Gone for good.
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The PI for the HER2-negative breast cancer IST, which has an abstract at ASCO,
is Alison Stopeck, MD, also an associate prof at U of A school of medicine.
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=87134255
http://azcc.arizona.edu/profile/alison-stopeck
The person named Michael Gordon quoted in this article is a medical advisor for Peregrine.
http://www.peregrineinc.com/about-us/medical-and-scientific-advisors.html
I don't understand what you are getting at. Chemo drugs bind proteins in cells which
makes them cytotoxic agents. There is no reason to expect that the chemo drugs will bind to beta2-GPI
and somehow interfere with Bavi binding to it. Is that what you are getting at?
phosphatidylserine, and all the other phospholipids, are not proteins, but lipids, so protein binding would not include them.
New paper published on PGN650-NIR imaging. This is similar to the poster presented at the recent AACR meeting
and available from Peregrine, but with more info.
Molecular Imaging June 2013
Measuring Response to Therapy By Near-infrared Imaging of Tumors Using A Phosphatidylserine-targeting Antibody Fragment.
Gong J, Archer R, Brown M, Fisher S, Chang C, Peacock M, Hughes C, Freimark B.
Abstract
Imaging tumors and their response to treatment could be a valuable biomarker toward early assessment of therapy in patients with cancer. Phosphatidylserine (PS) is confined to the inner leaflet of the plasma membrane in normal cells but is externalized on tumor vascular endothelial cells (ECs) and tumor cells, and PS exposure is further enhanced in response to radiation and chemotherapy. In the present study, we evaluated the potential of a PS-targeting human F(ab')2 antibody fragment, PGN650, to detect exposure of PS in tumor-bearing mice. Tumor uptake of PGN650 was measured by near-infrared optical imaging in human tumor xenografts in immunodeficient mice. PGN650 specifically targeted tumors and was shown to target CD31-positive ECs and tumor cells. Tumor uptake of PGN650 was significantly higher in animals pretreated with docetaxel. The peak tumor to normal tissue (T/N) ratio of probe was observed at 24 hours postinjection of probe, and tumor binding was detected for at least 120 hours. In repeat dose studies, PGN650 uptake in tumors was significantly higher following pretreatment with docetaxel compared to baseline uptake prior to treatment. PGN650 may be a useful probe to detect PS exposed in tumors and to monitor enhanced PS exposure to optimize therapeutic agents to treat tumors.
The paper is here:
http://mi.deckerpublishing.com/index.php/article/measuring-response-to-therapy-by-near-infrared-imaging-of-tumors-using-a-phosphatidylserine-targeting-antibody-fragment
The poster is here:
http://www.peregrineinc.com/images/stories/pdfs/jian_2013.pdf
Note that the imaging trial uses PGN650 bound to Iodine-124 for PET imaging, whereas in this paper,
and the poster, PGN650 is bound to 800CW, which is a probe for Near InfraRed (NIR) imaging.
http://www.clinicaltrials.gov/ct2/show/NCT01632696?term=Bavituximab+OR+Peregrine&recr=Open&rank=5
All the research done in any lab has to be funded, At universities/medical schools etc it is mostly funded
by the federal government (NIH) through competitive research grants, but also by pharma companies. You stated:
The only thing that matters is the increase in MOS for the treatment arm compared with the control arm.
There is no way to know if the disclosed PFS results will have any connection with the expected MOS results.
I am not even sure if it is possible to say that you could expect the first-line results to be better than the
second-line results. That would be true if you were talking about a trial comparing two chemotherapy regimens,
but we are not. Bavi is an immunotherapy and I can conceive of reasons for the second-line to be better than
first-line therapy, but to still expect very good first-line results. We know very little about the first-line trial.
We do not know anything about the patient characteristics. We do not even know what ECOG PS scores
are allowed. PS 0-2, or 0-1? The clinical trials webpage does not list this in the inclusion/exclusion criteria.
http://www.clinicaltrials.gov/ct2/show/NCT01160601?term=Bavituximab+OR+Peregrine&rank=4
Given all of this my expectations are for control MOS of 10 months and treatment MOS of 14-15 months.
