Gone for good.
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I just listened to the question put to Dr Gerber this morning and he said
at this time slightly more than 50% of the patients in the two arms remain alive
https://astro.webex.com/cmp0306ld/webcomponents/docshow/docshow.do?isPluginInstalled=yes&siteurl=astro&rnd=0.11428541360409594
or go here for link to recording
https://www.astro.org/News-and-Media/Media-Resources/Press-Kits/Thoracic-2012/2012-Thoracic-Symposium-Press-Kit.aspx
Yes, so maybe it is the data sent in to get the late-breaking plenary talk. So that would make it as of July 12,
since that was the last day to submit a late-breaking abstract! SO add another 6 weeks to those numbers.
That is what is always said. The moderator here probably doesn't know much about Bavi and so does not quite believe it , yet.
slides from the Gerber preview. Nothing new here.
https://www.astro.org/uploadedFiles/Main_Site/News_and_Media/Media_Resources/Press_Kits/Thoracic_2012/Gerber.pdf
Today's daily update. At the bottom of the page.
http://thoracicsymposium.org/Thoracic-Daily/tdaily_detail_97_5.html
I would guess that the OS numbers are interim numbers calculated by censoring the patients still alive.
How recent is this? Probably in the last two weeks or so? Even so it is fabulous!
That Avastin + CP trial was for first-line NSCLC, not second-line, and the MOS wasn't 13.4 months
it was 12.3 months, and the control arm MOS was 10.3 months.
Not correct. This trial was not a test of Avastin since both arms of the trial used Avastin.
It was a test of using pemetrexed in place of paclitaxel
Pem = pemetrexed
Cb = carboplatin
B = bevacizumab (Avastin)
Pac = paclitaxel
"The objective of this Ph 3 study was to compare Pem+Cb+B followed by Pem+B (Pem Arm) with Pac+Cb+B followed by B (Pac Arm) in pts with advanced NS-NSCLC."
"Conclusions: The primary endpoint of superior OS was not met in this trial, although Pem+Cb+B improved PFS. Toxicity profiles differed and both regimens demonstrated tolerability."
You are indeed correct about that.
He is getting desperate because what he said makes no sense.
Mojojo, nice graph! What I would question is the last part of the red curve. Because of the MOA of Bavi
being much different than standard chemo only it may not be a good assumption that the red curve
would continue down in a smooth fashion. It may be that at some point it flattens out and plateaus.
Hopefully tomorrow we might get a similar plot.
I am hoping to see that in the slides that Shan will be presenting tomorrow,
It doesn't matter, the only valid comparison is with the control arm of this trial. In any case, you can't
get much sicker than >90% in stage 4. If patients in all those other trials were sicker then you would
expect the MOS for their control arms to be much less than 5.4 months, not greater.
See Thurly's response to this.
Wake up people! The abstract for tomorrow's talk has been posted on the conference website.
The webcast by Shan will have more details I am sure, but the big news is out!
Results:Of the 121 patients randomized, no significant differences were seen in baseline characteristics (gender, age, ethnicity, ECOG or disease stage.) Based on 117 evaluable patients, the ORR was 7.9% for the D + P, 15.0% for the D + 1 mg/kg B and 17.9 % for the D + 3 mg/kg B cohorts, respectively. Median PFS was 3.0, 4.2 and 4.5 months, respectively. At the time the Independent Data Monitoring Committee (IDMC) recommended to unblind the trial, median OS had been reached at 5.4 months in the control group (61% death events), while <35% of death events had been observed in the bavituximab-containing groups. B + D was well-tolerated and no safety concerns were identified by the IDMC. Conclusions:In this double-blind, randomized, placebo-controlled, multicenter Phase II study in patients with Stage IIIB and IV non-squamous NSCLC, bavituximab in combination with docetaxel was well-tolerated and all endpoints (response, PFS and OS) demonstrated trends toward superiority for both experimental arms. Importantly, though median OS has not yet been reached in either bavituximab-containing cohort, there is a clear and persistent separation of the survival curves warranting further development of bavituximab.
