Cells Become Dormant During Chemotherapy

pip57

This research indicates that cancer cells can go dormant during tx so that the chemo drugs do not recognize them as a targets and pass them over.  They later reactivate and cause a relapse.  The researchers say that this points them towards the biological, instead of the genetic makeup, of these cells in order to find the cure.   

http://www.thestar.com/news/gta/article/1301826--cancer-cells-hide-by-going-dormant-princess-margaret-study-finds

 

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http://www.13wham.com/guides/health/story/stem-cell-facility-rochester-medical-center/IpWF2l58JUOJ6-DWOz22lg.cspx

CelineFlower

great article thank you!

gpawelski

This is the second significant cancer advance out of Toronto hospitals just this month, and the second to home in on the healthy tissues that lie in proximity to tumours.

In a major breakthrough, Toronto scientists have discovered a new approach to cancer treatment that would target the “normal” cells embedded around tumours.

In a study just released, researchers at Mount Sinai Hospital show that it’s the non-cancerous cells that grow in and around a tumour that actually coax it to spread to other parts of the body.

“Basically the normal cells and the cancer cells are engaged in a dialogue which is controlling (spread),” says Dr. Jeff Wrana, the study’s senior author.

“The tumour cells are tweaking the normal cells, causing them to misbehave a little bit and causing those normal cells to produce signals, words if you will, that flow back to the tumour cells and promote the tumour cell’s growth.”

Wrana’s study, which appears in the journal Cell, revealed that the words delivered by the normal cells, in a tiny protein vocabulary, were actually telling their cancerous counterparts to spread or metastasize.

In particular, his team identified a protein signal labelled Cd81 — a so-called exosome — as the key instructional culprit in kicking off tumour spread.

Classical oncology research has almost always searched for ways to kill or halt the mutant cancer cells themselves.

But Wrana’s team, at the hospital’s Samuel Lunenfeld Research Institute, suggested that stopping the successful transmission of Cd81 from normal to cancer cells could arrest metastasis, the tumour spread that causes most deaths from the disease.

“It (Cd81) is a mass of information, not just a word or two, but a whole collection of information,” Wrana says.

“And these signals weren’t just telling cancer cells to metastasize, what they were doing is sort of teaching the cancer cells how to use their own machinery to spread,” he says.

Wrana says scientists can now search for drugs that would stop normal cells from sending out their signals or that would block those Cd81 instructions from attaching to tumour cells.

Researchers at the Princess Margaret Cancer Centre speculated that some cancer cells evaded chemotherapy treatment by going dormant.

This dormancy, which would essentially hide them from cancer drugs, could well have been caused by instructions from the healthy tissues nearby, the Princess Margaret study said.

Wrana says the common understanding of cancer sees tumours as separate entities from normal tissues, an alien lump of horror growing inside one or other of our organs.

But cancer is in fact hooked into our normal tissues, dependent on them for food and — as it turns out — directions on how to spread.

“People think of cancer as a kind of independent tissue growing inside them, the same way they might think of a bacterial infection,” Wrana says.

“But in reality cancer grows within the context of the normal tissue that surrounds it. So cancer really is a part of us that’s transformed and changed.”

Normal cells sending out the spread signals could include the organ tissues in which a tumour is growing or the blood vessel and immune system cells that are actually embedded within.

Metabolism Is The Principal Driver Of Human Cancer