Hello,
First, my thanks for taking the time to review and comment. I actually wasn't looking for a critique, but rather someone to work with me to develop and execute assays. Sigma Aldrich may be willing to produce my zinc-finger configuration pro bono… I've already been invited up to the Institute for Advanced Biotechnology and Medicine to discuss my paper, and I've conversed with Dr. June and Dr. Wender (Bergstrom Professor of Chemistry, Stanford) among others about my proposed therapeutic and none expressed any concerns regarding neither the fundamentals nor feasibility of the approach I put forth.
I am surprised that you came to the conclusion that my proposed therapeutic involves a T Cell... it does not, it is a single chimeric protein having nothing to do with any lymphocyte… my apologies if my writing wasn't clear.
Also, again, although I appreciate your time, I take offense at your inferring that I simply read abstracts; I assure you I read several hundred pages (and a textbook or two) of research over several months and incurred a large expense acquiring those papers despite the fact that my tax dollars paid for much of the research.
I also disagree with (though appreciate :) ) just about every one of your assertions. I'll address the rest tomorrow, but just for starters… Take the Oncogenes... I wrote "but rather a change in transcription regulation, a substantial decrease in the ubiquitination-proteasome turnover rate, or its active state changing from induced to constitutive that is the actual driver of oncogenesis (8) (9). "
Each of those three assertions are accurate reflections of those made in the research I cited. In fact you wouldn't even have to read passed the title of the papers… referring to c-Myc; "hot spot mutations in lymphomas result in inefficient ubiquitination and decreased proteasome-mediated turnover"
even the Wiki article you linked states:
"an increase in protein (enzyme) activity… and a loss of regulation" and all but 3.2 specifically refer to regulation, not a change in primary function and even 3.2 refers to a change in state to constitutively active…
Thanks again,
Scott
On Monday, July 1, 2013 4:47:47 PM UTC-4, Mackenzie Cowell wrote:
--Passing your message on to the main list, Scott.---------- Forwarded message ----------
From: Scott Tarone <sta...@synapticsynthase.com>
Date: Sun, Jun 30, 2013 at 7:16 PM
Subject: Intein control in a targeted cancer therapy
To: con...@diybio.orgHello,
I'm not sure if your group is the right place for me to look for help, but I thought it worth a shot.
I am self-taught in the biosciences… Neuroscience, Genetics, Immunology, and Targeted Cancer Therapies. After watching a presentation on Chimeric Antigen Receptors on the NIH site, I had an idea on another approach that would remove the limitations inherent in the technique presented (though it was a fantastic step forward, and very successful). My approach is based on a constitutively active Caspase 3 mutant controlled by a molecular switch.
Long story short… I just wrote up a few paragraphs on my idea and sent it off to a few people in the field. One of them (a senior scientist from Pfizer) got back to me a few months later and said I may be on to something and that I needed to write a paper. I did that and then wrote an article on that paper with him and that was published in a small time online journal last year. Since then my paper and the article have been download several hundred times.
I didn't provide the links or an attachment as my first attempt to send this email was blocked by spam filters.. I will provide that information if you have interest. In the interim, you can search for "intracellular Caspase modulating Chimeric Antigen Receptor".
Thank you very much for your time…
Take care,
Scott
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