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paul, it's because I am a new editor. can you imagine?!
jrocket, you wrote you were surprised when whoever keeps the stock's price "lid" on allowed it to break above 1.10 a few weeks ago? Even wallstreet gnomes have to take a vacation (or w/c break) once in a while. welcome to the conspiracy theorist camp.
jrocket,nice. and yes,bought 5k mid-pm, that should scare all of you! have a good weekend
sumpin'positive for y'all.You'll LOVE the response, so read to the end. This is an email exchange today: a social acquaintence who, at a dessert and wine party function on Thursday evening, told me she had NSCLC.
2/18/2012 11:27:58 A.M. Pacific Standard Time,
Hi Madeline,
This is probably a bit premature because we need to wait to see what your blood work shows, but want you and [your oncologist]Dr. A..... to know about an anti-cancer agent in development which I have followed for several years, Bavituximab, manufactured by Peregrine Pharmaceutical. One of its clinical trials for "front-line" treatment of NSCLC has closed for patient enlistment, but there are Investigator Sponsored Trials ongoing which Dr.A.... could probably qualify to administer using Bavituximab in combination w. Pemetrexed and Carboplatin Chemotherapy. The Bavituximab (or any other experimental agent) may also be obtained for use (with other chemo- agents) under an FDA provision called "Compassionate use", a mechanism that allows patients to choose to use medications that are not fully FDA approved. There is a form to fill out on that, and if it seems appropriate, I'm sure Dr. A.... can/would help you with that too. I think the community is fortunate to have him.
All of this is an attempt to broaden your horizons to possibilities you and your doctors may not be considering...and there are others. As mentioned, though, this is one of my "pets". You can click on the web addresses below for more information. Best wishes, ....[ENTdoc]
http://www.peregrineinc.com/pipeline/bavituximab-oncology.html
http://clinicaltrials.gov/ct2/show/NCT00503347
Peregrine's Bavituximab Shows 50% Improvement in Overall Tumor ...
6 Dec 2011 ... "Across our bavituximab trials, the clinical data have been ... and best ORR was
determined at investigator sites using RECIST (Response ...
http://finance.yahoo.com/news/Peregrine-Bavituximab-Shows-iw-3497670049.html
This is a webcast from company president. Not sure you will be able to upload it:
http://www.veracast.com/bio/ceoinvestor2012/main/player.cfm?eventName=2024_peregr&appname=Microsoft Internet Explorer&os=Windows XP&wmversion=Yes - version 11.0.5721.5280&rmversion=Yes - no version info
Dear ....[ENTdoc],
I really appreciate receiving this information from you! Since we won't have the results on the Alk mutant gene test until next week, Dr. Anderson went ahead and has everything in place to start me on Chemo on Monday, Feb. 27. I went in yesterday to have a blood test, B-12 shot and talk with a nurse practitioner about Chemo. Actually, Dr. Anderson has prescribed the exact combination you have mentioned...using Bavituximab in combination with Pemetrexed and Carboplatin Chemotherapy. He also mentioned the possible use of Bavituximab as a maintenance drug after my six sessions of Chemo ends. So if the mutant gene tests negative, I'll begin Chemo on the 27th.
I'll let you know the mutant gene test results and Stanford's recommendations. I'll check out the information on the web sites you listed...thanks so much!!
Madeline
HeyCJ, monstrous ditto-thanks. Read and listened. The message was definitely low-key and "clean", with absolutely no hype. Wait for the post to follow.
freethemice, good work. thank you!
dear dog y dawg, here's my concept and I'm stickin' tooit:
The only way I've made money in this life is guessing right which way things are moving, and I think PPHM is moving the right direction...glacially. PPHM seems to me a natural "fiver" in a short while, but after the recent reverse one:five split that multiple looks anemic. Maybe it IS time to buy more because there's some evidence that "real" (as opposed to head fake) interest is picking up, and the "real" value of each stock is decreasing. I'm still here because of Thorpe's science; UTSWest,and all that implies; because the BOD is mostly attorneys; because the stock has not been artificially inflated and yoyo'd around in advance of real "beef" results; because PPHM science, instead if losing ground, is becoming more relevent, and because y'all are so charmin' and a whole lot of fun. My middlin' six figure losses in PPHM don't really count until my grandchildren sell.
