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The CREATE Pharmacogenetic Research Network
http://pharmacogenetics.wustl.edu/
Most pharmacogenetic strategies to date have focused on the role of single genes in the regulation of drug activity and have made important steps towards the goal of optimizing therapy for individual patients. However, there is clear evidence that medications, like most common diseases, are under the control of a network of genes, each contributing to the patient’s phenotype. The CREATE Pharmacogenetic Research Network (Comprehensive Research on Expressed Alleles in the Therapeutic Evaluation) will bring together infrastructure for the evaluation of pathways regulating drug activity. This will be achieved through the coordinated efforts of investigators from Washington University and University of California-San Francisco with expertise in the fields of Genomics, Pharmacogenetics, Clinical Pharmacology, Bioinformatics/Computational Biology, Molecular Genetics, Statistical Genetics, Population Genetics, Clinical Trials, and Translational Research. Together they are developing validation strategies for applied pharmacogenetics.
http://pharmacogenetics.wustl.edu/im/pgweb.nsf/0ee53e934810efcd86256a94005e5f7d/55b97591ff4c3a3a8625....
There are eight investigators from Washington University listed: Howard McLeod, C. Charles Gu, Mike Province, William Shannon, Gary Stormo, Mark Watson, Barbara Zehnbauer, and Alan Templeton. Now of course there is no direct connection between DNAP and any of these academics. Here’s the thing:
Province MA, Rice TK, Borecki IB, Gu C, Kraja A, Rao DC. Multivariate and multilocus variance components method, based on structural relationships to assess quantitative trait linkage via SEGPATH. Genet Epidemiol. 2003 Feb;24(2):128-38.
Gu CC, Rao DC, Stormo G, Hicks C, Province MA. Role of gene expression microarray analysis in finding complex disease genes. Genet Epidemiol. 2002 Jun;23(1):37-56.
Shannon WD, Province MA, Rao DC. Tree-based recursive partitioning methods for subdividing sibpairs into relatively more homogeneous subgroups. Genet Epidemiol. 2001 Apr;20(3):293-306.
As for Templeton:
Templeton AR, Weiss KM, Nickerson DA, Boerwinkle E, Sing CF. Cladistic structure within the human Lipoprotein lipase gene and its implications for phenotypic association studies. Genetics. 2000 Nov;156(3):1259-75.
Templeton AR, Clark AG, Weiss KM, Nickerson DA, Boerwinkle E, Sing CF. Recombinational and mutational hotspots within the human lipoprotein lipase gene. Am J Hum Genet. 2000 Jan;66(1):69-83.
BTW, here’s the latest paper by McLeod:
Marsh S, McLeod HL. Cancer pharmacogenetics. Br J Cancer. 2004 Jan 12;90(1):8-11.
Department of Medicine, Washington University School of Medicine, 660 South Euclid Ave, Campus Box 8069, the Siteman Cancer Center, and the CREATE Pharmacogenetic Research Network, St Louis, MO 63110-1093, USA.
The large number of active combination chemotherapy regimens for most cancers has led to the need for better information to guide the 'standard' treatment for each patient. In an attempt to individualise therapy, pharmacogenetics and pharmacogenomics (a polygenic approach to pharmacogenetic studies) encompass the search for answers to the hereditary basis for interindividual differences in drug response. This review will focus on the results of studies assessing the effects of polymorphisms in drug-metabolising enzymes and drug targets on the toxicity and response to commonly used chemotherapy drugs. In addition, the need for polygenic pharmacogenomic strategies to identify patients at risk for adverse drug reactions will be highlighted. British Journal of Cancer (2004) 90, 8-11. doi:10.1038/sj.bjc.6601487 www.bjcancer.com
Not sure what “studies assessing the effects of polymorphisms in drug-metabolising enzymes and drug targets on the toxicity and response to commonly used chemotherapy drugs” the paper concerns itself with.
A good example of how far ahead of the game DNAP is:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14672516&...
Am J Pharmacogenomics. 2003;3(6):361-70.
Pharmacogenomics and "Individualized Drug Therapy": high expectations and disappointing achievements.
Nebert DW, Jorge-Nebert L, Vesell ES.
Department of Environmental Health and Center for Environmental Genetics (CEG), University of Cincinnati Medical Center, Cincinnati, Ohio, USA.