I believe that Peregrine is waiting until approximately 80% of the treatment arm patients have died before announcing
the MOS results. This will eliminate second guessing about the effect censored patients would have on the ultimate result.
I also believe that the results will not be statistically significant because of the small trial size, but this is to be expected.
However, I do expect a good result for the hazard ratio. Remember that this is a phase IIb trial, not a phase III trial.
There is a big difference in expectations between the two.
Note that an increase of MOS of 40% would still be excellent and much better than the 19.4% seen in the Avastin + CP first-line NSCLC trial.
Here is an updated chart including 20 Phase III first-line NSCLC trials which had a control arm using carboplatin + paclitaxel (CP).
Every so often I have to get some fresh bait.
There are actually 21 trials listed for bavituximab or Peregrine, but only 5 are listed as "recruiting",
but that includes the IST for HER2-negative breast cancer which just completed enrollment.
http://www.clinicaltrials.gov/ct2/results?term=Bavituximab+OR+Peregrine
You are wrong, Dr. Brekken did not give the presentation in Chicago, It was Dr. David Gerber.
Please get your facts correct.
Yes, Dr. Brekken does have a lab at UTSW.
http://www.utsouthwestern.edu/labs/brekken/
Take that you scumbag!!!
NEW YORK, May 2 (Reuters) - A once prominent biotechnology investor was handed four years in prison on Thursday after pleading guilty to stock manipulation, the second time he has run afoul of U.S. securities laws.
David Blech, 57, pleaded guilty in May 2012 to securities fraud charges stemming from improper trades in biopharmaceutical companies Pluristem Therapeutics Inc and Intellect Neurosciences Inc.
Blech pleaded guilty in 1998 to similar charges of illegal trading, getting five years of probation rather than jail time. On Thursday, U.S. District Judge Colleen McMahon in Manhattan expressed anger at his repeat offense and rejected his lawyer's request for leniency.
"No, not this time," McMahon said. "No mercy. This time, punishment."
Blech was once dubbed the "King of Biotech" as a founder of companies and a major investor in the biotechnology sector.
The latest case stemmed from his sale of 50 million shares of Pluristem over several months in 2007. Rather than just selling the stock, he used several accounts held in other people's names to buy another 100 million shares and sell 150 million shares, the government said in court papers.
The result was that Blech was able to sell the 50 million shares for $1.2 million while propping up the price of Pluristem, which is lightly traded on the Over the Counter Bulletin Board, prosecutors said.
Blech committed a similar fraud in 2008, prosecutors said, when he sold shares in Intellect Neurosciences, a company he co-founded.
He had faced a maximum 40 years in prison. Prosecutors had sought 41 to 51 months in prison.
McMahon also ordered Blech to forfeit almost $1.34 million and sentenced him to a maximum three years of supervision after his jail term.
"I am ashamed to again be before a court pleading for its mercy," Blech said.
Blech still faces a separate civil lawsuit by the U.S. Securities and Exchange Commission related to the case.
The case is USA v David Blech, U.S. District Court, Southern District of New York, No. 12-cr-00372. (Editing by Matthew Lewis)
Radioactive Bacteria Targets Metastatic Pancreatic Cancer
http://www.sciencedaily.com/releases/2013/04/130422154753.htm
Treating cancer with radioactive bacteria
Three wrongs make a right
http://www.economist.com/news/science-and-technology/21576628-surprising-new-way-kill-tumours-three-wrongs-make-right/print
This is a very interesting story. Reading these articles immediately brought a few things to my mind.
1) Using the radioisotope attached to the bacteria is really just an indirect method of targeting the radioisotope to the tumor since
the immune response eliminated the bacteria elsewhere.
2) Cotara delivers the radioisotope Iodine-131 to the necrotic core of a tumor. So why not just use Cotara for metastatic pancreatic cancer?
3) How about attaching I-131 to bavituximab instead of I-124, as has been done before in imaging studies? I-131 is a beta emitter
(electrons), whereas I-124 emits positrons used for PET imaging.