jakedog, you made me laugh aloud. We should all take turns writing a letter we stockholders are undoubtedly going to receive from the chairman of the board. "We have decided that in the best interest of the stockholders...."
hey rrdog and until 2k, I've just always thought that PPHM was an R&D front for Roche. It makes every non-sequitur we've talked about here make sense, including a royal stockholder screving when the curtain comes down on this long-running charade. They've succeeded in beating us senseless until almost everyone here would go for a 5:1 "premium". I'm with until2k:I'll continue to follow the science.
north40k,freethemice, thanks. one(of several)phenoms that keep me hanging in here is just this phenomenon: a publication in 2012 on "new" science we have been submerged in for several years. an interesting phenomenon indeed considering the explosion of IT. Let's hope tech doesn't pass us by before IT catches up. regards!
djohn, good question. I read it about 5 times, and all I can tell is that it is definitely positive re Cotara-like drug used in malignant thyroid cancer metastatic to lungs.
RRdog, a well-reasoned post. Thanks, agree.
David,I share your concern about Cotara fate, but was reassured on this board that the "virtual" meeting with the FDA in December, which involved cloud computing, skype, and texting will soon result in another iteration of that product's course down the pipeline ...or something like that. With that reassurance (ne admonishment)I've tried to temporarily put Cotara out of mind. Hope this helps you. It didn't help me.
cloaked,good post.It's perfectly EMblematic/Euphemistic for PPHM and interest in stockholder value.Let's see how long it takes to do something about it...again.
geo: post73469:careful who you get into bed with: new years thoughts of Bavi+ Ribavirin trials:
-Ribavirin MOA (mechanism of action) is to reduce intracellular
synthesis and storage of guanine, a nucleotide “building
block” necessary for DNA and RNA synthesis.
-Ribavirin thus inhibits viral replication and body immune cell replication?
-Ribavirin interferes with reproduction of rapidly proliferating
cells. Also, cells with a high rate of protein turnover.
-Therefore ribavirin side effects include nausea and immunosuppression.
- Ribavirin alone (monotherapy) has little effect on HCV {hepatitis C virus}RNA levels, and is associated with a decline in serum ALT, suggesting that ribavirin may not be acting as an
antiviral agent, but rather as a modulator of immune
system function.
-Ribavirin monotherapy for HCV is ineffective, and the drug is only approved for use in combination with interferon.
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/Inf%20and%20Rib_08.pdf
The implications of this are mind-boggling.
you asked, "Isn't it also known that Bavi will work best if paired with another agent that increases the PS on bad cells (chemo, irradiation, etc)?
jonrocket,absolutely agree. if the stock price takes off like amgen, genentec, imclone, etc.etc. there might be forgetting and forgiveness, but if the company is sold for even what appears to a resonable person to be a reasonable multiple, we have all gotten _chewed, in spades. I've never seen anything like it, and hope I never do again.
freethemice, nice.thanks. question remains whether FDA is shifting toward CLINCAL significance (quality of life,etc) in addition to squeaking by with statistical significance.
