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Evolusi , bukan hanya mutasi , mendorong perkembangan kanker

Memecahkan ' Peto Paradox , ' model baru menunjukkan tekanan seleksi dari jaringan sehat membuat sel-sel dengan mutasi kanker di cek

Date:

July 21, 2015

Source:

University of Colorado Anschutz Medical Campus

Summary:

Sebuah artikel baru berpendapat terhadap pegangan umum  ' akumulasi mutasi ' model onkogenesis mendukung model yang tergantung pada tekanan evolusi bekerja pada populasi sel 

............ " Kami sudah berusaha untuk membuat obat yang menargetkan mutasi pada sel-sel kanker . Tapi jika itu ekosistem tubuh , dan tidak hanya mutasi penyebab kanker , yang memungkinkan pertumbuhan kanker , kita juga harus memprioritaskan intervensi dan pilihan gaya hidup yang mempromosikan kebugaran sel-sel sehat dalam rangka untuk menekan munculnya kanker , " kata James DeGregori , PhD , associate director untuk ilmu dasar di University of Colorado Cancer Center , dan penulis senior  ....more

Evolution, not
just mutation, drives development of cancer

Solving 'Peto's Paradox,' new model shows selection pressure of healthy
tissue keeps cells with cancerous mutations in check

Date:

July 21, 2015

Source:

University of Colorado Anschutz Medical Campus

Summary:

A new article argues against the commonly held 'accumulation of mutations'
model of oncogenesis in favor of a model that depends on evolutionary pressures
acting on populations of cells.

..........................

A paper published today in theProceedings of the National Academy of
Sciences argues against the commonly held
"accumulation of mutations" model of oncogenesis in favor of a model
that depends on evolutionary pressures acting on populations of cells.
Basically, the paper states that the ecosystem of a healthy tissue landscape
lets healthy cells outcompete ones with cancerous mutations; it is when the
tissue ecosystem changes due to aging, smoking, or other stressors, that cells
with cancerous mutations can suddenly find themselves the most fit, allowing
their population to expand over generations of natural selection.

This new thinking about oncogenesis has profound implications for cancer
therapy and drug design.

"We've been trying to make drugs that target mutations in cancer
cells. But if it's the ecosystem of the body, and not only cancer-causing
mutations, that allows the growth of cancer, we should also be prioritizing
interventions and lifestyle choices that promote the fitness of healthy cells
in order to suppress the emergence of cancer," says James DeGregori, PhD,
associate director for basic science at University of Colorado Cancer Center,
and the paper's senior author.

The proposed model helps to answer a longstanding question in cancer
science known as Peto's Paradox -- if cancer is due to random activating
mutation, larger animals with more cells should be at greater risk of
developing the disease earlier in their lives. Why then do mammals of vastly
different sizes and lifespans all seem to develop cancer mostly late in life?

"Blue whales have more than a million times more cells and live about
50 times longer than a mouse, but the whale has no more risk than a mouse of
developing cancer over its lifespan," DeGregori says.

The answer that DeGregori and CU Cancer Center colleague Andrii Rozhok, PhD
propose is that in addition to activating mutation, cancer may require
age-associated changes to the tissue landscape in order for evolution to favor
the survival and growth of cancer cells over the competition of healthy cells.

Consider the following two evolutionary scenarios: In a grassy lawn, the
health of the lawn is the best defense against dandelions; and in the time of
the dinosaurs, the environment selected for giant lizards until the meteor hit
at which point the new context favored the evolution of new species better
adapted to the changed environment, including larger mammals.

Let's start with the lawn: "Healthy cells are optimized for the
ecosystem of the healthy body. But when the tissue ecosystem changes, such as
with aging or smoking, cancer-causing mutations are often very good at
exploiting the conditions of a damaged tissue landscape," DeGregori says.
In this scenario, DeGregori's suggestion to explore the development of
interventions supporting the fitness of healthy tissues is like applying
fertilizer to the lawn rather than herbicide to the weeds.

DeGregori's model is supported by studies showing that mutations that can
cause cancer do not necessarily increase a cell's fitness. "In fact,
healthy cells are so optimized to the healthy tissue landscape that almost any
mutation makes them less fit," DeGregori says.

For example, some cancer cells mutate in a way that allows them to survive
in the oxygen-poor tissue environments found in the center of developing
tumors. But this adaptation only confers a fitness benefit in oxygen-poor
tissues. In a healthy, oxygen-rich tissue, this mutation would not confer this
advantage. In healthy tissue, cells with this mutation lose the evolutionary
race to the healthy cells; cancer cells are outcompeted and they die, or at
least their population is held in check and remains insignificantly small.

But what happens when the tissue landscape changes? This brings us to the
dinosaurs. Sixty-five million years ago, a warm, wet planet favored dinosaurs,
though a few early mammals scurried among them. Then the giant meteor hit
(among other environmental changes happening around this time), altering the
basic dynamics of the ecosystem. It was this adjustment to the ecosystem that
allowed furry and feathered, warm-blooded creatures to eventually dominate
earth.

It seems as if new, successful species are produced by new, successful
genetic changes. But in this example, as in cancer, individuals with these
"new" genetics may already exist and it is changes to the ecosystem
that allow them to flourish. Yet cancer biologists focus on how cancer risk
factors like aging and smoking create new mutations, instead of focusing on how
these contexts alter tissue landscapes and thus alter selection for already-existing
mutations. Supporting this idea, DeGregori points out that studies modeling
stem-cell pools show that selection pressure from the tissue landscape is more
powerful than mutations at deciding the makeup of a population of stem cells.

"When the body changes due to aging, smoking, inherited genetic
differences or other factors, it changes the tissue ecosystem, allowing a new
kind of cell to replace the healthy ones," DeGregori says.

Certainly, cancer development requires mutations and other genetic alterations.
But how do these mutations cause cancer? It may not be that these mutations
create accidental "super cells" that immediately run amok. Oncogenic
mutations are often or always present in the body, but are kept at bay by
selection pressures set against them. That is, until the tissue ecosystem and
its pressures change in ways that make cells with cancerous mutations more
likely to survive than healthy cells, over time allowing the population of
cancer cells to overcome that of healthy cells.

We can avoid some of these tissue changes by lifestyle choices, such as by
not smoking. Unfortunately, we can't put off aging forever. But there may be
features of the tissue landscape that, with new therapies and new
understanding, could be reinforced in ways resist cancer better, longer.







Story Source:

The above post is reprinted from materials provided
byUniversity of Colorado
Anschutz Medical Campus. Note: Materials may be edited
for content and length.







Journal Reference:

1.   
Andrii I. Rozhok, James DeGregori. Toward an evolutionary model of
cancer: Considering the mechanisms that govern the fate of somatic mutations. Proceedings
of the National Academy of Sciences, 2015; 201501713 DOI:10.1073/pnas.1501713112

http://www.sciencedaily.com/releases/2015/07/150721134835.htm

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