4) If the problem of treating metastatic pancreatic cancer is that the patients die too quickly for bavi to have much effect then using
I131-PGN635, or Cotara, can instead use their targeting ability to deliver the radioiostope which will immediately start killing the
surrounding tumor.
5) What about using bavi and Cotara together for metastatic pancreatic cancer? They should complement eachother, maybe having a
synergistic effect.
Jason Stafford's Ph.D. dissertation from 2011 is available online.
http://repositories.tdl.org/utswmed-ir/handle/2152.5/1038
Here is the concluding paragraph from chapter 3, followed by Figure 3.6. Note that 124I-IN11 F(ab')2
is now renamed as the imaging agent 124I-PGN650.
So it is all about maintaining the confidentiality of the percentages paid for licensing.
New Confidential Treatment Order extending past orders
http://ir.peregrineinc.com/secfiling.cfm?filingID=9999999997-13-8647&CIK=704562
I hope this is good, but who knows? There is no reason for Peregrine not to present details
in a PR since they are not bound by ASCO disclosure policies. I expect to hear the
news once the "event horizon" has been crossed.
Three poster abstracts at ASCO confirmed. Only the titles until May 15th. Nothing for the first-line NSCLC trial.
http://iplanner.asco.org/am2013/am2013.aspx
Abstract #8095
Randomized, blinded, placebo-controlled phase II trial of docetaxel and bavituximab as second-line therapy in locally advanced or metastatic non-squamous non-small cell lung cancer.
Mikhail Shtivelband, MD
Abstract #567
Phase I clinical trial of bavituximab (Bavi) and paclitaxel (P) in patients (pts) with HER2-negative metastatic breast cancer (MBC).
Pavani Chalasani, MD, MPH
Abstract #4054
Randomized, open-label, phase II trial of gemcitabine with or without bavituximab in patients with nonresectable stage IV pancreatic adenocarcinoma.
Shuchi S. Pandya, MD
This may be old news, but maybe not to all.
Two Oncology Drugs Deemed Breakthrough Therapies
New program is intended to speed the path to approval by boosting company–FDA interactions.
Swiss drugmaker Novartis announced in mid-March that its investigational compound LDK378, an inhibitor of anaplastic lymphoma kinase (ALK), received a “Breakthrough Therapy” designation from the U.S. Food and Drug Administration (FDA) for treatment of patients with ALK+ metastatic non–small cell lung cancer who cannot tolerate crizotinib (Xalkori; Pfizer) or whose disease progressed while taking it.
Novartis is the second company to reveal that one of its oncology drugs was granted the special status. In February, Janssen and Pharmacyclics received 2 Breakthrough Therapy designations for ibrutinib, a Bruton tyrosine kinase inhibitor under investigation for the treatment of patients with relapsed or refractory mantle cell lymphoma who have received prior therapy, and also for patients with Waldenstrom macroglobulinemia. The companies are collaborating to develop ibrutinib.
The Breakthrough Therapy program, introduced last summer under the mandate of the FDA Safety and Innovation Act, is intended to expedite the development and review of drugs that treat serious and life-threatening conditions and that have demonstrated substantial improvement over existing therapies on at least one clinically significant endpoint. Companies whose drugs earn this status are entitled to interact more frequently with the FDA to discuss the clinical trial design, ensure the collection of appropriate data, and streamline the drug development program.
As of March 13, the FDA had received 32 requests for Breakthrough Therapy designation, of which 9 have been granted and 10 denied; the remainder are pending review. The program is open to all types of drugs, not just anticancer agents. Vertex Pharmaceuticals announced in January that 2 of its drugs for cystic fibrosis earned the designation.
“Breakthrough Therapies allow us to take the most promising drugs—those that will have a transformative effect on the practice of oncology, the crème de la crème drugs—and task our review staff to move these applications quickly and have frequent interactions with the company,” explains Richard Pazdur, MD, director of the Office of Hematology and Oncology Products in the FDA's Center for Drug Evaluation and Research.
