Biology I – Article Abstract 6 – 25 Points
INSTRUCTIONS: Read this article and outline
its important points by answering the questions at the bottom.
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Are cancers newly evolved species?
By Robert Sanders, UC Berkeley NewsCenter, July 26,
2011
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.
“Cancerous
tumors are parasitic organisms,” he said. 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.
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, said Duesberg. 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, 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.
Carcinogenesis
and evolution
The idea that
cancer formation is akin to the evolution of a new species is not new, with
various biologists hinting at it in the late 20th century. Evolutionary
biologist Julian S. Huxley wrote in 1956 that “Once the neoplastic process has
crossed the threshold of autonomy, the resultant tumor can be logically
regarded as a new biologic species.”
Last year,
Dr. Mark Vincent of the London Regional Cancer Program and University of
Western Ontario argued in the journal Evolution that carcinogenesis and the
clonal evolution of cancer cells are speciation events in the strict Darwinian
sense.
The evolution
of cancer seems to be different from the evolution of a grasshopper, for
instance, in part because the cancer genome is not a stable genome like that of
other species. “The challenging question is, what has it become?”¯Vincent said
in an interview. Duesberg’s argument from karyotype
is different from my argument from the definition of a species, but it is
consistent.
Vincent noted
that there are three known transmissible cancers, including devil facial tumor
disease, a parasitic cancer that attacks and kills Tasmanian devils. It is
transmitted from one animal to another by a whole cancer cell. A similar
parasitic cancer, canine transmissible venereal tumor, is transmitted between
dogs via a single cancer cell that has a genome dating from the time when dogs
were first domesticated. A third transmissible cancer was found in hamsters.
“Cancer has
become a successful parasite,” Vincent said.
Mutation
theory vs. aneuploidy
Duesbeg’s arguments derive from his
controversial proposal that the reigning theory of cancer “that tumors begin
when a handful of mutated genes send a cell into uncontrolled growth,“ is wrong. He argues, instead, that carcinogenesis is
initiated by a disruption of the chromosomes, which leads to duplicates,
deletions, breaks and other chromosomal damage that alter the balance of tens
of thousands of genes. The result is a cell with totally new traits “that is, a
new phenotype.”
“I think Duesberg is correct by criticizing mutation theory, which
sustains a billion-dollar drug industry focused on blocking these mutations,”
said Vincent, a medical oncologist. Yet very, very few cancers have been cured
by targeted drug therapy, and even if a drug helps a patient survive six or
nine more months, cancer cells often find a way around it.¯
Chromosomal
disruption, called aneuploidy, is known to cause disease. Down syndrome, for
example, is caused by a third copy of chromosome 21, one of the 23 pairs of
human chromosomes. All cancer cells are aneuploid, Duesberg said, though proponents of the mutation theory of
cancer argue that this is a consequence of cancer, not the cause.
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. 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 said.
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 said. Within these margins it
remains stable, despite its flexibility.¯
Karyographs display karyotype variability
Duesberg and his colleagues developed karyographs as a way to display the aneuploid
nature of a cell’s karyotype and its stability across numerous cell cultures. Using
these karyographs, he and his colleagues analyzed
several cancers, clearly demonstrating that the karyotype is amazingly similar
in all cells of a specific cancer line, yet totally different from the
karyotypes of other cancers and even the same type of cancer from a different
patient.
HeLa cells
are a perfect example. Perhaps the most famous cancer cell line in history,
HeLa cells 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.
“Once a cell
has crossed that barrier of autonomy, it’s a new species,” Duesberg
said. HeLa cells have evolved in the laboratory and are now even more stable
than they probably were when they first arose.
The
individualized karyotypes of cancers resemble the distinct karyotypes of
different species,, Duesberg
said. While biologists have not characterized the karyotypes of most species,
no two species are known that have the same number and arrangement of
chromosomes, including those of, for example, gorillas and humans, who share 99
percent of their genes.
Duesberg argues that his speciation theory
explains cancer’s autonomy, immortality and flexible, but relatively stable,
karyotype. It also explains the long latency period between initial aneuploidization and full blown cancer, because there is
such a low probability of evolving an autonomous karyotype.
“You start
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,” he said. The rare viable aneuploidies of
cancers are, in effect, the karyotypes of new species.
Duesberg hopes that the
carcinogenesis-equals-speciation theory will spur new approaches to diagnosing
and treating cancer. Vincent, for example, suspects that cancers are operating
right at the edge of survivability, maintaining genomic flexibility while
retaining the ability to divide forever. Driving them to evolve even faster, he
said, might push them over the edge.
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1. List the
title of the article, the author, where it was published, and the date it was
published.
2. What does
the author think Cancerous tumors are?
3. This means
that each cancer is a what? He suggested that each cancer depends on its host
for
food, but otherwise operates independently and often to the
detriment of its host.
4. How does a
Pap smear indicate chromosomal problems that could lead to cervical cancer?
5. Down
syndrome is caused by what sort of mutation?
6. How did a young
black woman named Henrietta Lacks contribute to the study of cancer?