Posted by: Oliver Tomas in Health News on July 24th, 2011

In the Sacramento and Davis regional area, UC Davis researchers are studying bladder cancer because at present, the survival rate five years post-diagnosis, for patients with advanced bladder cancer is about 50%. Although many studies conducted previously have provided evidence that survival rates can improve if surgery is preceded by chemotherapy, this rarely translates into clinical practice, as only less than 50% of patients respond positively.

Can holistic medicine work better on parasites than chemotherapy if cancer cells are a newly evolved species? That’s what scientists continue to ask as research moves forward.

Physicians hesitate to use this as a treatment option as many patients can suffer significant adverse events without receiving any benefit at all. But an hour’s drive away at UC Berkeley, scientists have stated in a news release published today that cancerous tumors are parasitic organisms.

Check out the July 26, 2011 news article by Robert Sanders, Media Relations , “Are cancers newly evolved species?” Studies at the Sacramento and Davis area University of California and at UC Berkeley have stated that cancer patients may view their tumors as parasites taking over their bodies, but this is more than a metaphor for Peter Duesberg, a molecular and cell biology professor at the University of California, Berkeley. According to the scientist, cancerous tumors are parasitic organisms, he explained in that UC Berkeley news release. Each one is a new species that, like most parasites, depends on its host for food, but otherwise operates independently and often to the detriment of its host.

Just look at the graph in the article which shows the chromosomes of 20 individual cells of a normal human male. Each cell has precisely two copies of 22 chromosomes and one copy of each sex chromosome, demonstrating that human cells have a fixed and stable karyotype. But in a paper published in the July 1 issue of the journal Cell Cycle, Duesberg and UC Berkeley colleagues describe their theory that carcinogenesis – the generation of cancer – is just another form of speciation, the evolution of new species.

Cancer is comparable to a bacterial level of complexity, but still autonomous, that is, it doesn’t depend on other cells for survival; it doesn’t follow orders like other cells in the body, and it can grow where, when and how it likes,” scientist Peter Duesberg explained in that news release. “That’s what species are all about.”

This novel view of cancer could yield new insights into the growth and metastasis of cancer, Duesberg said in the news release, and perhaps new approaches to therapy or new drug targets. In addition, because the disrupted chromosomes of newly evolved cancers are visible in a microscope, it may be possible to detect cancers earlier, much as today’s Pap smear relies on changes in the shapes of cervical cells as an indication of chromosomal problems that could lead to cervical cancer.

Key to Duesberg’s theory is that some initial chromosomal mutation – perhaps impairing the machinery that duplicates or segregates chromosomes in preparation for cell division – screws up a cell’s chromosomes, breaking some or making extra copies of others. Normally this would be a death sentence for a cell, but in rare cases, he said, such disrupted chromosomes might be able to divide further, perpetuating and compounding the damage. Over decades, continued cell division would produce many unviable cells as well as a few still able to divide autonomously and seed cancer.

Duesberg asserts that cancers are new species because those viable enough to continue dividing develop relatively stable chromosome patterns, called karyotypes, distinct from the chromosome pattern of their human host. While all known organisms today have stable karyotypes, with all cells containing precisely two or four copies of each chromosome, cancers exhibit a more flexible and unpredictable karyotype, including not only intact chromosomes from the host, but also partial, truncated and mere stumps of chromosomes.

“If humans changed their karyotype – the number and arrangement of chromosomes – we would either die or be unable to mate, or in very rare cases become another species,” Duesberg said in the news release. But cancer cells just divide and make more of themselves. They don’t have to worry about reproduction, which is sensitive to chromosomal balance. In fact, as long as the genes for mitosis are still intact, a cancer cell can survive with many disrupted and unbalanced chromosomes, such as those found in an aneuploid cell, he added in the news release.

The karyotype does change as a cancer cell divides, because the chromosomes are disrupted and thus don’t copy perfectly. But the karyotype is “only flexible within a certain margin,” Duesberg explained in the news release. “Within these margins it remains stable, despite its flexibility.”

Did you know that cancer cells taken from a woman in 1951 are still alive and dividing? Why don’t they run out of steam? They are called HeLa cells, which were obtained in 1951 from a cervical cancer that eventually killed a young black woman named Henrietta Lacks. The 60-year-old cell line derived from her cancer has a relatively stable karyotype that keeps it alive through division after division.

What happens is that a cancer cell can cross the barrier of autonomy and become a new species. HeLa cells have evolved in the laboratory and are now even more stable than they probably were when they first arose. It all starts with a chromosomal mutation, that is, aneuploidy perhaps from X-rays or cigarettes or radiation, that destabilizes and eventually changes your karyotype or renders it non-viable. The rare viable aneuploidies of cancers are, in effect, the karyotypes of new species.

Why do cancer cells retain the ability to divide forever? Could a cure be in driving them to evolve even faster to push them over the edge? That’s what scientists are pondering.

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