The new FDA program is the fourth to be introduced over the past 2 decades as part of the agency's commitment to make the drug approval process speedier and more fluid:
The Fast Track designation, reserved for drugs that treat serious diseases and fill an unmet medical need, includes more frequent meetings and correspondence with the FDA and rolling review of sections of its application for approval.
Accelerated Approval hastens approval of drugs for serious diseases that fill an unmet need through the use of surrogate endpoints in trials; later confirmatory trials must verify the anticipated clinical benefit.
Priority Review status may be granted to drugs that offer significant advances in treatment or provide a treatment for a condition for which no adequate therapy exists. The FDA aims to complete a Priority Review in 6 months rather than the standard review timeline of 10 months.
Breakthrough Therapy status conveys all the benefits of the Fast Track program and even more intensive FDA guidance.
The various designations are not mutually exclusive. For example, a drug can be declared a Breakthrough Therapy and receive Accelerated Approval and Priority Review.
Although the FDA will likely be more discriminating about which drugs receive the designation than it is with the Fast Track distinction, the specifics of the program aren't entirely clear yet, says Christopher-Paul Milne, DVM, MPH, JD, director of research at the Center for the Study of Drug Development at Tufts University in Boston, MA.
By law, the FDA must issue a draft “guidance document” before the end of 2013 to aid companies in preparing submissions and planning trials. The lack of such guidance now, however, isn't likely to deter many in industry from seeking the designation.
“It really shouldn't cost them much in the way of resources to apply,” notes Milne, adding that a Tufts survey completed several years ago found that the average time spent by companies preparing Fast Track materials was about 60 hours. Such an average isn't available yet for the new classification, but it's likely to be a relatively small investment of time—one that could get a drug to market months, or even years, sooner.
The designation may also boost a company's value. When the FDA takes that level of interest in a candidate drug, says Milne, “it certainly helps maintain investor interest.” –Suzanne Rose, with additional reporting by Megan Scudellari
What makes a “Breakthrough”?
According to the 2012 U.S. Food and Drug Administration (FDA) Safety and Innovation Act, a Breakthrough Therapy is a drug intended to “treat a serious or life-threatening disease or condition and preliminary clinical evidence indicates that the drug may demonstrate substantial improvement over existing therapies on one or more clinically significant endpoints, such as substantial treatment effects observed early in clinical development.”
However, the FDA has not yet issued guidance on what constitutes “substantial treatment effects” or the amount of data required for a drug to be considered a Breakthrough Therapy. Public data on 2 oncology drugs that have received the designation—LDK378 (Novartis) and ibrutinib (Janssen and Pharmacyclics) may offer some insight.
At last fall's European Society of Medical Oncology annual congress, researchers presented results of a phase I study of LDK378 in patients with ALK+ malignancies. Data showed an 80% response rate in patients with non–small cell lung cancer whose disease had progressed despite treatment with crizotinib (Xalkori; Pfizer). Novartis subsequently launched 2 phase II single-arm trials of LDK378: one in patients previously treated with chemotherapy and crizotinib and the other in patients with no previous exposure to the drug.
Ibrutinib was tested in a phase I trial of 56 patients with various relapsed or refractory B-cell lymphomas; 7 of 9 patients with mantle cell lymphoma and 3 of 4 patients with Waldenstrom macroglobulinemia responded to the drug. Data from a phase II trial of the drug in patients with mantle cell lymphoma were presented at the American Society of Hematology Annual Meeting in December 2012. Among the 110 patients who were evaluated for their response to treatment, 68% experienced a complete or partial response to the drug.
©2013 American Association for Cancer Research.
http://cancerdiscovery.aacrjournals.org/content/early/2013/03/28/2159-8290.CD-ND2013-008.abstract
We may know something before the ASCO abstracts are released on May 15th.
Since we know that Peregrine's clinical trials don't qualify for late-breaking status
the title(s) should show up here.
Late-April 2013: iPlanner launch
Plan your schedule online through the Annual Meeting website or a mobile application. Search for sessions, speakers, titles of Abstracts, or topics of interest and create a customized schedule to print or download onto your mobile device.
http://chicago2013.asco.org/meeting-program-timeline
Recent paper on PS receptors, PS and viruses in PLOS Pathogens, March 2013.
