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One Answer to Cancer
03-21-2008, 04:40 AM,
One Answer to Cancer
I don't remember who, but a couple of other people here have cancer. I haven't read it all yet, but this looks promising. Top Words have link to book (Free), also a short video.
03-21-2008, 06:44 AM,
One Answer to Cancer
Wow, there goes the supressed truth about curing cancer.
[Image: Palestinian_Dawn_by_Palestinian_Pride.jpg]
03-22-2008, 02:18 AM, (This post was last modified: 03-22-2008, 02:28 AM by drew hempel.)
One Answer to Cancer
After a quick glance it looks like spirulina should do the trick -- plus garlic I'm sure. Enzymes. I just loaded up on spirulina -- cleans the blood -- after another quick glance, this is one of the most bizarre, fascinating models of science I've seen:


When all is said and done, cancer is a normal growth of tissue (a placenta) due to the development of a basic germ cell in the wrong place (outside of the uterus). Sometimes this placenta also has a "baby" or begins a tumor inside of it much like a normal pregnancy — only it is in the wrong place. (When dissecting tumors Pathologists often find partially formed teeth, toenails and other types of tissue, such as lung tissue, within the tumors.)
03-24-2008, 03:15 AM,
One Answer to Cancer
Thanks Hilly, as always.
03-24-2008, 03:19 AM,
One Answer to Cancer
Your welcome
04-17-2008, 11:20 PM,
One Answer to Cancer
Wow this "conspiracy" has just been confirmed, in a recent New Scientist article:

doi:10.1016/S0262-4079(08)60638-7 How to Cite or Link Using DOI (Opens New Window)
Copyright © 2008 Reed Business Information Ltd, England Published by Reed Business Information Ltd.
This Week

Fetal enzyme helps cancers grow

Andy Coghlan

Available online 15 March 2008.

An enzyme responsible for driving the explosive growth of fetuses may explain how cancers grow

NO WONDER tumour cells can grow and multiply so rapidly. It turns out that they reawaken an enzyme responsible for driving the explosive growth of fetuses.

Healthy cells use most of their glucose “fuel” to produce energy, rather than for building components of new cells, such as fats and DNA. But in cancer cells, the opposite happens. Now, Lewis Cantley of Harvard Medical School in Boston and his colleagues have identified the enzyme responsible for triggering this switch – a fetal form of pyruvate kinase, called PKM2.

“It's a bit like building materials being brought to a house,” says Cantley. “Usually, cells burn all the material to make energy, but if you burn it all you can't use it to make a new house.” In cancer cells, PKM2 blocks the burning of the building materials so that new tumour cells can be made instead.

Usually cells burn all their fuel to make energy. In cancer cells, PKM2 blocks the burning so new cancer cells are made instead

As well as explaining how cancer cells grow and multiply so rapidly, the finding may also help explain why almost all types of cancer cell absorb much more glucose than healthy cells, yet switch to an apparently less efficient way of burning it to make energy. This switch allows them to divert more glucose into cell multiplication.

This effect was discovered 80 years ago by the German chemist, Otto Warburg. He noticed that, unlike healthy cells which make energy from glucose and oxygen in chambers called mitochondria, cancer cells make energy by a less efficient process called glycolysis, even when plenty of oxygen is available.

Warburg argued that this switch was responsible for triggering cancer, but other researchers disagreed and the “Warburg effect” was ignored until last year, when experiments with a drug called dichloroacetate showed that it could switch energy production back to the mitochondria and reverse cancer in rats (see New Scientist, 20 January, 2007). A human trial to test DCA is under way at the University of Alberta in Edmonton, Canada.

Cantley's team has now worked out why the Warburg effect happens: to divert resources into tumour cell-building and multiplication.

Crucially, they've discovered that cancer cells switch over to glycolysis by re-activating PKM2. In healthy adult cells, energy production involves PKM1, the adult form of pyruvate kinase. But in all cancer cells studied by Cantley, the fetal form of the enzyme had been reactivated and the adult form silenced (Nature, DOI: 10.1038/nature06734).

Moreover, Cantley's team showed that if they used molecular blockers called small hairpin RNAs to reverse the switch, the cancer cells stopped growing, both in the lab and in animals.

Evangelos Michelakis, the researcher in Edmonton who is testing DCA, says that the new results vindicate Warburg. “They support the concept of metabolism being a driver of cancer, not a consequence,” he says.

However, Joanna Peak at Cancer Research UK in London says it is too early to know if the findings can be applied to human cancers outside the lab. “More research is needed before we can consider developing cancer treatments that target this process,” she says.

The gene that makes cancer more deadly

A master gene has been identified that makes breast cancers more aggressive and helps them to spread, which is usually what kills people. By blocking the gene, called SATB1, it might be possible to stop the cancer in its tracks.

Terumi Kohwi-Shigematsu of the Lawrence Berkeley National Laboratory in California describes SATB1 as a “genome organiser”, that simultaneously controls hundreds of other genes. It does this by physically reshaping chromosomal DNA, creating interlocking loops which unite hundreds of genes at once. This network of captive genes can then be activated en masse to make breast cancer cells more aggressive and capable of invading other parts of the body.

When Kohwi-Shigematsu and her colleagues disabled SATB1 in aggressive breast cancer cells, they ceased to be invasive. “Deleting SATB1 not only abolished their metastatic activity, but also their growth,” says Kohwi-Shigematsu. Likewise, when she switched it on in otherwise non-aggressive breast cancer cells, they turned nasty.

The team, whose results appear in Nature (DOI: 10.1038/nature06781), is hoping to develop treatments that switch SATB1 off, perhaps by sabotaging it with fragments of short interfering RNA. Any method will have to target the gene in breast cancer tissue alone to avoid harming healthy cells in the thymus, which also rely on SATB1 to programme the immune system's T-cells.

“This fascinating piece of research suggests that the way DNA is arranged within cells may contribute to cancer,” says Kat Arney at Cancer Research UK. “It could provide an exciting lead for treating breast cancer in the future.”

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