Since 1965 there have been more than 800 pharmacogenetics/genomics reviews - most suggesting that we are on the verge of offering individualized drug therapy to everyone. However, there are numerous reasons why this approach will be extremely difficult to achieve in the foreseeable future. Drug treatment outcome represents a complex phenotype, encoded by dozens, if not hundreds, of genes, and affected by many environmental factors; therefore, we will almost always see a gradient of response. Phenotyping assays of blood enzyme activities (if feasible) are generally more successful than DNA genotyping for predicting unequivocal outcomes of drug therapy in each and every patient. Phenotyping with probe drugs has generally not succeeded, because of the overlapping substrate specificities not only of drug-metabolizing enzymes but also transporters, receptors, ion channels, transcription factors, and other drug targets; drug-drug interactions, enzyme induction and inhibition, and multiple (enzyme, transporter, second-messenger, signal transduction) pathways also present enormous problems. Genotyping to predict drug disposition, efficacy, toxicity, and clinical outcome has been proposed, but the success of genotyping in individualized drug therapy currently appears unlikely because of the many shortcomings (frequency of DNA variant sites, ethnic differences, admixture) and complexities (plasticity of the genome, multiple mechanisms for determining sizes and locations of haplotype blocks) of this approach.Genomics is an important tool in basic research; yet, it is unrealistic to include genotyping within the realm of tests available to the practicing clinician in the foreseeable future. The same can be said for transcriptomics and proteomics, which also rely on available sources (tumors, biopsies, excreta). The newly emerging fields of metabonomics and phenomics might offer solutions to anticipating and decreasing individual risk for adverse drug reactions in each individual patient; however, tests based on these approaches are not expected to become available to the practicing clinician for at least the next 5-10 years.
Genetics article
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14704187&...
Genetics. 2003 Dec;165(4):2071-83.
Sequences associated with human iris pigmentation.
Frudakis T, Thomas M, Gaskin Z, Venkateswarlu K, Chandra KS, Ginjupalli S, Gunturi S, Natrajan S, Ponnuswamy VK, Ponnuswamy KN.
DNAPrint Genomics, Sarasota, Florida 34236.
To determine whether and how common polymorphisms are associated with natural distributions of iris colors, we surveyed 851 individuals of mainly European descent at 335 SNP loci in 13 pigmentation genes and 419 other SNPs distributed throughout the genome and known or thought to be informative for certain elements of population structure. We identified numerous SNPs, haplotypes, and diplotypes (diploid pairs of haplotypes) within the OCA2, MYO5A, TYRP1, AIM, DCT, and TYR genes and the CYP1A2-15q22-ter, CYP1B1-2p21, CYP2C8-10q23, CYP2C9-10q24, and MAOA-Xp11.4 regions as significantly associated with iris colors. Half of the associated SNPs were located on chromosome 15, which corresponds with results that others have previously obtained from linkage analysis. We identified 5 additional genes (ASIP, MC1R, POMC, and SILV) and one additional region (GSTT2-22q11.23) with haplotype and/or diplotypes, but not individual SNP alleles associated with iris colors. For most of the genes, multilocus gene-wise genotype sequences were more strongly associated with iris colors than were haplotypes or SNP alleles. Diplotypes for these genes explain 15% of iris color variation. Apart from representing the first comprehensive candidate gene study for variable iris pigmentation and constituting a first step toward developing a classification model for the inference of iris color from DNA, our results suggest that cryptic population structure might serve as a leverage tool for complex trait gene mapping if genomes are screened with the appropriate ancestry informative markers.
Now, before anybody tries to spin the 15% figure quoted above, don't forget that the work described in this article represents about 20% of that which had been undertaken and which is necessary to correctly infer iris color. Here is the relevant quote:
http://www.dnaprint.com/2003/pressreleases/pr_11_20_03.htm
During the presentation, DNAPrint(TM) also announced that some of the early work on human iris color has been accepted for publication in the peer- reviewed journal "Genetics". The paper "Sequences Associated with Human Iris Pigmentation" will appear in the upcoming December issue, and represents the first systematic post-genome era study of human iris color to have yet been published. DNAPrint(TM) was one of the first to identify more markers and prior to this work, few markers for human iris color were known, and it had not been possible to predict iris color from DNA (nor any other anthropometric trait) with good sensitivity and/or specificity. Several of the markers described in this paper are necessary (but not sufficient) to infer iris color from DNA; the paper represents about 1/5th of the research conducted by DNAPrint(TM) in this area.
OT: Fascinating story behind this as well. The Eunuch Admiral in question (not sure I'd have been queuing up for the role of Admiral) eventually got taken out by the mother of all Tsunamis.