Open access:
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1003232
TIM-family Proteins Promote Infection of Multiple Enveloped Viruses through Virion-associated Phosphatidylserine
Stephanie Jemielity 1, Jinyize J. Wang 1, Ying Kai Chan 2, Asim A. Ahmed 1, Wenhui Li 3, Sheena Monahan 4,
Xia Bu 5, Michael Farzan 2¤, Gordon J. Freeman 5, Dale T. Umetsu 4, Rosemarie H. DeKruyff 4,
Hyeryun Choe 1¤*
1 Division of Respiratory Diseases Children’s Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America, 2 New England Primate Center,
Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, United States of America, 3 National Institute of Biological Sciences,
Beijing, China, 4 Division of Immunology, Children’s Hospital Boston, Harvard Medical School, Boston, Massachusetts, United States of America, 5 Department of Medical
Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts, United States of America
------------------------------------------------------------------------------------------
Some quotes from the paper:
[snip]
Several recent findings suggest that negatively-charged phospholipids
like PS might play a role in mediating virus entry. PS was
shown to be exposed on the membranes of various enveloped
viruses, including Pichinde virus, vesicular stomatitis virus (VSV)
and the intracellular mature virion form of Vaccinia virus [32,33].
This is likely a common feature of most enveloped viruses, as virusinfected
cells were shown to overexpress PS on their plasma
membranes [32–34]. In addition, the entry of lentiviral pseudoviruses
bearing the GPs of Sindbis (SINV), Ross River (RRV) and
Baculo virus was enhanced in a PS-dependent manner by the
TAM receptor tyrosine kinase Axl [35]. Axl has also been shown
to promote EBOV and MARV entry [11]. Finally, an antibody
targeting anionic phospholipids effectively rescued rodents from
lethal challenges by either Pichinde virus or mouse cytomegalovirus,
demonstrating in vivo contribution of anionic phospholipids
to the infectivity of these viruses [33].
[snip]
PS receptors form a complementary, widely expressed
network of receptors that is characterized by functional rather
than structural conservation. These particular features of PS
receptors likely contribute to their exploitation by viruses as
attachment factors. Notably, several PS receptors, including
TIM4, are highly expressed on mammalian macrophages and
dendritic cells. These cells play critical roles in the initial stages
of infection of filoviruses and flaviviruses in particular [55,56,65],
and PS receptors may thus play correspondingly important roles
in establishing these infections. PS receptors may be more
important still for viruses like DENV, WNV, EEEV and CHKV,
which are borne by insect vectors. The role of PS as apoptotic
marker is conserved in insects [66], and compared to mammalian
cells the membranes of insect cells are generally enriched
with PE [67,68], which binds several PS receptors. Thus
mosquito-delivered virions may especially benefit from PS
receptor-mediated enhancement of infection.
In conclusion, our results indicate that hTIM1, hTIM4, hAxl
and potentially other PS-binding receptors can enhance the entry
of a number of highly divergent viruses. As demonstrated for
hTIM1, the enhancement conferred by all of these receptors is
likely PS dependent and does not require any viral entry protein.
Accordingly, these proteins cannot properly be described as viral
receptors, although the nature of the viral entry protein clearly
impacts the relevance of PS receptors to infection. In some cases,
PS receptors may play critical roles in establishing or maintaining
an in vivo infection, which could affect disease severity. Thus our
results support the proposal of Soares et al., demonstrated for
Pichinde virus and mouse cytomegalovirus [33], that therapeutic
strategies targeting PS and other anionic phospholipids may be
broadly effective against a wide range of viruses.
-----------------------------------------------------------------------------------
Notes:
[33]. Soares MM, King SW, Thorpe PE (2008) Targeting inside-out phosphatidylserine
as a therapeutic strategy for viral diseases. Nat Med 14: 1357–1362.
Gordon Freeman gave a seminar at UTSW, hosted by Dr. Thorpe, at the end of February.
