
Tasmanian devils 'adapting to coexist with cancer' - pseudolus
https://www.bbc.com/news/science-environment-47659640
======
abhinai
Can someone please explain why this is happening only now and why the species
isn't already extinct? From the way this article is written, it seems the main
culprit is the animals biting each other. However, they must have done this
for tens or hundreds of thousands of years. So why are they suddenly getting
face cancer? And why is the species threatened by this problem only now? What
information are we missing here?

~~~
notavalleyman
Just speculating here, but there might not be anything temporally "special"
about the spread of infection right now. We might find that every N years a
new disease emerges, spreads, and then is adapted to - and we're just lucky
enough to be around to observe this current wave

~~~
TheSpiceIsLife
Further to this, isn't this the basis for evolution?

Some selective pressure emerges that didn't previously exist, whether that be
a predator; change in nutrient availability; disease; climate; etc.

It's possible the loss of habitat in Tasmania has either _slowed_ spread of
the DFTD, because the Devils are more widely dispersed, or _hastened_ the
spread because there are fewer Devils reproducing to potentially adapt to it.

I find it interesting to ponder how it has come about that the Earth isn't
just covered in, say, that pathogenic fungus¹ reported on recently, but rather
something like 8.7 million species².

1\.
[https://news.ycombinator.com/item?id=19515362](https://news.ycombinator.com/item?id=19515362)

2\.
[https://www.nature.com/news/2011/110823/full/news.2011.498.h...](https://www.nature.com/news/2011/110823/full/news.2011.498.html)

~~~
akiselev
_> I find it interesting to ponder how it has come about that the Earth isn't
just covered in, say, that pathogenic fungus¹ reported on recently, but rather
something like 8.7 million species²._

Existing inside an organism with a functioning immune system long enough to
cause death requires completely different adaptations than existing outside of
one. By their very nature, most pathogens spend too much energy on
biochemistry that does diddly squat (without an immune system to fight) to
help them compete against the innumerable species of garden variety bacteria
floating around.

------
DoreenMichele
To give a different perspective, this is how genetic disorders in humans
develop. Sickle cell is protective against malaria. Cystic fibrosis is
protective against one or two infections that swept through Europe repeatedly,
which is why it is a predominantly Caucasian condition and is much less common
in other ethnicities.

This article is kind of celebrating the birth of a new genetic disorder as a
form of survival.

I actually find that aspect of it moderately disturbing.

~~~
FreeFull
The interesting thing about sickle cell anaemia is that you get it if both
copies of the gene are abnormal, you get the disease, but if just one of them
is abnormal you don't get the disease but still get the resistance to malaria.

~~~
DoreenMichele
Cystic fibrosis (CF) is also homozygous recessive.

Presumably, both disorders developed for the same reason: One copy of the gene
is protective, but not crippling. Two copies are crippling.

So those with one copy had higher survival rates when epidemics of certain
diseases hit. This meant that more of their children survived, even though
some of their children were born with terrible impairment and worse survival
rates.

People with CF tend to not reproduce. In fact, 97 percent of males with CF
lack a vas deferens, making them effectively sterile. It's mostly the carriers
who create new people with CF. Some of them had no idea they were carriers
until they had a child with CF.

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PavlovsCat
[https://en.wikipedia.org/wiki/Devil_facial_tumour_disease](https://en.wikipedia.org/wiki/Devil_facial_tumour_disease)

> In 2007, it was predicted that populations could become locally extinct
> within 10–15 years of DFTD occurring, and predicted that the disease would
> spread across the entire range of the Tasmanian devils causing the devils to
> become extinct within 25–35 years.

Oh man :(

Is this kind of stuff "normal" (historically), or is it likely to be another
result of our general poisoning of everything? There is this,

> In 2004, Kathryn Medlock found three oddly shaped devil skulls in European
> museums and found a description of a devil in London Zoo dying, which showed
> a similarity to DFTD

but that's a.) not much and b.) the source for that is dead or had the URL
changed, and I can't find it:
[https://www.google.com/search?q=abc+%22Devil+Disease%22+medl...](https://www.google.com/search?q=abc+%22Devil+Disease%22+medlock+2004)

~~~
stareatgoats
Might not be the fault of humans in this case. The Wikipedia article [0] gives
some interesting context, and suggests that the cancer is spread through
allograft (i.e. a form of direct transfer of the cancer from one individual to
another). It also reports that "The devils have, in a way, fought back the
extinction by developing the gene that is immune to face tumors" \- a positive
development in the long run.

