
Crispr Wins Key Approval to Fight Cancer in Human Trials - adventured
http://www.bloomberg.com/news/articles/2016-06-23/crispr-wins-key-approval-to-fight-cancer-in-human-trials
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cioc
If you think stuff like this is cool, and you'd like to be a part of the
software engineering effort at Parker Institute for Cancer Immunotherapy, msg
me. ccary@parkerici.org

We are building out our platform for bioinformatics. Some engineering topics:

* Large scale data processing (Cloud & on-prem HPC based)

* Bioinformatics / ML algorithms

* Data storage & retrieval (File systems & databases)

~~~
wfunction
Yes, please elaborate on what the software engineering effort involves! Is
this a bioinformatics thing? What kind of work does it involve? Does it
require a strong theoretical background? etc.

(Edit: Thanks! Just noticed you added it.)

~~~
leeoniya
maybe WRT to
[https://www.google.com/search?q=genome+sequencing+algorithms](https://www.google.com/search?q=genome+sequencing+algorithms)
which would be needed to find unique patterns among billions of base pairs for
CRISPR to target. it's microscopic big data :D

[1] [http://benchling.engineering/dna-regex-
search/?hn](http://benchling.engineering/dna-regex-search/?hn)

[2] [http://benchling.engineering/optimizing-
crispr/](http://benchling.engineering/optimizing-crispr/)

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baldfat
Having lost a sister and a son to cancer I hope for this to work. The issues
are tremendous for this technique and I don't have high hopes for its use on
cancer. I am still having high hopes on immune system techniques that helps
the body to mark cancer cells and attack the cells for most cancers.

CRISPR big hope is that it can change the cell to stop reproducing or stop
invading other cells. Simply put cancer cells are cells that grow that don't
stop AND can spread to other cells. If you get one of the two you win.

HIGHLY RECCOMENDED : list to Radio Lab Famous Tumors
[http://www.radiolab.org/story/91713-famous-
tumors/](http://www.radiolab.org/story/91713-famous-tumors/)

~~~
j_jochem
Isn't the idea with CRISPR that you patch the patient's t-cells in such a way
that they are able to recognize cancer cells as diseased cells, allowing the
immune system to clear them away?

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alextheparrot
The holy grail would be fixing commonly occurring mutations that cause the
cancer, but to my knowledge the edit/correction rate is too low for this to
work currently, plus the possibility of causing more cancer by bad edits.

Thus, the T-cell approaches are more promising currently as it allows for
direct modification of cells to fight cancer with known anti-cancer antigens,
using a modified immune system.

~~~
rudolf0
Could this theoretically be used to fight all pathogen-based illnesses as
well?

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robbiep
Theoretically, it could be used to get a person to grow a new set of arms. But
technology that doesn't exist yet is all speculation.

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zymhan
I hope that by the time I'm succumbing to the effects of aging, we'll have
techniques with tools like CRISPR to make it easier.

~~~
ddorian43
And are you doing something about it (donating/investing/working/etc) ?

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ceejayoz
Chances are anyone in a developed-world democracy is investing/donating via
their tax dollars.

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JoshTriplett
Not very effectively or with the focus you might want, though.

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ceejayoz
I tend to believe the NIH is better at administrating grants than I am.

~~~
JoshTriplett
I'd absolutely agree they're better than I am personally, since I'm neither a
medical researcher nor an expert at evaluating medical research. But I don't
believe they're better than an organization focused on solving a specific
problem.

As a random example of inefficiency: there's a lot more money going into
research on specific degenerative diseases than into the causes and solutions
for degeneration. Solve the root cause, not the symptoms.

~~~
ejstronge
While the idea of pursuing a 'root cause' is attractive, in many cases,
including the one you point out, there is not a clear cause to be attacked.

Neurodegeneration is a pattern of response to multiple disease processes - we
can only understand the response by studying the cases in which it arises.

For the tech-minded crowd, this is like wanting to create responsive designs
without actually making websites to demonstrate them.

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noam87
As someone about to start PD-1 inhibitors after failing Ipilimumab (now in
lungs (1))... well it'd be just plain stupid to die now with all these
treatments on the horizon.

\---

(1) This just happened this month. The Doctor called me with the results
literally the week after I handed in my notice at a secure job to join an
early-stage startup.

Life really _is_ short!
([http://www.paulgraham.com/vb.html](http://www.paulgraham.com/vb.html))

No I don't regret my decision :)

(Also thank Jeebus I live in Canada where my current lack of benefits does not
preclude me from getting the best treatment.)

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c-slice
If you want to better understand the CRISPR patent dispute, this article lays
out the arguments very clearly. [https://www.statnews.com/2016/03/18/crispr-
patent-dispute/](https://www.statnews.com/2016/03/18/crispr-patent-dispute/)

~~~
SapphireSun
Ha, are you sure you didn't mean
[http://www.cell.com/cell/fulltext/S0092-8674(15)01705-5](http://www.cell.com/cell/fulltext/S0092-8674\(15\)01705-5)
;D

(For those of you who aren't in on the joke, "The Heroes of CRISPR" was
written by the director of the Broad Institute, which incidentally has Feng
Zheng on its payroll. For that reason Eric Lander has been roundly criticized
for attempting to weigh in on the history early. My friends who work in and
around Kendall Square say that some of the criticism is overblown, the article
points out a lot of people who didn't get much recognition prior, but still...
it's a bit skeevy so you might want to take the latter half of the article
with a grain of salt as it's not necessarily factually wrong, but the emphasis
might be distorted and there is a risk of omissions.)