hey jonnyrocket. I'll take that on. Usually I have a hard time getting past all the clinical and preclinical PPHM information above the board entries. Now I can't even find it to get those signal seeking results. Got a website address for a lazy guy? You asked, "the data that came in - is it stat sig when compared to SOC?" If it were possible to answer the question accurately, it would have been answered already. The study was labeled "signal seeking" precisely because it cannot be tagged statistically for a number of reasons. A full college level course in statistics would be necessary for a full understanding. My recollection of that data is that some was only statistically significant to 95% confidence level,meaning that in 5 similar trials out of 100 the positive findings would not be there. Is that good enough for you? Usually a higher standard than that is required. The data is analyzed to see at what confidence level it conforms to. Those results are then compared to SOC results in a similar way to see if the difference between the trial results and SOC is, in fact, a statistical difference at an acceptable "confidence level". That accomplished, strangely enough, a result that is positive and statistically significant, (i.e. 4 days of additional survival vs. 1 day = 4 times the survival length), considering risk, expense, and side-effects does not always translate into a real clinical benefit (quality of life, etc.). After being "steeped" in the statistical method for long enough, one can often "feel" with some degree of accuracy what the likely outcome will be...and that's where the gambling comes in here...as of today. And I would say (at about the .01 confidence level!) that the more courses in statistics you've had the better off you are in determining the eventual outcome here. This, and all previous posts, IMO only.
freethemice,don't you think when sumpin' is this big there are bound to be challenges to patent coverage? I am surprised it has come as a frontal attack on PS rather than a backdoor approach to another membrane phospholipid like PE (phosphatidylethanoleamine), etc. Duke probably thinks they see an opening, and decided to see if they could squeeze through it...
pphmtoolong, a guess: could be that Bavi loses some specificity for docking site when one arm is tied up with a payload. I cannot imagine that issue, if it is one, to be a long-term problem in subsequent constructs. There are some real pluses to "keeping it simple" with regard to safety studies. At this point, given Bavi safety, efficacy appears to be a virtual no-brainer with a payload. Then we don't need to try to beat a dead immune system into fighting a large solid cancer.
dia76ca, agree with your insightful post...while watching the very green Oregon Ducks struggle against Wisconsin boxcars and trucks. One huge problem is the need for a paradigm shift in cancer treatment, a need that has been present for decades, but a catch-22 we can't seem to extract ourselves from, and that is use of cytotoxic, immunosuppressive agents in the presence of immunocompromised patients, by definition. My post about Ribavirin was to point out some of the apparent futility of wanting positive results from immunostimulatroy agents like Bavituximab being used in combination with immunosuppressants. If Bavituximab stimulates what's left of the body's immune system to produce specialized scavenger cells, how that that synch with its use with a compound like Ribavirin that is known to inhibit new cell and specialized protein production? I know you were shuckin', but I don't look for Bavi to be packing Ribavirin OR intereron ANYwhere.
freethemice
Agreed.And thanks for all your "inside" scientific observations here throughout the years. observations from the point of vieIn these two preclinical breastConsistently on the mark. And how about the April 2010 report of tumor studies conducted at the University of Missouri-Columbia, where a bavituximab-equivalent antibody 2aG4 was used in combination with PRIMA-1, a small molecule investigational drug that targets abnormal p53, a protein present in half of all breast cancer cases--one that suppresses apoptosis, or normal cell death. Among its multiple anti-tumor effects, PRIMA-1 increases tumor cell apoptosis which in turn exposes PS, the target for Peregrine's antibodies.
Results of that study showed the combination therapy was more effective than either treatment alone at reducing the tumor growth rate and the incidence of lymph node metastasis in two different breast tumor models. In one model 30% of all tumors were completely eradicated following combination therapy, compared to none in the control group animals. As you said, IFN-gamma, antibody-IL-2, and even TTF-like small molecules are waiting to hitch a ride on fully humanized missile Bavituximab.
North4k, short answer,'yes'. It appears that one of PPHM's Bavituximab immunostimulatory MOAs during irradiation therapy is to excites production of specialized scavenger cells which helps eliminate the "logjam" around cancer cells being killed wholesale by irradiation. If a solid cancer is like a stadium full of bad guys, you can imagine the confusion when the gamma/alpha-ray gun start shooting and there are cancer bodies all over the field and bleachers. Bavi facilitates ingress and egress of ambulances to clear the dead cells and cell parts to help focus on remaining live cancerous cells.