Abstract to be presented at the annual meeting of the American Association of Immunologists (AAI),
Sunday, May 5th in Honolulu. Hawaii.
http://www.immunology2013.org/index.html
CURRENT ABSTRACT TOPIC CATEGORY: Immunotherapy and Vaccines
TITLE: Combined targeting of exposed phosphatidylserine, CD47 and CD54 on
human pancreatic tumor cells in a mouse xenograft model of human pancreatic cancer
(P4455)
AUTHORS (FIRST NAME, LAST NAME): Shihong Ma 1, 2, Philip Thorpe 3, Ellen
S. Vitetta 2, 4, 5, Jeffrey Meyer 1
INSTITUTIONS (ALL): 1. Department of Radiation Oncology, UT Southwestern
Med. Ctr., Dallas, TX, United States.
2. Cancer Immunobiology Center, UT Southwestern Med. Ctr., Dallas, TX, United
States.
3. Department of Pharmacology, UT Southwestern Med. Ctr., Dallas, TX, United
States.
4. Department of Microbiology, UT Southwestern Med. Ctr., Dallas, TX, United
States.
5. Department of Immunology, UT Southwestern Med. Ctr., Dallas, TX, United
States.
ABSTRACT BODY: Phosphatidylserine (PS) is normally intracellular but becomes
exposed on the luminal surface of vascular endothelium in tumors and can also be
expressed on tumor cells themselves. Studies have shown that targeting PS with an
antibody enhances the antitumor effect of chemotherapy or radiation on several
tumors, and induces antitumor immunity in mice. Combination of this anti-vascular and
antitumor antibody with an antibody (anti-CD47) that blocks the “don’t eat me” signal
CD47 commonly expressed on human tumors may lead to synergistic antitumor
activity. Similarly, synergistic antitumor activity might be obtained by combining the
PS-targeting antibody with anti-CD54, an antibody that has been demonstrated to have
pan antitumor activity in xenograft models and is safe in humans. Our objective is to
evaluate combinations of these antibodies in a xenograft model of human cancer.
Studying these combinations requires determining the expression of CD47 and CD54
on several cancer cell lines. To this end, MDA-MB-231 (breast), NCI-H157 (lung),
Du145 (prostate), PANC-1 and BxPC-3 (pancreatic) were analyzed for surface
expression of CD47 and CD54. All five cell lines expressed CD47 (>87% of cells
positive). All tested cell lines were also highly CD54 positive (>84% of cells positive)
except for MDA-MB-231 (~50% positive). The effects of anti-PS antibody in
conjunction with anti-CD47 or anti-CD54 on tumor growth are currently being
analyzed in SCID mice bearing BxPC-3 pancreatic tumors.
Funding Support: Supported by the Horchow Foundation, the department of
Radiation Oncology and the Cancer Immunobiology Center, UT Southwestern Medical Center
CONTROL ID: 1641664
PRESENTATION TYPE: Oral and Poster
Academic medicine, and academic science, doesn't work that way. No one assigns a "lead" to a lab.
It is all about the grant money. Only faculty members can be principal investigators (PIs) and
apply for grants. The lab exists only because there is grant money to pay for the research and the
salaries of all the personnel. The university will skim 40-50% off the top to pay for overhead expenses.
Nobody "owns" the research. Any patent rights arising from the research will be shared between UTSW,
the inventors, and possibly the funding agency (NIH). I think the grants currently in place will keep paying
until they are exhausted. After that new grants will have to be obtained. That is why PIs spend so much
of their time writing grant proposals. In today's environment the rate of success is low. Someone
like Thorpe who had a long history of grants may have an advantage. Going forward, what was Thorpe's
lab will not exist because it was only "Thorpe's lab" because of the grants that Dr. Thorpe received.
Here is a list of the people in Thorpe's lab.
Dr. Huang will have to establish his own lab now. Everyone else will scatter. The grad student will
need a new faculty member as advisor, the postdocs will need to find another lab with grant money
available, the research associates and assistants will have to find another lab that has money
to pay them, etc. In short, this is the end of the Thorpe lab.