[0]
[https://en.wikipedia.org/wiki/Devil_facial_tumour_disease#Hi...](https://en.wikipedia.org/wiki/Devil_facial_tumour_disease#History)

~~~
PavlovsCat
I did read that. Right after the bit I quoted:

> Calicivirus, 1080 poison, agricultural chemicals, and habitat fragmentation
> combined with a retrovirus were other proposed causes. Environmental toxins
> had also been suspected.

But the source for that is also kinda useless... someone with the last name
Owen wrote a book in 2005, great. I'm used to footnotes containing quotes from
the material they reference, and even when it links to a source, since link
rot is out of their scope, that doesn't really help.

> suggests that the cancer is spreads though allograft (i.e. a form of direct
> transfer of the cancer from one individual to another)

Yes, but why is that a recent disease? 1996 is _super_ recent.

> It also reports that "The devils have, in a way, fought back the extinction
> by developing the gene that is immune to face tumors" \- a positive
> development in the long run.

The long run is the last 100k years, IMO. When I think about cancer
historically, I am interested in that timeframe, not starting with 1996.

 _I wrote this reply 21 minutes after your comment, but apparently I was
throttled so I had to keep the tab open to post it much later. I 'm done here,
good luck and bye everybody._

------
sabujp
is it possible to learn the secrets of such abilities?

~~~
gus_massa
Probably yes, but it will probably not help too much with human cancers.

In humans, each cancer is unique and the cancerous cells are just mutated
versions of the cells of the person, so they are very related. A difficult
task of the inmune system is to distinguish the normal cells, from the
cancerous cells. Another problem is that the mutations in each person are
different, son what is useful to cure one person may not work to cure another
person.

In the Tasmanian devil case, all of them have exact same cancer. [Actually,
there are two transmisible types. Most of them have one transmissible type, a
few have the other transmissible type, and I guess that a small minority has
it's own non transmissible variant, like in humans. To simplify the
discussion, let's ignore all but the first type, and assume that all of them
have the exact same cancer.] This cancer is transmissible, the cell are
mutated versions of the cells of a Tasmanian devil that died many years ago. A
bunch of cells go from the cancer in one devil to another devil, and start to
grow. This is very difficult because the cells of the cancer are very
different from the cell of the new devil, so they should be an easy
identificable target for the inmune system. For this reason, transmisible
cancer are very rare in mammals, there are only 3 or 4 known cases.

I'm not sure what is happening here, but a usual trick to distinguish the
cells is that each cell produce some molecules that are a mix of some kind of
sugar and some king of protein. There are many sugars to select and many
protein parts to select, so there is a lot of possible variation. Each person
produces only some of them, not every variant, so the inmune system can learn
which of this are the normal one, and if it finds a cell with another
combination will attract it.

This is one of the reason why organ transplant is so hard. The inmune system
of the host detect that the cells in the new organ have a different variants,
and start to attack the organ. This is also the reason why transmisible cancer
are so rare. Even if a part of the cancer goes to another person, the inmune
system of the new host will detect the unknown molecules and attack them.

Somehow, in the Tasmanian devil case the transmissible cancer can avoid this
check and continue growing in the new host.

My guess of the "cure" is that some of the offspring of the Tasmanian devil
mutated and get a new molecule that is not in the cells of the cancer that are
like the cells of the very ancient Tasmanian devil. Or perhaps the mutation
was to not build one of the molecules, or build a different variant. So the
inmune system of the new mutated Tasmanian devil can learn that the old
protein is not normal, and attack the cells without/with it. I'm not sure what
happened here.

Once the mutant Tasmanian devil with the weird molecule survives, it increase
the probability of having offspring, that may inherid the mutation, and
increase the probability or survival, that increase the number of offspring,
... And sooner or later you get a world full of Teenage Mutant Tasmanian
Devils :).

And, as this cancer is transmissible and all have the same kind of cells, the
mutation will make the mutated offspring inmune too. [There are actually two
transmissible cancers in the Tasmanian devil, so to survive they probably will
have to be double mutated, perhaps they can inherit one mutation from the
father and other from the mother, or a mutated one can get a new mutation.]

The cancer may also mutate to be more difficult to be detected producing the
new version of the molecules, and then the devils will have to wait until one
of them get a lucky mutation, and so on ...

The problem to copy this to humans is that each humans gets it own version of
cancer, with cells that have the same molecules than the person. So you must:

a) Modify the cancer cells (and not the normal ones) to make them produce a
weird molecule so the inmune system identify and attack them. But this is very
difficult.

b) Modify the normal cells (and not the cancer ones) to make them produce a
weird molecule, and retrain the inmune system to make it attack the cells with
the old version of the molecule. I think this is even more difficult, or to be
more precise totally impossible.