Having said that, this "wire" idea is cool, but there are a couple non-sequiturs that limit practical application in most cases. In brief (and there are exceptions all over the place to what I'M going to say here). In general, if a cancer is surgically resectable, it is resected. What's left to put a wire into? If there are micro-metastases, they are usually either not visible, or too small for the naked eye to insert a wire into, or too many of them, etc. The concept is similar to Cotara's principle of hitting cancer from the inside out, and "the wire" could certainly have application in areas we can't get into (ie GBMs deep inside vital brain tissue)but can reach percutaneously. Yada. A big part of the engineering of "the cure" does relate to a safe, cost-effective, specific delivery system. Seems like we're moving right along with PPHM's anti-PS platform in that regard. Cheers!
puzzlinger&puzzlinger:
-Someplace along the way to market double-armed MAB missile Bavituximab, capable of carrying a cancercidal payload directly to tumor vasculature, is found to be mildly stimulating to the immune system when used unarmed, or "naked", against cancers and viruses.
-Bavi is then paired with Ribavirin to treat HCV, and Ribavirin is a drug which, if used alone, has little if any effect on HCV {hepatitis C virus}RNA levels; is associated with a decline in serum ALT; is probably an immunomodulator; might even be immunosuppressive; and can only be used for HCV paired with interferon.
some possible conclusions while trying to connect the dots...
anyone?
trial design?
FDA barriers to new drug entry?
who on earth paid for this trial?
benefits of pairing Bavi with immunosupprssant chemo agents?
maybe interferon + Bavi makes more sense.
using Bavi in end-stage disease when the immune system is spent rather than in early disease?
careful who you get into bed with: new years thoughts of Bavi+ Ribavirin trials:
-Ribavirin MOA (mechanism of action) is to reduce intracellular
synthesis and storage of guanine, a nucleotide “building
block” necessary for DNA and RNA synthesis.
-Ribavirin thus inhibits viral replication and body immune cell replication?
-Ribavirin interferes with reproduction of rapidly proliferating
cells. Also, cells with a high rate of protein turnover.
-Therefore ribavirin side effects include nausea and immunosuppression.
- Ribavirin alone (monotherapy) has little effect on HCV {hepatitis C virus}RNA levels, and is associated with a decline in serum ALT, suggesting that ribavirin may not be acting as an
antiviral agent, but rather as a modulator of immune
system function.
-Ribavirin monotherapy for HCV is ineffective, and the drug is only approved for use in combination with interferon.
http://www.hcvadvocate.org/hepatitis/factsheets_pdf/Inf%20and%20Rib_08.pdf
The implications of this are mind-boggling
hey gang, after reading today's posts I decided to send a special NewYears wish to all on this board who daily make it better in so many ways...from the relatively silent guidance of our hardworking moderators to (almost)all contributors. I started to give special recognition to mojo and freethemice for today's learned discussion of PGN632, and then djohn and cheynew on Proven and Phage, but then realized that virtually every contributor on my page of 40 posts deserves kudos...and a welcome back to jbeck. Another "marker" for the quality of the posts here is that lately I am reading almost every one! My sense of the patent application is consistent with my usual first paranoid response, and sense, at minimum, a probable double-cross and patent question which will put UTSW and Duke on a science-driven competition the likes of which we will be pleased to witness. Let's be very clear about anti-PS at this point...no matter what else. Duke and Barton Haynes joining the -PS pack, regardless of claim jumping,means there's "there" there. And Thorpe probably won't be too offended to share the Nobel with Haynes. Ariba!(AND Aruba).
sunstar, one-word explanation for a well-known phenomenon: "stoichiometry". It has plenty of precedence in the world of chemistry.
FreeNorth,excellent question, post#73319)in which you asked, "Since the exposure of phosphatidylserine (-PS) on a cell's surface flags it as apoptotic to the immune system and needing removal, what additional benefit does Bavituximab add to the removal of the cell?"