RRdog, I don't think they are extreme anymore.
At this point I am not making any more estimates because we are in uncharted territory.
No telling how long those patients will remain alive.
The 5.4 months for the control arm also tells us that this patient group was pretty sick. King has said that
over 90% were stage 4 (metastatic disease). If you look back at my table for the second-line NSCLC phase 3 trials,
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=77206110
you can see that 5.4 months is less than all of them. That makes the current situation all the more remarkable.
Great! 5.4 months for the control MOS, that makes the MOS for the treatment arms even better in comparison.
If less than 35% treatment arm patients had died by the end of April (is that when it was unblinded)
this could go on for a while. It could get to 3X the control arm MOS. The treatment arm patients may
be on a plateau if plotted on a KM survival curve. At some point you could say their cancer is controlled,
or cured. I think the emphasis on CRs is wrong because CRs are defined by the RECIST criteria and are
measured during the treatment cycles. It is possible to have a CR, as defined by those criteria, and then
to later progress and not be a CR. CR does not mean cure. On the other hand it can go the other way too.
We are now in a place where we don't really know what is going on inside those patients still alive, all we
know is that they are still alive.
I think you are assuming a lot if you think he understands anything about Bavi. He will understand MOS numbers,
but to think he understands the potential is a big stretch.
CP, if Bavi is internalized by the tumor cell, something which has never been shown in any of the preclinical
papers, then it would be enclosed inside the cell. How could it then interact with the immune system?
The macrophages and dendritic cells would not be able to bind to the Fc part of the antibody. Furthermore,
it would likely then be degraded by enzymes. This assumption of yours doesn't work.
The dosage does matter, but because at 1 mg/kg it is near saturation what matters is if the dosage were
less than that, not more.
While we are waiting another amazing story is here.
http://www.nytimes.com/2012/09/06/science/far-from-junk-dna-dark-matter-proves-crucial-to-health.html?ref=global-home
http://www.sciencedaily.com/releases/2012/09/120905140913.htm
What is relevant about this is that understanding cancer using the old gene-centric
approach just got way more complicated because now you need to look at all the
"dark matter" DNA too. More redundant pathways that tumor cells can use to defeat "targeted" drugs.
This makes the immune approach even more attractive.
From the NYT article:
“These papers are very significant,” said Dr. Mark A. Rubin, a prostate cancer genomics researcher at Weill Cornell Medical College. Dr. Rubin, who was not part of the Encode project, added, “They will definitely have an impact on our medical research on cancer.”
In prostate cancer, for example, his group found mutations in important genes that are not readily attacked by drugs. But Encode, by showing which regions of the dark matter control those genes, gives another way to attack them: target those controlling switches.
Dr. Rubin, who also used the Google Maps analogy, explained: “Now you can follow the roads and see the traffic circulation. That’s exactly the same way we will use these data in cancer research.” Encode provides a road map with traffic patterns for alternate ways to go after cancer genes, he said.
Dr. Bernstein said, “This is a resource, like the human genome, that will drive science forward.”
The system, though, is stunningly complex, with many redundancies. Just the idea of so many switches was almost incomprehensible, Dr. Bernstein said.
There also is a sort of DNA wiring system that is almost inconceivably intricate.
It is an oral presentation so I don't think there is any abstract to be released tomorrow,
except for the poster on the first-line NSCLC trial.
I looked at this a while back and found some, but more in the control arms than
the treatment arms. I think 5% CRs would be very good.
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=77608580
I saw this. I think it is like MDSC, or Dendritic suppressor cells, or D2 dendritic cells, like M2 macrophages.
This was the first time I heard a mention of a subset analysis. I wonder what subset, or subsets, they are.
That could be interesting.