Thorpe Lab Members
Gustavo Barbero - Research Associate
Olivier Belzile, Ph.D. - Postdoctoral Researcher
Annie Best - Graduate Student
Xianming Huang, Ph.D. - Assistant Professor
Janie Iglehart - Research Assistant
Lisa Li - Research Associate
Shuzhen Li - Research Scientist
Kristi Lynn, Ph.D. - Postdoctoral Researcher
Stacey McCabe - Senior Administrator
Alan Schroit, Ph.D. - Adjunct Professor
Dan Ye, M.D. - Senior Research Associate
Yi Yin, M.D., Ph.D. - Instructor
However, that does not mean that the research will disappear. Dr. Thorpe published many, many
papers over the last 20 years. This area of research will survive, but it will be in other labs spread
around the world. Maybe someone at UTSW will carry forward with some of it, maybe not. It all depends
on whether or not they can get funding for the research. I know these things because I work in a
research lab in a university medical school. I never met Dr. Thorpe, but I had communicated with him
over the last 5 years. He had given me good feedback for ideas I had sent to him. He will be missed.
This has been a very sad time for me.
This is what it is all about.
http://well.blogs.nytimes.com/2013/03/28/using-former-smokers-to-spur-others-to-quit/
I read it a year ago. Just wondering why it was on Fox news now.
This is news from a year ago! Note in the link you have:
"The results of these experiments were published yesterday (March 26, 2012, submitted in Dec. 2011) in the Proceedings of the National Academy of Sciences, under the title: The CD47-signal regulatory protein alpha (SIRPa) interaction is a therapeutic target for human solid tumors (Willingham et al, 2012)"
I know for a fact that it is not Pfizer, but Celgene. Who are you going to believe, me or Sierra?
All opinions are for entertainment purposes only. Have a nice day.
I too am hoping that the survival results from the first-line NSCLC are very good. I just wanted to point out that
the ORR, and PFS results are not necessarily indicative of the survival results. As we have learned, the
MOA for bavi may lead to longer survival without a big change in the ORR or PFS, so those results from
the first-line trial may just be a consequence of small numbers of patients and not due to any tampering.
This is very interesting stuff. What they didn't mention in this article from Reuters is that all the patients required
bone marrow transplants after the T-cell therapy. Also, that one of the 5 patients was not eligible for a bone
marrow transplant and he was the one that died. It was mentioned in this article from the NY Times.
http://www.nytimes.com/2013/03/21/health/altered-t-cell-therapy-shows-promise-for-acute-leukemia.html?ref=research&_r=0
This is highly experimental stuff and is in no way going to show up as a general treatment for ALL in the near
future. It does show the power of the immune system.
Mojojojo, I am worried that it has now come to the point that any setback for Peregrine is considered
another potential case of sabotage. We all know that most biotech companies fail because their drugs fail.
Are we to believe that it is all due to sabotage? Yes, we do have evidence that Peregrine has been the
victim of foul play, but there is also a danger in becoming the "victim". When things fail in a clinical trial we are
reminded that we don't know everything, that in fact we know very little of what is actually happening with the
cancer and its response to the treatment. It is a time to learn from the failures so that our understanding of
the underlying reality may be increased. That said, where is the line to be drawn?
Any investor that invests in any biotech stock and thinks it is a "sure thing" is a fool. If they rely on
anonymous internet forums for their "research" into any biotech stock they are even a bigger fool.
I agree with you. Looking forward to the subgroup analysis at ASCO.
That is what I was thinking, they were probably having a hard time getting patients.
You know nothing. Mycobacterium tuberculosis is an intracellular bacterium. The bacteria invade macrophages
and survive in them for some time while they multiply. PS is expressed on the macrophages as it is on cells
that have been infected by a virus. This poster from 2011 shows that this also happens with
Francisella tularensis (tularemia) and Yersinia pestis (plague).
Outside chance that liver trial data could be presented here?
http://www2.kenes.com/liver-congress/Pages/Home.aspx
I mentioned this here:
http://investorshub.advfn.com/boards/read_msg.aspx?message_id=85707746