interest in the subject. She had reposted the piece and received a response from another friend referring us to a review paper on drugs that shut down the Chk1 pathway the mutation turns on. The results there throw the entire thing into doubt.

There is, however, a difference between what the researchers were looking at in the review paper and what the mutation researchers at Case have discovered. The earlier researchers were trying to block the Chk1 pathway because it is involved in repairing damaged DNA. The mutation, however, activates that pathway, which somehow seems to stop the cancer–even though logic says it should not.

The review paper had me convinced this was not something that would not work. Then, when I looked at the press release again, I was not so sure. But I have also been a reporter and been interviewed by reporters, so I know that what we say and what a reporter hears are not always the same thing.

And then further confusion

I have now read the abstract of the paper from the Case researchers–unfortunately the full text is only available to subscribers or those with $35 to spend for a single day’s access–and am still baffled by how this works. They do say that how Chk1 works is “not well understood.”

I’d really like to see full text of the paper. I’d like to know what they did, how they did it, and what precisely happened. I especially want to know why activating something we thought we wanted to shut down kills the cancer cells.

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