Here is an interesting set of data from a new article in Cancer Research:
Why RECIST Works and Why It Should Stay
Antonio T. Fojo and Anne Noonan
http://cancerres.aacrjournals.org/content/early/2012/08/31/0008-5472.CAN-12-0733.abstract
This is in response to another article:
RECIST: No Longer the Sharpest Tool in the Oncology Clinical Trials Toolbox
Manish R. Sharma Michael L. Maitland and Mark J. Ratain
http://cancerres.aacrjournals.org/content/early/2012/08/31/0008-5472.CAN-12-0058.abstract
The interesting thing is the OS data for these drugs and how small the increase is. Note especially the drugs for NSCLC.
From the first article with the table:
"Summarized therein are drugs approved by the FDA in
metastatic solid tumors over the past 10 years. Cytotoxic and
targeted therapies are itemized, including many of the therapies
that promised so much, but ultimately disappointed. The
29,312 patients enrolled represent a fraction of those evaluated,
as this number does not include patients enrolled in the phase
II trials that preceded these phase III studies and the thousands
enrolled in confirmatory phase III trials. The median gain
achieved in PFS with our new therapies in these past 10 years
is a marginal 2.15 months. The median gain in OS has been 2.16
months. No one can look at these data, which include 48 FDA
drug approvals over 10 years, and argue that our "screening
threshold" is too high and that we are missing active agents."
I only have a free membership also. To go to any post just put the number in the white box in the blue bar
above the highlighted items and press "Go to Post". Whether you want to read it or not is up to you.
Well, I do have a theory that there is a connection.
See my post # 87274.
It is actually a picture of Dr. William B. Coley, who is considered by some the father of cancer immunotherapy.
http://en.wikipedia.org/wiki/William_Coley
I want to thank all of you who have expressed appreciation of my work here. I hope that it has helped you
to evaluate the science of Dr. Thorpe and Peregrine. Thank you for educating me on matters I knew little of,
such as the financial aspects of biotech companies. There is a lot more science yet to come. I don't think
the medical community has yet grasped the impact this science will have. I feel that it is of fundamental importance.
Hope to meet some of you at the Annual Shareholders Meeting next month.
You will never see me on Facebook, since I don't use it and don't want to. I am sure
there are others that feel the same.
Fine with me, but I would really like to see Gerber et al. submitting a paper
to NEJM before long. Got to sell it to the oncologists too.
I think they are bound by the rules under which they submitted the late-breaking abstract.
The data can not be released before 1:40 PM CDT on Friday. What is the big deal? There can
be a big story in the Sunday edition of the NYT. Don't more people buy the Sunday edition
anyway? It is still before Monday's open of the market.
Thanks CJ, even better than I thought.
Not sure. If I remember correctly, I read that most universities got 5-10%. Maybe
RRdog has some info on that?
RRdog, don't forget they also have patents for phosphatidylethanolamine (PE) which we haven't
heard a lot about yet. PE is included in several of their patent applications including the latest.
Compositions and Methods Comprising Phosphatidylethanolamine-Binding Peptide Derivatives
20120164071
June 28, 2012
I don't know what their cut is, maybe 5%? Thorpe will be very popular there at UTSW.
WE OWN IT. I haven't heard much mention of the fact that there are no competitors to
Peregrine as far as anti-phospholipid antibodies for the treatment of cancer and viral
diseases. I think the patents in place pretty much have it locked up tight. That is a huge
advantage for Peregrine, and for us the shareholders.
Mojojo, thanks, very nice graph. I think it is the effect on the survival curve that is most relevant,
as shown in the graph on my post # 89243. Bavi does seem to be similar to avastin in PFS, although
better than control. Here are survival curves from the poster at AACR 2012 on cure of TRAMP mice with
CRPC. Think of the black line as the control arm, and the green line as the bavi treatment arm(s).
and the model survival curve to demonstrate how delayed separation of survival curves can violate the
assumption of proportional hazard.