Ineverunderstoodasinglewordhesaid
One for you Sarasota residents (or visitors)
http://www.sarasotanewsandbooks.com/January%20events.htm
Thursday, January 8
GAVIN MENZIES, 1421: The Year Columbus Discovered America, William Morrow, a division of Harper Collins
Lecture, Discussion and book signing. 7:00 PM. First United Methodist Church, 104 S. Pineapple Ave.
The incredible true story of the New World discovery before Columbus was even born. Gavin Menzies’ extraordinary story of Chinese exploration begins in 1421 when four huge fleets set sail from the country’s new capital, Beijing. The ships, 450 foot long junks made from the finest teak, were led by the Emperor’s loyal Eunuch admirals, first among whom was the ‘Admiral of the Western Sea’ Zheng He. Their mission was to discover and unite the whole world in the benefits of Confucian harmony – or, put another way, to bring the whole world into the Chinese trade system. Their journeys would last over two years and circle the entire globe encountering many previous unknown territories.Following Gavin Menzies’s lecture at the Royal Geographical Society in London in March 2002, a flood of new information from all over the world has been investigated and is included in the American edition.
But more importantly, Sarasota based DNAPrint Genomics headed by Dr. Tony Frudakis, has been hired to corroborate Menzies' controversial theories using advanced DNA technology. Dr. Frudakis will appear with Mr. Menzies in a lively and provocative discussion.
The January Popular Science article for those that haven't read it:
http://www.popsci.com/popsci/medicine/article/0,12543,567794-1,00.html
The connection?
http://www.a-imbn.org/organizational_structure.htm
Program Committee includes "Koh Chong-Lek, Prof. & Coordinator of Genetics & Molecular Biology, Institute of Biological Sciences, University of Malaya, Malaysia"
Dr. Gurinder Shahi
Executive Director/Coordinator
Asia-Pacific IMBN Secretariat
Tel: +65-774 9462
E-mail: gurinder.shahi@a-imbn.org
This is the project in a bit more detail:
http://www.nbbnet.gov.my/research%20project/exe%20summary/DrKoh.htm
Dr Koh Chong Lek is the main researcher:
http://www.um.edu.my/FS/StaffDetail.asp?SCode=200
BIOVALLEY UKM Genomics Laboratory is the interim laboratory of the National Institute for Genomics and Molecular Biology. One of it's approved projects is "Analysis of the Human Genomic Diversity in the Malaysian Population for Potential Medical and Forensic Application" which is described here:
http://202.185.32.213/genomicslab/content/approve_project.php
Human Genome Diversity: Analysis of the Human Genomic Diversity in the Malaysian Population for Potential Medical and Forensic Application
Malaysia is blessed with a multiracial population that offers diversity at the human genomes, both nuclear and mitochondrial. These diverse genomes have been under investigation since 1993 with the view of establishing the genotype and allele frequencies at a number of highly variable loci, in order to use them to identify individuals in forensic investigations and parentage testing. To extend the expertise and to improve capability and capacity in genome-scale analysis of the diverse human genomes of ethnic and indigenous groups in Malaysia, this project aims to investigate human genomic variations of medical and evolutionary importance using standard and advanced technologies for disease and forensic applications. Data obtained from the study will contribute to the understanding of SNPs involvement in diseases and their application in forensic science.
Straits Times article
http://straitstimes.asia1.com.sg/commentary/story/0,4386,227176,00.html
Take the guesswork out of prescriptions
By Andy Ho
MY DAUGHTER recently developed a chest infection with wheezing. She was put on an antibiotic and an anti-asthma drug respectively for each problem. Later, her doctor substituted the former with another antibiotic, and threw in a steroid for good measure. She's okay now.
You probably also know someone who is going through different medications for hypertension, or a relative with cancer who's had to change her chemotherapy regimen, and so on.
Unquestionably, there is money to be made if you can develop a test that tells me beforehand whether a drug will work for me.
After all, most of us know from experience that prescribed drugs often fail to work. Still, it was a bombshell dropped when a top executive of Europe's largest pharmaceutical maker admitted as much recently.
Dr Allen Roses, senior vice-president of genetic research at GlaxoSmithKline (GSK), said at a recent scientific meeting in London that 'the vast majority of drugs - more than 90 per cent - only work in 30 to 50 per cent of the people'.
Citing figures, Dr Roses, a geneticist by training, said that drugs for Alzheimer's disease worked in only one out of three patients. The record for cancer drugs was even worse, working in only one in four patients, while drugs for migraine, osteoporosis and arthritis did slightly better, being effective half the time.
So when a doctor writes out a prescription, he is typically just trying to see which cocktail will work in a particular case.
