Redplate has a new gig.
TapImmune Appoints Mark Reddish to Its Management Team as Vice President Product Development
Former Executive at ID Biomedical and Biomira Inc Brings Broad Experience and Expertise in Cancer and Biodefense Product Development
>>The development of started 14 years ago. I don't remember you being in the room at the time when the decision was made to go after the ICRF patents, or even down in the lab when the actual work started.<<
This doesn’t refute that muc1 has been investigated for 20-30 without proof of efficacy.
>>Oh ya you don't actually contribute as a hack, just snipe from the sidelines 14 years later.<<
I don’t like to talk about my accomplishments.
Most scientists try very hard to not make statements that are untruthful. Science is a process used to gain knowledge and this process is hampered when misinformation is spread. Because of the importance of truth it tends to hurt a scientist’s reputation if constantly corrected for making things up; you shake it off like water on a duck’s back. On the topic of explaining why the phase II T cell response rate is low you have been caught lying twice. The first time you said it was critical to perform the assays immediately after taking the samples. The rest of the immunology field disagrees with this opinion as evident by the near universal use of frozen cells. Next we heard there wasn’t enough cells to perform the assays. This is a common refrain found in many of the papers in which you’re listed as a co-author. However, this is incongruent with the number of assays described in publications; 78 patients at several time points. And these aren’t the only misstatements you’ve made during my short presence here. I still can’t understand how you could take the 13/17 positive T cell response when blood is taking from health donors and the vaccine is given ex vivo and mistakenly call it phase I safety trial. What, were they testing the safety of drawing blood? The lies have been many and your immunology is pedantic and outdated. Even when presented with evidence that the immunology field is putting less importance on killing assays and more importance on other markers you continue without contemplation, http://messages.finance.yahoo.com/Stocks_%28A_to_Z%29/Stocks_O/threadview?m=ts&bn=72373&tid=74454&mid=74454&tof=-1&rt=1&frt=2&off=1
I would consider that just a minor difference of opinion. More remarkable are the out right gaffs. Here you are asked to compare anti-ctla4 and stimuvax.
“Interesting the adjuvant MPLA is also a CTLA4 agonist, which makes Stimuvax sort of like ipilimumab, but doesn't make ipilimumab quite like Stimuvax. In theory they would be nicely complimentary to each others stated functions.
There is a source of immune suppression, and it is why we are here. T cell become down regulated via encounters with mUC1 mucin, the literature calls this anergy. One paper that addresses this shows that IL2 being added can also help to overcome this anergic blockade. See this little diddy here from Nature Medicine. Publishing here has a tad more credibility than publishing a hack piece at Seeking Alpha
Agrawal, B., Krantz, M.J., Reddish, M.A. and Longenecker, B.M. (1998) Cancer-associated MUC1 mucin inhibits human T-cell proliferation which is reversible by IL-2. Nature Med. 4(1):43-49.”
There are two very large things wrong about the above. First, MPLA is not a CTLA4 agonist. I don’t understand how an immunologist can be so completely ignorant about ctla4. Finding a means to block peripheral tolerance has been described as the search for holy grail for over a decade. Even worse though is citing your IL-2 paper. Not the citing your own work, although that is creepy, but the IL-2/anergy theory isn’t in favor. This paper cites other authors with a competing theory involving regulatory T cells. Which theory is the stimuvax trial based on? The regulatory T cell theory and not the theory postulated by their own scientists.
So, thanks for all the contributions (lies, sophistry, and discredited ideas) hack.
The development of started 14 years ago. I don't remember you being in the room at the time when the decision was made to go after the ICRF patents, or even down in the lab when the actual work started.
Oh ya you don't actually contribute as a hack, just snipe from the sidelines 14 years later.
>>The IP you mention has no relationship to the IP and development that underlies Stimuvax.<<
My mistake- the muc1 license came from the Imperial Cancer Research Fund not UofA.
The timing however stands. It’s been 24 years since the first muc1 paper was published in 1987-
Cloning of partial cDNA encoding differentiation and tumor-associated mucin glycoproteins expressed by human mammary epithelium
<<false The IP you mention has no relationship to the IP and development that underlies Stimuvax. >>
Appears these shorts' whole basis for shorting is flawed.
COVER NOW OR GO BROKE YOU FOOLS!!!
"The intellectual property rights developed by Dr. Antoine A. Noujaim and Dr. B. Michael Longenecker were licensed to Biomira in 1986. It’s been 25 years already."
The IP you mention has no relationship to the IP and development that underlies Stimuvax.
>>Stimuvax has been 14 years in development, 12 in the clinic.<<
The intellectual property rights developed by Dr. Antoine A. Noujaim and Dr. B. Michael Longenecker were licensed to Biomira in 1986. It’s been 25 years already.
>>Yields of cells was responsible for over half of the samples giving having 'no data' which was due to insufficient cell numbers for the assays. <<
“T-cell proliferation assays were performed on 78 (88.6%) of 88 patients in the L-BLP25 arm before immunization and at several time points after immunization.”
78 patients tested at several time points. 6% of the stage III LR sub-group showed a positive T cell response as defined as a single time point positive by LPA.
It’s not like all the samples come in at once. If the first samples showed insufficient cell numbers they would have asked for a larger blood draw at later time points.
OK, so even if "Yields of cells was responsible for over half of the samples giving having 'no data'" (convenient that this is in some nebulous presentation which you can't prove exists) there were still only 16 patients in the phase 2b study will T-cell proliferation out of 78 assayed. Now, 16/78 is not a big proportion, but neither is 16/38.
Also, and this is small point, but "there is data" is incorrect. You should have written "there are data". Details are important.
Actually there is data and Butts mentioned it in a presentation/poster. Yields of cells was responsible for over half of the samples giving having 'no data' which was due to insufficient cell numbers for the assays.
The rest of your claims of what i said is false and deliberately so. Butts made the statement made on the data regarding sample viability and cell yields that prevented half of the data from ever being collected.