You bet it's coming stocky!! Here's another $8.95 million for ya'!

Moffitt receives $8.95 million drug discovery grant from NCI


Tampa, FL (May 16, 2007) – The H. Lee Moffitt Cancer Center & Research Institute has been awarded an $8.95 million grant from the National Cancer Institute. The long-term goal of research being conducted through the grant is the discovery of novel drugs for the treatment of cancer based on disrupting aberrant signal transductions circuits in human tumors.

“At this time in history, a project of this caliber is considered a monumental accomplishment,” said Said Sebti, Ph.D., program leader of the Drug Discovery Program and principal investigator on the grant.

The five year grant will cover five projects and three cores or shared facilities. The cores include administration overseen by Sebti, high throughput drug screening overseen by Wayne Guida, Ph.D. and chemistry, overseen by Harshani Lawrence, Ph.D. Each of the five projects is lead by two researchers: a biologist and a chemist.

• Jiandong Chen, Ph.D., Nicholas Lawrence, Ph.D., and Mark McLaughlin, Ph.D. will develop small molecules to disrupt mdmx binding to p53
• Srikumar Chellapan, Ph.D. and Nicholas Lawrence, Ph.D. will identify Raf/Rb association inhibitors
• Said Sebti, Ph.D. and Mark McLaughlin, Ph.D. will develop proteasome antagonists
• Hong-Gang Wang, Ph.D., Nicholas Lawrence, Ph.D., and Mark McLaughlin, Ph.D. will identify Bcl family antagonists
• Jerry Wu, Ph.D. and Nicholas Lawrence, Ph.D. will develop SHP2 phosphatase inhibitors

The project’s central hypothesis is that disruption of these circuits will induce apoptosis (cell death) and inhibit malignant transformation.

Researchers will work to develop drugs that will help break down the hallmarks of cancer which include: uncontrolled cell division, resistance to tumor apoptosis, invasion and metastasization and angiogenesis, the formation of new blood vessels, especially blood vessels that supply oxygen and nutrients to cancerous tissue.

Additionally, the "Method" incorporating "Ancestry", has been validated and "Patented".

Filing Date:04/11/2002 Publication Date:09/12/2006

These past 4 years of listening to nonsensical hyperbole by posters on this board is OVER.

You know who you are.

THE COMPANYS METHODS ARE VALIDATED. CASE CLOSED...

Methods for the identification of genetic features for complex genetics classifiers

http://www.freepatentsonline.com/7107155.html

No doubt... The AIM testing package now being utilized by Emory University is "REVOLUTIONARY"

Using ancestry-informative markers to define populations and detect population stratification
Mary-Anne Enoch
Pei-Hong Shen

Ke Xu

Colin Hodgkinson

David Goldman

Laboratory of Neurogenetics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA

A serious problem with case-control studies is that population subdivision, recent admixture and sampling variance can lead to spurious associations between a phenotype and a marker locus, or indeed may mask true associations. This is also a concern in therapeutics since drug response may differ by ethnicity. Population stratification can occur if cases and controls have different frequencies of ethnic groups or in admixed populations, different fractions of ancestry, and when phenotypes of interest such as disease, drug response or drug metabolism, also differ between ethnic groups.

Although most genetic variation is inter-individual, there is also significant inter-ethnic variation. The International HapMap Project has provided allele frequencies for approximately three million single nucleotide polymorphisms (SNPs) in Africans, Europeans and East Asians. SNP variation is greatest in Africans. Statistical methods for the detection and correction of population stratification, principally Structured Association and Genomic Control, have recently become freely available. These methods use marker loci spread throughout the genome that are unlinked to the candidate locus to estimate the ancestry of individuals within a sample, and to test for and adjust the ethnic matching of cases and controls.

To date, few case-control association studies have incorporated testing for population stratification. This paper will focus on the debate about the quantity and methods for selection of highly informative marker loci required to characterize populations that vary in substructure or the degree of admixture, and will discuss how these theoretically desirable approaches can be effectively put into practice.

http://jop.sagepub.com/cgi/content/abstract/20/4_suppl/19

DNAPrint posts first-quarter profit

http://www.heraldtribune.com/apps/pbcs.dll/article?AID=/20070518/BUSINESS/705180656

slug...you do understand that Ancestry is "extremely useful" for identifying a certain locus on the gene associated with trait, disease, toxicity, etc... Don't you?