That sounds like a lot of guesswork, but rest assured that no malice was intended by Dr Roses - or your doctor when he prescribes for you.
GSK later released a statement decrying the way the British press had misrepresented Dr Roses, whose point was really that drugs on the market do work for about half of us. The rest are usually people who carry genes that interfere with medicine in some way.
The solution is obvious: have tests that can identify people with genetic profiles that enable them to respond to and benefit from a particular drug.
This is the new field of pharmacogenomics, of which Dr Roses is a recognised leader. It tries to target drugs to a smaller number of patients with specific genetic inheritances. The holy grail is personalised medicine - whereby prescriptions are tailored to one's unique genetic make-up.
What's new about it?
Until now, researchers have generally focused on trying to identify which genes cause what disease - with not much success especially in terms of developing therapies.
For example, Singapore's Institute of Molecular and Cell Biology reported this week that it had identified a gene called 'u-boot' that determines how muscle cells develop in an embryo.
This discovery may well provide insights into how inherited muscle diseases arise. Yet a huge leap remains from that to a safe, effective form of therapy on the market.
The new approach, instead, is to sequence genomes to find, not genes, but much tinier genetic variations in individuals called 'snips' or single nucleotide polymorphisms.
Suffice to say that each individual has a unique set of 'snips' called a haplotype, which he inherits from his father and mother. Some haplotypes 'red flag' susceptibility to a disease or likelihood of responding well or adversely to a specific drug.
For example, a United States-based biotech firm called Genaissance has already compiled a database of 5,000 haplotypes and linked some of them to how well patients respond to cholesterol-lowering drugs called statins.
With such data in hand, various drugs can be quickly and safely tested in people who are likely to respond to them.
All good for new drug discovery, but can such knowledge be translated soon into something useful to patients in the clinic?
Yes, if we develop enough of these genetic tests to eliminate people who won't respond to specific drugs.
And those tests are already on their way to the market.
This week, Swiss-based drug firm Roche announced an impending genetic test that is 85 per cent accurate in predicting whether various asthma and hypertension drugs will work for an individual. Conversely, GSK had announced last year a genetic test that identifies those patients likely to develop a serious allergy to its HIV drug called abacavir.
Personalising prescriptions with the help of such tests would make treatment safer and more effective, thus encouraging patients to take their drugs more faithfully. The net effect would be an increased availability of effective drugs for a finely segmented market.
You would think that would be good news for the pharmaceutical industry.
Not quite for every drug maker, it seems.
The drug industry has always employed armies of salesmen to sell as many drugs as possible to as many patients as they can get through their doctors. Like it or not, this mass marketing approach has made drug firms among the most profitable companies around - even if their drugs are useless half the time.
If new tests make doctors change their prescribing habits, they could erode the market share for certain drugs, especially those with more limited effectiveness rates.
But whether the big drug firms like it or not, personalised medicine is on the horizon. If they are reluctant to invest in developing genetic tests to enable the new medicine, it can only mean a market opportunity for others who will.
To invert an old adage, one man's poison is another man's meat. So here is one New Year resolution for Singapore's life-science effort: Focus on this emergent market niche and start developing simple, inexpensive but precise genetic tests that will enable personalised prescriptions.
stakddek, I thought that as well the first time I saw the selected populations. This is the answer:
http://www.hapmap.org/abouthapmap.html.en
Most of the common haplotypes occur in all human populations; however, their frequencies differ among populations. Therefore, data from several populations are needed to choose tag SNPs. Pilot studies have found sufficient differences in haplotype frequencies among population samples from Nigeria (Yoruba), Japan, China and the U.S. (residents with ancestry from Northern and Western Europe, collected in 1980 by the Centre d'Etude du Polymorphisme Humain (CEPH) and used for other human genetic maps) to warrant developing the HapMap with large-scale analysis of haplotypes in these populations. The HapMap developed with information from these populations should be useful for all populations in the world. However, to assess how much more information would be gained by including other populations, a parallel study will examine haplotypes in a set of chromosome regions in samples from several additional populations.
The DNA samples for the HapMap will come from a total of 270 people: from the Yoruba people in Ibadan, Nigeria (30 both-parent-and-adult-child trios), Japanese in Tokyo (45 unrelated individuals), Han Chinese in Beijing (45 unrelated individuals), and the CEPH (30 trios). These numbers of samples will allow the Project to find almost all haplotypes with frequencies of 5% or higher. All of the new samples collected for the Project are being obtained with protocols approved by the appropriate ethics committees, after culturally appropriate processes of community engagement or public consultation and individual informed consent. The community engagement process is designed to identify and attempt to respond to culturally specific concerns and give the participating communities direct into the informed consent and sample collection processes.