I think the key concept is the use of the term "flags it". Actually, the opposite. Apoptosis and inverted -PS is a normal process that is all but ignored by the body, and those dying cells are left for the usual "weekly garbage collectors" rather than specialized detox cells. It is thought that the production of cancer cells also allows these early cell clones to fly below the radar of the specialized 'self-non-self' hazmat crew that brings in cytokines, and full-blown allergic/inflammatory response to invasion.
Anti-PS agents such as Bavituximab grab onto all flipped -PS, whether from normal apoptotic cells or cancerous cells, and especially on the specialized endothelial cells of blood vessels nourishing cancers.
What we found on the way to the bank (!!apropos of today's discussions!!) is that somehow Bavi excites the rapid inggress of the hazmat crowd of dendritic cells, etc. to the region, and thus acts as a non-specific immunological stimulus at tumor sites. This is, perforce, a relatively weak, but apparently measureable effect, and that is what is being measured now in clinical trials. We know that similar non-specific immunological enhancers have relatively weak effect, but if it is measureable, repeatable, and free of side-effects...why not use it? We have only begun to scratch the surface of this vast new technology, and are privileged to be on the forefront of a true phenomenon with vast potential for good. The key is that time and again the platform (anti-PS MAB) is being shown to be relatively safe. Imagine what the warhead can be armed with. This website might help for basic definitions: http://www.caring4cancer.com/go/cancer/treatment/other
I posted the following 6 month-old (non-Thorpian) article a couple days ago, and it is absolutely fascinating in its implications for stem cells and for genetically engineered molecules:
"This study was performed...to identify potential targets for the development of novel therapy to treat cancer with poor outcome or treatment efficacy. We show that the negatively charged phospholipid phosphatidylserine (PS) is exposed in the outer leaflet of the plasma membrane not only in tumor cell lines, but also in metastases and primary cultures thereof, which contrasts with a lack of PS exposure by differentiated non-tumorigenic counterparts. Studied tumor cell lines were derived from non-tumorigenic and malignant melanomas, prostate- and renal cancer, glioblastoma and a rhabdomyosarcoma. Importantly, also metastases of melanoma expose PS and [!]there is a correlation between malignancy of melanoma cell lines from different stages of tumor progression and PS exposure[!]. The PS exposure we found was neither of apoptotic nor of experimental artificial origin. Finally potentially [!]malignant and non-malignant cells could be differentiated by sorting of a primary cell culture derived from a glioblastoma based on PS exposure[!], which has so far not been possible within one culture due to lack of a specific marker. Our data provide clear evidence that PS could serve as uniform marker of tumor cells and metastases as well as a target for novel therapeutic approaches based on e.g. PS-specific host defense derived peptides. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175029/
http://cancerres.aacrjournals.org/content/early/2011/03/16/0008-5472.CAN-10-3894.abstract
corporal,you said, "We will know if the HCV program has life if somebody pays something for it". I'll add...or if company announces follow-on study plans...or if the company continues to monitor the patients even outside the study time-frame parameters. That is low-risk and low-cost. Not a lot anyone can do to fudge certified hematology lab results.
north40k, a reasonable analysis. I too followed MDX-010 from the early days and agree. Further, PPHM's Bavituximab has at least the same potential, and probably much greater potential than MDX-010. The overarching considerations to keep sight of here are:
-safety...first. the record in lower animals and now in humans appears to be quite good.
-specificity: excellent. PPHM has a lock on a newly described docking site present on the vasculature of virtually all solid cancers, and on the cell surface of many. The docking site is "flipped" cell membrane aminophospholipids
-exclusivity: PPHM has the recipe; it has the FDA-approved lab to manufacture the monoclonal antibody.
-All the evidence to date shows a significant synergy of Bavituximab with irradiation therapy for cancer. No trials have begun.
-All the evidence to date shows at least some immunomodulatory effects of Bavituximab in host vs. cancer.
