Throw away what you thought you
knew about cancer. The new model
described here shows us that a reduction in oxygenation forces a switch to a
far less effective solution which then drives blood vessel proliferation. These forms of cancer thus have nothing whatsoever
to do with genetic failure and that is a completely false lead.
This is wonderful bit of research
detective work and should lead to far better therapies. Bravo!
In the past two years, I have
seen a couple of anti cancer protocols come along that kick over the apple cart
and I suspect that we could well see this disease off sooner than later. My sense is that critical mass has already
been achieved in the lab at least.
Low Oxygen Levels Could Drive Cancer Growth, Research Suggests
ScienceDaily (May 3, 2012) — Low oxygen levels in cells may be a
primary cause of uncontrollable tumor growth in some cancers, according to a
new University of
Georgia study. The
authors' findings run counter to widely accepted beliefs that genetic mutations
are responsible for cancer growth.
If hypoxia, or low oxygen levels in cells, is proven to be a key driver
of certain types of cancer, treatment plans for curing the malignant growth
could change in significant ways, said Ying Xu, Regents-Georgia Research
Alliance Eminent Scholar and professor of bioinformatics and computational
biology in the Franklin College of Arts and Sciences.
The research team analyzed samples of messenger RNA data-also called
transcriptomic data-from seven different cancer types in a publicly available
database. They found that long-term lack of oxygen in cells may be a key driver
of cancer growth. The study was published in the early online edition of
the Journal of Molecular Cell Biology.
Previous studies have linked low oxygen levels in cells as a
contributing factor in cancer development, but not as the driving force for
cancer growth. High incidence rates of cancer around the world cannot be
explained by chance genetic mutations alone, Xu said. He added that
bioinformatics, which melds biology and computational science, has allowed
researchers to see cancer in a new light. Gene-level mutations may give cancer
cells a competitive edge over healthy cells, but the proposed new cancer growth
model does not require the presence of common malfunctions such as a sudden
proliferation of oncogenes, precursors to cancer cells.
"Cancer drugs try to get to the root -- at the molecular level --
of a particular mutation, but the cancer often bypasses it," Xu said. "So
we think that possibly genetic mutations may not be the main driver of
cancer."
Much of cancer research so far has focused on designing drug treatments
that counteract genetic mutations associated with a particular type of cancer.
In their study, the researchers analyzed data downloaded from the Stanford
Microarray Database via a software program to detect abnormal gene expression
patterns in seven cancers: breast, kidney, liver, lung, ovary, pancreatic and
stomach. The online database allows scientists to examine information from microarray
chips, which are small glass slides containing large amounts of gene material.
Xu relied on the gene HIF1A as a biomarker of the amount of molecular
oxygen in a cell. All seven cancers showed increasing amounts of HIF1A,
indicating decreasing oxygen levels in the cancer cells.
Low oxygen levels in a cell interrupt the activity of oxidative
phosphorylation, a term for the highly efficient way that cells normally use to
convert food to energy. As oxygen decreases, the cells switch to glycolysis
to produce their energy units, called ATP. Glycolysis is a drastically less
efficient way to obtain energy, and so the cancer cells must work even harder
to obtain even more food, specifically glucose, to survive. When oxygen levels
dip dangerously low, angiogenesis, or the process of creating new blood
vessels, begins. The new blood vessels provide fresh oxygen, thus improving
oxygen levels in the cell and tumor and slowing the cancer growth-but only
temporarily.
"When a cancer cell gets more food, it grows; this makes the tumor
biomass bigger and even more hypoxic. In turn, the energy-conversion efficiency
goes further down, making the cells even more hungry and triggering the
cells to get more food from blood circulation, creating a vicious cycle. This
could be a key driver of cancer," Xu said.
Xu explained that this new cancer-growth model could help explain why
many cancers become drug resistant so quickly-often within three to six months.
He stressed the importance of testing the new model through future experimental
cancer research. If the model holds, researchers will need to search for
methods to prevent hypoxia in cells in the first place, which could result in a
sea change in cancer treatment.
Additional authors of this study include Juan Cui, Xizeng Mao and
Victor Olman, all of UGA, and Phil Hastings of Baylor College
of Medicine. Xu also has a joint appointment with Jilin
University in China .
2 comments:
In 1938, Dr. Otto Warburg received the Nobel Prize for proving that cancer is anerobic. He successfully treated and CURED cancer by administering O2 Therapy to cancer patients. Later, it was discovered that cancer also feeds off sugar. go to www.cancertutor.com, www.mercola.com, www.naturalnews.com. Lookup Dr. Budwig, FlaxSeedOil2@yahoogroups.com. 3 parts DMSO + 1
part baking soda transdertmally CURES cancer. DiMethylSufOxide-DMSO@yahoogroups.com. Former cancer patient, Bruce
thanks for the reference. That readily explains the efficiency of the maple syrup baking soda combination that has been used successfully also and why a pure vegan diet is also beneficial.
Like yourself, i am becoming convinced that cancer is curable.
after saying that, i find outright scientific ignorance blocks most from taking advantage of the obvious tricks and that sadly includes doctors who mistake a vast knowledge for wisdom.
If we can cure willful blindness then we may have a winner.
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