GE, best wishes to your son and family.
A perfect illustration of the futility of trying to engage some of you, and how some try to make mischief when the intent here was to help an investor with a serious question to the extent that I am able. There has been no attempt to improperly influence investor opinion on anybody's part. However, it is clear that the posting of any information is going to be increasingly problematical, so perhaps the best course is not to post in these forums at all.
Frog, can I refer you back to the first post I made on this subject (and my previous statements about confidentiality).
OK, have a look at this quote from the following post that is public domain:
http://ragingbull.lycos.com/mboard/boards.cgi?board=DNAP&read=274308
"Frudaky did the Orchid deal which is undoubtedly going to blossom into something beautiful. You simply do not have the facts yet. By the way, BECKMAN NOW OWNS THIS OPTION .... Beckman is a good friend to DNAPrint. You connect the lines and wait for the PRs."
I would like to respond to your question but am not able to, sorry.
66fan, that is interesting. Incidentally, SLE is one of the diseases that Shriver and company are interested in:
Molokhia M, Hoggart C, Patrick AL, Shriver M, Parra E, Ye J, Silman AJ, McKeigue PM. Relation of risk of systemic lupus erythematosus to west African admixture in a Caribbean population. Hum Genet. 2003 Mar;112(3):310-8.
Article about Mark Shriver
http://magazines.ivillage.com/goodhousekeeping/hb/news/article/0,,ajc_2003_12_14_NS_36047067-0005-Ho....
Raising Flags on Health Risks
December 14, 2003
BILL HENDRICK, Staff
The Atlanta Journal-Constitution
DNA tests might one day provide physicians clues about our genetic predisposition to a slew of health conditions such as obesity, high blood pressure, diabetes and osteoporosis, according to an international team of researchers headed by Mark Shriver, a molecular anthropology professor at Penn State University.
Shriver helped develop a test that looks at dozens of specific markers in DNA molecules that shed light on peoples' ancestries. He says certain ethnic groups are more likely than others to contract often deadly diseases. Most people identify with one race or another, but in reality, all human populations are practically identical, genetically speaking.
It's well-known that women of European ancestry have a higher rate of osteoporosis than African-American women, who have a higher prevalence of obesity. But obesity in African-American women doesn't seem to be as dangerous to them as it is for European-American women. Research is also clear that:
> African-American women are three times as likely to die of heart disease as white counterparts.
> African-Americans are more likely to have asthma and prostate cancer.
> Jewish women of European origin are more likely to develop breast cancer than non-Jewish females from the same areas.
> Among Mennonites in Lancaster County, Pa., a tightly knit group, 1 in 400 is born with a rare metabolic disease --- but the risk in the general population is 1 in 200,000.
Copyright 2003 The Atlanta Journal-Constitution
The article is also here on the AJC site, together with two other articles that have been posted previously:
http://www.ajc.com/sunday/content/epaper/editions/sunday/living.html
Putting the gene in genealogy
Bill Hendrick - Staff
Long before Alex Haley's "Roots" miniseries transformed genealogy from a methodical pastime to a raging passion for millions of Americans, Tina Dunkley already had been wondering "who I was, where I came from and why I felt a hole in my soul." Now she's got some answers --- for $350 and a dab of saliva.
Raising flags on health risks
Bill Hendrick - Staff
DNA tests might one day provide physicians clues about our genetic predisposition to a slew of health conditions such as obesity, high blood pressure, diabetes and osteoporosis, according to an international team of researchers headed by Mark Shriver, a molecular anthropology professor at Penn State University.
African-American DNA Roots Project: A genetic map to past
Bill Hendrick - Staff
Two researchers are soliciting DNA from African-Americans, hoping it helps blacks better explain the four-century chasm between today and their ancestral origins, say the creators of the African-American DNA Roots Project. Geneticists Bruce Jackson at Boston University and Bert Ely at the University of South Carolina say their database may help today's African-Americans trace their roots to ethnic groupings (formerly called tribes) in Africa.
I actually missed that bit in my (obviously too quick) review of the document. Got distracted by some "noise"...
chig, that's the key paragraph. That should stop the discussion on that particular point...
OT, unless he's a southpaw eom
Straw5, you know that I do not disagree with you. It is the way that questions are posed that is the issue, and that gives rise to concern in some quarters...