-Bavituximab is capable of carrying cancercidal small molecules directly to cancer
-Bavituximab's fully humanized iteration is on the near-horizon.
The future of the entire platform, IMO, remains stellar. The question is, how long will it take before a reasonable infusion of cash is brought to the program to move it forward with appropriate speed.
sunstar...anyone...is it possible to petition for lengthening of this trial? At this point tend to agree with JRocket succinct analysis (post 73190). All becoming interestinger and interestinger, but without numbers all remains hopeful fiction, not science. Fascinating looking at all the holes this month and none of the data. That said, I haven't seen anything that makes me want to divest. Au contraire.
Thanks for your patience with me on this guys. I just want to know who sent the ambulance and white coats to my home tonight!
thanks cj, I think I need a vacation: "we have opened a dialogue with the FDA to determine the critical elements of our pivotal trial protocol"...OMG!
rrdog, I've admired your style of expressing an unique, over-arching viewpoint, but am having difficulty unjangling what you just wrote, that"...PPHM telegraphed a meeting in the fourth quarter with the FDA which morphed into a virtual meeting with written iterations." The points of departure are, specifically, "telegraphed", "morphed", "virtual meeting", and "written iterations". I won't parse each of those terms. I'll simply say that I find them, uh, disturbing? You wrote,"PPHM did not promise hard information beyond that." True. There have been, and remain, no promises. "... or an FDA decision." True again> Nobody has anticipated an FDA decision. We have been told specifically that there would be a meeting by this time. I'd like to know why...if...it has happened. Iteration, morph, virtual, or telegraphed. Period.
rr & lurker: here's hoping such a big and generous set of suppositions are correct. The least management could do is unequivocably clarify where we are with Cotara at this point. I remain stuck with the idea that we were going to get some information this month... more than that a dialog continues...and I had read all the info. lurker thoughfuly posted.
RRreally? you wrote,"I like that at present I hear no Cotara discussion about any other subject than the shape of Phase III..."
What happened to the December FDA meeting? Everyone here believe no news=good news? Again?Always? Ridiculous. Gawd.
cj,nicefind. Any ideas re.Dec2011 Cotara/FDA update? Thanx.eom
Cloaked:the following is a bit of my own due diligence on the subject this morning for about 30 minutes. Hope it helps
Adv Cancer Res. 2011;111:39-96.
The essential role of evasion from cell death in cancer.
Kelly GL, Strasser A.
SourceThe Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia.
Abstract
The link between evasion of apoptosis and the development of cellular hyperplasia and ultimately cancer is implicitly clear if one considers how many cells are produced each day and, hence, how many cells must die to make room for the new ones (reviewed in Raff, 1996). Furthermore, cells are frequently experiencing noxious stimuli that can cause lesions in their DNA and faults in DNA replication can occur during cellular proliferation. Such DNA damage needs to be repaired efficiently or cells with irreparable damage must be killed to prevent subsequent division of aberrant cells that may fuel tumorigenesis (reviewed in Weinberg, 2007). The detection of genetic lesions in human cancers that activate prosurvival genes or disable proapoptotic genes have provided the first evidence that defects in programmed cell death can cause cancer (Tagawa et al., 2005; Tsujimoto et al., 1984; Vaux, Cory, and Adams, 1988) and this concept was proven by studies with genetically modified mice (Egle et al., 2004b; Strasser et al., 1990a). It is therefore now widely accepted that evasion of apoptosis is a requirement for both neoplastic transformation and sustained growth of cancer cells (reviewed in Cory and Adams, 2002; Hanahan and Weinberg, 2000; Weinberg, 2007). Importantly, apoptosis is also a major contributor to anticancer therapy-induced killing of tumor cells (reviewed in Cory and Adams, 2002; Cragg et al., 2009). Consequently, a detailed understanding of apoptotic cell death will help to better comprehend the complexities of tumorigenesis and should assist with the development of improved targeted therapies for cancer based on the direct activation of the apoptotic machinery (reviewed in Lessene, Czabotar, and Colman, 2008).