With hundreds of single nucleotide polymorphisms (SNPs) in a candidate gene and millions of SNPs across the genome, selecting an informative subset of SNPs to maximize the ability to detect genotype-phenotype association is of great interest and importance. In addition, with a large number of SNPs, analytic methods are needed that allow investigators to control the false positive rate resulting from large numbers of SNP genotype-phenotype analyses. This dissertation uses simulated data

http://digitalcommons.library.tmc.edu/dissertations/AAI3110199/

THIS IS EXACTLY WHAT DNAPRINT HAS ACCOMPLISHED
---------------------------------------------------------------

Ancestry informative marker (AIMs) polynucleotides that contain a single nucleotide polymorphism or that contain an insertion or deletion, are provided, as are methods of using panels of the AIMs to draw an inference as to a trait of an individual. The trait can be, for example, biogeographical ancestry, a pigmentation trait, responsiveness to a drug, or susceptibility to a disease. Also provided are methods of determining the proportional ancestry of an individual. Reagents and kits also are provided.


A method of inferring, with a predetermined level of confidence, a trait of an individual, comprising: a) contacting a sample comprising nucleic acid molecules of a test individual with hybridizing oligonucleotides, wherein the hybridizing nucleotides can detect nucleotide occurrences of single nucleotide polymorphisms (SNPs) of a panel of at least about ten ancestry informative markers (AIMs) indicative of a population structure correlated with the trait, and wherein said contacting is performed under conditions suitable for detecting the nucleotide occurrences of the AIMs of the test individual by the hybridizing oligonucleotides; and b) identifying, with a predetermined level of confidence, a population structure that correlates with the nucleotide occurrences of the AIMs in the test individual, wherein the population structure correlates with a trait, thereby inferring, with a predetermined level of confidence, the trait of the individual.

http://www.freepatentsonline.com/20040229231.html

---------------------------------------------------------------

The study showed that some of the 16 genetic polymorphisms are linked to toxic side effects during more than one treatment phase; and some caused more than one type of toxicity. Certain polymorphisms were linked to the pharmacokinetics of specific drugs— how drugs are absorbed by the body, distributed, chemically modified or broken down and eliminated. Variations in pharmacokinetics can alter the levels of drugs in the body, leading to ineffective or toxic levels in individual patients.

For example, during the induction phase, when a variety of different types of chemotherapy drugs are used, polymorphisms in the two genes that were part of a biochemical pathway that breaks down chemotherapy drugs were linked to gastrointestinal toxicity and infection, respectively. In the consolidation phase, when drugs called antifolates were the main treatment, a folate was linked to gastrointestinal toxicity, as it was during the continuation phase. And in all three phases, one polymorphism was linked to hyperbilirubinemia, or jaundice, partly caused by the drug methotrexate.


http://www.eurekalert.org/pub_releases/2007-05/sjcr-igl051107.php

Address Ancestry, St. Judes, Leukemia...or go away. You're more of a gnat than a frog.

Jever, I bought more today. When you think it's gonna go up? TIA

frogdreaming,

you stated, and was the basis of your argument:

So please don't try to suggest that the concept of ancestry, as it applies to the relationship between genetic variation and genetic based physiological effect, is in any way revolutionary

sad slug....

What's "revolutionary" is the "concept" (as you call it), is now a reality: A genetic marker being scientifically associated with disease.

As far as treatment is concerned...population stratification based on ancestral origins and groups is the only way to categorize patients and target succeptibility to disease.

I do realize that this collapses all of your arguments for many, many years now.

I'm feelin' for ya' buddy... I just can't reach ya'..

poor froggy... I didn't expect that you wouldn't be able to distinguish b/w what Frudakis has labeled "recreational genomics" and what is quickly being recognized as revolutionary.

Can you please explain the validity of Ancestry for the board? You seem to keep avoiding the question.

Ancestry and pharmacogenetics of antileukemic drug toxicity

http://bloodjournal.hematologylibrary.org/cgi/content/abstract/109/10/4151

-------------------------------------------------------------

Inherited genes linked to toxicity of leukemia therapy
St. Jude researchers discover that variations in genes that affect the behavior of leukemia chemotherapy drugs in the body are linked to drug toxicity, a finding that will likely help clinicians predict how patients will respond to specific agents

http://www.eurekalert.org/pub_releases/2007-05/sjcr-igl051107.php

ben,

Shareholders

As February 15, 2007 there were 1,034 owners of record of our common stock.

slog...obviously, you are in denial pertaining to the scope of this technology. That in conjunction with an indiscernable, less-than-fluid, comprehension of said technology...leaves you at a distinct disadvantage.

In future I will certainly keep this in mind; as I sense these characteristic "limitations" are...no doubt...an issue for you on many levels. ROTFLMAO

Cardiovascular and Psychiatric Risks with ADHD Drugs
FDA Patient Safety News: Show #63, May 2007

Patients with Attention Deficit Hyperactivity Disorder(ADHD) who are taking stimulant drugs such as Adderall (amphetamine-dextroamphetamine), Ritalin (methylphenidate) and Strattera (atomoxetine hydrochloride) will soon be given a Patient Medication Guide each time the prescription is filled.