Itsonlymuni, in a nutshell:
And speaking of biased opinons and agendas, it has been my observation that you and w2p (amoung others) usually react with sometimes rabid fervur and ridicule to anything and anyone who posts in a negative manner. I am not alone in this observation, as it has been pointed out by others whom I will not name at this time.
I can name them for you: Dragon, Spook, TD, Indy, Long, Frog, Phil and TonyTox. Did I miss anybody out?
Again, I'll ask you, are you willing to repost the positive aspects of this company I have pointed out in the past?
You have obviously confused me with somebody that you think works for you.
With all that said, I am done with this discussion as I can see it serves no usefull purpose at this time to continue.
Agreed. I suggest that you go back to RB where you can indulge in the sort of "balanced" discussion that you crave.
Some updates on the civil suit can be found here
http://www.clerk.co.sarasota.fl.us/srqapp/civdetail.asp?tb_searchby=Company&tb_searchfor=2003+CA...
The hearing is now scheduled for January 8 2004
http://www.clerk.co.sarasota.fl.us/srqapp/cache/27923851.pdf
"Given the current posture of the case", DNAP have requested that the impounded computer is now examined.
http://www.clerk.co.sarasota.fl.us/srqapp/cache/60146070.pdf
mjam, W2P is THE MAN! lol
Itsonlymuni, you seem to want evidence, facts, links and validation - or rather others to provide them for you. Here is a recent example from RB:
1USGrant, first you have to provide evidence that what he posts is untrue and missleading. Can you do that? And provide facts with links that validate your assertions? All of Dragon's posts can be backed up. All you have to do is read the company's Sec filings, it's all in there in black and white with no need to spin. Good luck, you'll need it.
However, when it comes to your own posts you seem to content yourself with possibilities:
Btw, can you prove that all of the possibilities related by me in the posts you reposted are not possible? If you cannot, then why repost them? If it was to simply remind me and all others of the very real negative possibilities in relation to our company then I say "good job, you did well".
I post mainly facts and reasonable interpretations based on analysis of those facts. I am the first person to ask questions based on e.g. statements in SEC returns which raise potential issues, and have a history of so doing. I have no issue with examining all of the facts and both sides of any argument, in an open manner and in order to maintain an "honest forum" as you put it. What I do object to is the clever and subtle manipulation and non-ending posting of negative arguments, biased opinion and spin merely to further an agenda; as we typically see elsewhere and increasingly see here. That does not constitute a "balanced" view or an "honest" forum IMO.
Arch, I have to disagree with you. I believe that this poster does indeed have a clue (along with several others) and has a history of introducing FUD directly or by subtle reference. Here are some examples from posts on this board. I personally see a clear pattern here:
“W2p's response to Phil seemed naive and immature and, at the very least, out of line. Philipabel presented arguments that should be of absolute concern to any investor.”
“This suggests Tony is the only one working on R&D.”
“The jury's still out on whether those share are restricted or not. If not, when all those shares hit the float, and if nobody's buying, .0135 will look good.”
“And as we all know, some of those steps have been and might possibly be again into something not too pleasant and usually found in barnyards.”
“Looks like just another bitter pill to swallow if you want to stay long. As always, more shares equals dilution now or later no matter how they are derived. Demand will be our only savior. If that demand can be created in a realistic way, we can look for reward. If not, the damage will be slow, painfull, and steady. Proceed at your own risk.”
“On reading of the development of Ancestry 2.0 into 2.5 and 3.0 I can't help but wonder who is performing all of this development work? The Indian scientists appear to be gone and Tony has been busy with bio conferences both here and abroad. There seems to be an obvious disconnect with reality here. Who is performing all the work? It is all so impressive on the face but it seems insurmountable for a seven employee company with only one very busy scientist (Tony) to accomplish all that is hoped for. I guess I just don't get it.”
“Are the Indian scientists still working for Dnap? If they are no longer with the company, who is working to further develop Ancestry, Witness, Statnome and Ovinome? Has Dnap discontinued development of these products in favor of pursuing the development of drugs?”
“Sorry Ming, but that answer isn't good enough. Have you walked into Dnaprint's lab and found him hard at work? Who did you get that answer from? And why could you get that answer and not me? Did you just assume it since nobody has said anything to the contrary? Their new website certainly doesn't supply it and is ominously vague about many things. The old website gave a much more detailed description and much was eliminated from the new one. Why did that happen? Legal reasons? It seems there are so many open questions that demand answers and these are just a few.”
“66fan, thanks, do you live in the area? Were they quite busy and was Zack also still present? How about the Indian scientists, any of them still there? Did you get a count on the total employees. Tia.”