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victoriadanahy
No doubt, CRISPR is the next big thing that will make sense for everyone.

I work for Synthego and we make synthetic RNA for CRISPR/Cas9 Genome
Engineering. Our process is fully automated with robots and an architected LAB
synthesizer.

We are actively hiring:

* Full Stack Engineers with strong DB and Python skillS * Robotics/Mechanical Engineers with automation experience AND who think outside the box! *Extraordinary Human Beings are welcome too

If you are interested --> email me: victoria.danahy@synthego.com :-)

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DigitalSea
>rewrite the blueprints of life itself

Something unsettling about how that is worded, but this awesome. There hasn't
really been any major breakthrough like this in a very long time, as the era
of antibiotics ends, new treatments like this might open the door for a new
wave of medical treatments.

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astazangasta
I'm calling it here, this trial will fail hard.

The basic idea is this: the cancer has a number of mutations that produce
novel antigens that don't exist in normal cells. If we can train T-cells to
recognize these, they can attack the tumor with great specificity and kill
those cells.

The problem is, all the tumor has to do to evade this targeting is shed the
problematic mutation, which is easily done - tumors are great at acquiring
novel mutations to become resistance to therapy, losing a mutation is even
easier. All you have to do is ditch one arm of a chromosome, revert the
mutation, or otherwise eliminate the novel mutation, and your tumor cell is
now resistant to this therapy.

Add to this the fact that we are basically shit at predicting which mutant
proteins will produce neoantigens and you have a recipe for total failure,
even in concept.

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maxander
Depends on what you mean by "fail hard," I suspect. Sure, cancer cells can
gain or lose mutations, but if we target a mutation important for cancer
development only a fraction of the target cancer will survive the treatment.
We might achieve nice-to-have results like reduction in tumor size and
increased patient life expectancy, or a "cure" in lucky patients with less
agile cancers, which would put this radical new intervention in line with most
standard cancer treatments. As a total _cure_ for cancer it will "fail," but
then, so have all the breakthrough cancer treatments that have collectively
shattered the mortality rates of cancer patients.

(You mention you're involved in cancer research, so you presumably know all
this already- I'm wondering if there's a more nuanced reason for this
pessimism.)

The best theory I've heard so far as to how we'll "cure cancer" altogether is
that we'll simply develop a big enough armory of anticancer treatments that no
individual cancer case could evolve fast enough to beat them all. Unlike
bacteria or viruses, cancers evolve on their own and when they're done their
evolutionary innovations die with them. Our technology lives on, though, so we
can hope to eventually just totally outclass their capabilities. If CRISPR
gives us another source of these partial treatments, we're just that much
closer to that level.

~~~
astazangasta
This method is not targeting mutations important for cancer, this is targeting
"passenger" somatic mutations. You can't use this mechanism to target
important mutations because only a minority of patients are going to be able
to present an oncogenic mutation (e.g. BRAF V600E) as an antigen (because of
differing HLA types). In those rare cases perhaps this therapy might succeed,
although the tumor probably still has ways of evading (downregulating the
offending HLA for example).

As for the "kitchen sink" approach, so far none of the methods we've developed
are free from side effects. Cancer patients are often on the edge of death;
each successive therapy will probably do more damage to them. As it is most
people fail on current immunotherapies because of autoimmune reactions. So
relentless application of therapies is not necessarily going to work, though
of course having more weapons in our arsenal is great.

~~~
danieltillett
I was under the impression that the major reason for the failure of current
immunotherapy treatments is due to non-response, not excessive autoimmunity.

~~~
astazangasta
Sorry, you're absolutely right. I should say 'many', not 'most', my comment
was hasty. It varies with the therapy and only a minority of patients fail
because of adverse immune events, and the drug matters - ipilimumab (anti-
CLTA4) had 10-15% severe immune-related adverse events, whereas anti-PD1 is
much better tolerated (probably because the immune checkpoint is later).
Combination therapies (ipi + nivo) have much higher adverse event rates,
unsurprisingly.

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Dowwie
Well, it's worth a shot.

[http://i.imgur.com/BbgL7x3.gif?noredirect](http://i.imgur.com/BbgL7x3.gif?noredirect)