Copyright © 2011 Elsevier Inc. All rights reserved.
Biochim Biophys Acta. 2011 November; 1808(11-15): 2638–2645.
doi: 10.1016/j.bbamem.2011.07.026 PMCID: PMC3175029
Copyright © 2011 Elsevier B.V.
In search of a novel target — Phosphatidylserine exposed by non-apoptotic tumor cells and metastases of malignancies with poor treatment efficacy
Sabrina Riedl,a1 Beate Rinner,b1 Martin Asslaber,c Helmut Schaider,be Sonja Walzer,d2 Alexandra Novak,b Karl Lohner,a and Dagmar Zweyticka
aInstitute of Biophysics and Nanosystems Research, Austrian Academy of Sciences, Schmiedlstraße 6, A-8042 Graz, Austria
Received April 1, 2011; Revised July 19, 2011; Accepted July 19, 2011.
This document may be redistributed and reused, subject to certain conditions.
This document was posted here by permission of the publisher. At the time of the deposit, it included all changes made during peer review, copy editing, and publishing. The U. S. National Library of Medicine is responsible for all links within the document and for incorporating any publisher-supplied amendments or retractions issued subsequently. study was performed in the aim to identify potential targets for the development of novel therapy to treat cancer with poor outcome or treatment efficacy. We show that the negatively charged phospholipid phosphatidylserine (PS) is exposed in the outer leaflet of their plasma membrane not only in tumor cell lines, but also in metastases and primary cultures thereof, which contrasts with a lack of PS exposure by differentiated non-tumorigenic counterparts. Studied tumor cell lines were derived from non-tumorigenic and malignant melanomas, prostate- and renal cancer, glioblastoma and a rhabdomyosarcoma. Importantly, also metastases of melanoma expose PS and there is a correlation between malignancy of melanoma cell lines from different stages of tumor progression and PS exposure. The PS exposure we found was neither of apoptotic nor of experimental artificial origin. Finally potentially malignant and non-malignant cells could be differentiated by sorting of a primary cell culture derived from a glioblastoma based on PS exposure, which has so far not been possible within one culture due to lack of a specific marker. Our data provide clear evidence that PS could serve as uniform marker of tumor cells and metastases as well as a target for novel therapeutic approaches based on e.g. PS-specific host defense derived peptides.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3175029/
Annu Rev Physiol. 2003;65:701-34. Epub 2002 May 1.
Aminophospholipid asymmetry: A matter of life and death.
Balasubramanian K, Schroit AJ.
Cancer Res. 1991 Jun 1;51(11):3062-6.
Elevated expression of phosphatidylserine in the outer membrane leaflet of human tumor cells and recognition by activated human blood monocytes.
Utsugi T, Schroit AJ, Connor J, Bucana CD, Fidler IJ.
Anatomic Pathology / Annexin-V in Ovarian Carcinoma
CME/SAM
Evaluation of Cell Surface Expression of
Phosphatidylserine in Ovarian Carcinoma Effusions
Using the Annexin-V/7-AAD Assay
Clinical Relevance and Comparison With Other Apoptosis
Parameters
Hiep Phuc Dong, MSc,1 Arild Holth, BSc,1 Lilach Kleinberg, PhD,1 Marit Gunhild Ruud, BSc,1
Mari Bunkholt Elstrand, MD,2 Claes G. Tropé, MD, PhD,2,3 Ben Davidson, MD, PhD,1,3
and Björn Risberg, MD, PhD1,4
http://ajcp.ascpjournals.org/content/132/5/756.full.pdf
Threes,me lad,enlighten me re. what am I missing of "advances of Contara-in-China". I've been awaiting positive news with profound chest retractions.
thanks threes,you said,"as China-TNT becomes a greater success while our TNT technology fights for a market.." Did I miss sumpin' good out of China re TNT?