“Anybody besides me think the company would better served if Tony stayed home in the lab and did research rather than touring the globe hitting all these forensics conferences? It may look impressive to see his name as speaker at a conference a half world away but I fail to see how that will ever add to the bottom line. Just an added expense and Tony gets a paid vacation on us. If we were an established company with a firm grip on a market niche with many devoted customers firmly emplaced it would make sense to try to branch out internationaly by attending international conferences to get the word out. But not at this point when we are struggling towards respectable revenues and accepting dubious financing. Jmho.”
Bag8ger, the bottom line is perhaps best summarized in the "Recent studies and future directions" section at the end of the article (which I have further precised in bold):
Several theoretical and practical studies indicate that AM approaches promise to be suitable for identifying genes causing complex diseases. Methodological advancements have been made to offset the potential problems arising from association between unlinked loci by conditioning on parental admixture, and to detect and correct for population stratification. Use of Bayesian AM can take into consideration various uncertainties, including missing data values for estimating admixture proportions, and can overcome problems arising out of mis-specification of parental allele frequencies and promises to be an effective tool for admixture studies. This method, which is different from the classical disequilibrium-based approach that is more commonly used, is perhaps more suitable for disease gene mapping in admixed populations and has already been successfully used for mapping (he refers to his skin pigmentation work here). Table 2 summarises recent studies showing associations between ancestry and phenotypes/diseases and instances where AM was used to identify genes. Currently, the primary impediment to exhaustive AM genome scans is the lack of verified AIM panels. Sufficient numbers of markers are available as candidate AIMs, but effort and resources are required to confirm these markers and to generate accurate parental allele frequencies. Efforts are currently underway in several laboratories to identify more AIMs for this purpose. It seems inevitable that more such studies will be carried out in the near future to utilise the immense potential of this approach.
We have known for some time about the work on MALD using AIMs (or Ethnic Difference Markers, or whatever other people want to call them) for some time. Some relevant quotes from the December 2002 newsletter:
"DNAPrint was the first (and to date, the only) company to mine the human genome sequence for AIMs necessary for the MALD/AM approach."
"DNAPrint was the first to not only mine the human genome for AIMs, but the first to develop methods for using these AIMs to determine individual ancestral admixture proportions."
"(DNAPrint) was the very first to Mine the human genome for candidate AIMs Validate these mined candidate AIMs against an international panel of individuals to establish their allele frequencies in the world’s populations. File patent on the human genomes best AIMs (with Fst over 0.40, of which we have identified about 8,000). Develop methods for the determination of individual ancestry admixture proportions, which are necessary for the MALD/AM approach. DNAPrint exercises a virtual monopoly on this method, not only for the present because we are the only ones with the resources to perform the method, but by virtue of our patent, which effectively precludes others from performing the method efficiently. Our patent application filed last year covers about 8,000 of the human genomes best AIMs (all others are of substandard character for MALD/AM). It also describes how ancestral admixture proportions can be calculated for individuals. We expect that no other group will be able to effectively perform MALD/AM screens without violating this patent. Since the MALD/AM is the only cost-effective means by which to screen a genome, this places DNAPrint in a powerful position."
So, the patent application (and the associated 8,000 AIMs) is the key thing here. The article in question clearly post-dates (by over six months) the newsletter references. Back to your question. I believe (IMHO) that Shriver/DNAP have a lock on the AIMs by virtue of the patent application, and that the agreement between Shriver and DNAP means it is in their best interests to commercialize this approach (directly or through licences). I am delighted to see so many others (Smith, Seldin, Altschuler, etc) using MALD. I firmly believe that this is in our own best interests going forward, and that the only impediment would be the patent application not being accepted.
mjam, no I didn't see DNAP mentioned anywhere on the slides, but the fact that they were in the list probably meant that they were mentioned somewhere! Quite why they would be mentioned in a presentation to GSK is another matter...
Here is an interesting presentation (made to GSK) on the future of the pharmaceutical industry.
http://www.globalchange.com/ppt/gsk/
BTW, in the panel on the left after the slide text there are a number of "related issues". I can see one company referenced here...
A number of pending publications were listed in an updated version of Mark Shriver's CV previously:
http://www.anthro.psu.edu/cv/shriver.pdf
One in particular was potentially going to be very interesting:
Halder, I. and Shriver, M.D. (in review) Measuring and using admixture to study the genetics of complex disease.
Well, here is a link to the paper, which was published November 2003 in the new journal Human Genomics, and which nicely summarizes work to date and the future potential of MALD:
http://www.henrystewart.com/journals/hg/Review%20paper.pdf
Another initiative, which could be seen as competitor or opportunity:
http://www.azcentral.com/business/articles/1212tgen12.html
TGen, ASU to market lab testing
For-profit venture needs Regents' OK
Jodie Snyder
The Arizona Republic
Dec. 12, 2003 12:00 AM
The Translational Genomics Research Institute wants to create a for-profit company in conjunction with Arizona State University that would specialize in diagnostic tests.
The company is tentatively named Nanobiomics and would be run by Ron Van Horssen, chairman of the Cottonwood Group, a small private investment company.
Van Horssen has had experience in commercializing magnetic-resonance-imaging research.
The Arizona Board of Regents must approve the move, and Richard Love, TGen's chief operating officer, said approval could come as soon as the end of January.
Nanobiomics would commercialize findings from labs at TGen and ASU.
Van Horssen said it would focus on miniaturizing laboratory tests so they could be self-contained disposable devices.
They would also look at forensic analysis involving DNA testing and biowarfare-agent detection.
The company would manufacture the tests and could grow to a "significant size," Van Horssen said.
He also emphasized that the company is in the planning stages and that he doesn't have specific numbers on possible employees.
Love said there were no revenue projections available for the operations. Nanobiomics would look to venture-capital funds for its financing, Van Horssen said.
TGen and ASU's Arizona Biodesign Institute would have equal shares in the project, but a reserve would be held for the company's employees, Love said.
Some relevant links:
http://www.tgen.org/
http://www.azbio.org/
http://www.azbio.org/leadership.html
Our Director
World-renowned researcher, scholar and science policymaker George Poste has been named director of the Arizona Biodesign Institute, Arizona State University's new and path-breaking biodesign and biotechnology enterprise.
The Lee's pharmaceutical website is now available again:
http://www.leespharm.com/EN/channel_2511.html
Gurinder Shahi (DNA Phenomics SAB) quoted in this Straits Times article today:
http://straitstimes.asia1.com.sg/commentary/story/0,4386,224880,00.html
The Republic, notes life sciences entrepreneur Gurinder Shahi, has managed to bring in people and set up credible research institutes very quickly, despite its weak foundation in scientific R&D compared to New Zealand and Australia.
It has also succeeded in building venture capital, but is still behind its more developed counterparts in terms of ideas and innovations.
What it can do is to mine the rich capabilities of countries like New Zealand, where much of the technology is undervalued, compared to overpriced markets like the United States.
Singapore, rich in commercial funds, should look at New Zealand as 'a place for smart investments', suggests Dr Shahi, who is the chairman and CEO of BioEnterprise Asia, a full-service incubator for life-sciences start-ups.
'It would be well worth our while identifying areas of mutual interest that we can work to build together.'
BTW, he is also speaking at this event in April 2004:
http://www.sachsforum.com/global4_fs.html
Team, this one is Hector "A" Gomez - I think ours is Hector "J" Gomez.
OT: Ann, Haven't been there, but I did know the USMC were stationed there before and during WWII.
Ann, you might have missed the subsequent events. Tony resigned as a member of GMED's Scientific Advisory Board, and the Genotyping Contract did not proceed due to GMED's inability to obtain the requisite funding. The agreement is effectively dormant currently.
Ann, Lee Pharma (P) Ltd. (www.leepharma.com), is a private pharmaceutical company in India; not the same as (but easy to confuse with) Lee's Pharmaceutical Holdings Limited (www.leespharm.com), the publicly quoted company in Hong Kong.
The Lee's Pharma site was definitely not under construction previously so this is a re-construction lol.
Here's the previous post about Hector that mentions PRB:
http://www.investorshub.com/boards/read_msg.asp?message_id=1247532
Doug, one of the interesting things about this particular group is the connections with people like Michael Lai in the US, Benjamin Li and John Tam in Hong Kong, and others in Taiwan and Mainland China.
There is also a connection back to Zengen through Lee's Pharmaceuticals. For instance Zengen owns 3.3% of Lee's and James Lipton (Zengen CSO) is on Lee's Scientific Advisory Board. Lee's are also involved with a pre-clinical study using Zengen's peptide technology. Lee's have an interesting multi-faceted relationship with both Zengen and PRB, and potentially offer a gateway to Greater China.
You might notice that there is also a "focus" on eye disease amongst some of the PRB Scientific Advisors and the CSO...
What do PRB/Lee's have that we want? That remains to be seen, but I think there are several possible ways that this could develop and there is certainly plenty of scope for synergy.
BTW, I know for a fact that W2P has been waiting for months for the PRB website to be completed!