The medication guide will warn that there have been reports of sudden death in children and adolescents with pre-existing structural cardiac abnormalities or other serious heart problems who were taking stimulant drugs to treat their ADHD. Sudden death, stroke and MI have also been reported in adults with underlying risk factors for these events who took ADHD drugs.

http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/psn/printer.cfm?id=519

----------------------------------------------------------------

DNAPrint genomics Licenses Ritalin-Like Compounds Targeting Enhanced Treatment of Drug Addiction and Attention Deficit
Market Wire, October, 2005


DNAPrint genomics, Inc. (OTC BB: DNAG) today announced it has licensed a series of methylphenidate analogs or Ritalin(TM)-like compounds targeting the clinical development of enhanced pharmaceuticals for the treatment of drug addiction, attention deficit hyperactivity disorder (ADHD), and depression. This is the second drug project that will be developed by DNAPrint Pharmaceuticals. Inc., the Company's wholly owned, recently formed pharmaceutical subsidiary focused on personalized medicine.

http://findarticles.com/p/articles/mi_pwwi/is_200510/ai_n15738616

---------------------------------------------------------------

"Other therapies in our product pipeline include Ritalin(tm)-like compounds for the potential treatment of drug abuse, attention deficit hyperactivity disorder (ADHD), and depression," Dr. Gomez said. "These compounds are analogs of Ritalin, a well-known drug used for treatment of ADHD and designed specifically to take effect slowly but last longer, thus reducing the potential for cardiovascular complications, abuse and a patient's required daily dosage."

http://www.primenewswire.com/newsroom/news.html?d=101142

----------------------------------------------------------------

Methylphenidate Analogs and Methods of Use Thereof US11/256063


PCT/US2005/038030

Eureka, I would suggest they focus 80% of their resources at one product, and get it to market as quickly as possible. This would give them needed leverage in funding, partnership, and alliance negotiations.

I suspect there are a number of diagnostic/theranostic tests DnaPrint will develop asociated with cd-59. Type II diabetes, cardiovascular...will also have oncological applications:

2007 Jan 26

Small-Molecule Inhibition of the Interaction between the Translation Initiation Factors eIF4E and eIF4G.

[My paper] Nathan J Moerke , Huseyin Aktas , Han Chen , Sonia Cantel , Mikhail Y Reibarkh , Amr Fahmy , John D Gross , Alexei Degterev , Junying Yuan , Michael Chorev , Jose A Halperin , Gerhard Wagner

Assembly of the eIF4E/eIF4G complex has a central role in the regulation of gene expression at the level of translation initiation. This complex is regulated by the 4E-BPs, which compete with eIF4G for binding to eIF4E and which have tumor-suppressor activity. To pharmacologically mimic 4E-BP function we developed a high-throughput screening assay for identifying small-molecule inhibitors of the eIF4E/eIF4G interaction. The most potent compound identified, 4EGI-1, binds eIF4E, disrupts eIF4E/eIF4G association, and inhibits cap-dependent translation but not initiation factor-independent translation. While 4EGI-1 displaces eIF4G from eIF4E, it effectively enhances 4E-BP1 association both in vitro and in cells. 4EGI-1 inhibits cellular expression of oncogenic proteins encoded by weak mRNAs, exhibits activity against multiple cancer cell lines, and appears to have a preferential effect on transformed versus nontransformed cells. The identification of this compound provides a new tool for studying translational control and establishes a possible new strategy for cancer therapy.

http://209.85.165.104/search?q=cache:tq4JpGcCzFMJ:lib.bioinfo.pl/auth:Chorev,M+Dr.+Michael+Chorev+20....

--------------------------------------------------------------

Inhibitor of CD59 Activity as an Adjunct to Antibody-Based Cancer Therapy

http://otd.harvard.edu/technologies/tech.php?case=2887

--------------------------------------------------------------

Abstract: Type 2 diabetes mellitus (T2DM) can lead to death without treatment and it has been predicted that the condition will affect 215 million people worldwide by 2010. T2DM is a multifactorial disorder whose precise genetic causes and biochemical defects have not been fully elucidated, but at both levels, calpains appear to play a role. Positional cloning studies mapped T2DM susceptibility to CAPN10, the gene encoding the intracellular cysteine protease, calpain 10. Further studies have shown a number of noncoding polymorphisms in CAPN10 to be functionally associated with T2DM while the identification of coding polymorphisms, suggested that mutant calpain 10 proteins may also contribute to the disease. Here we review recent studies, which in addition to the latter enzyme, have linked calpain 5, calpain 3, and its splice variants, calpain 2 and calpain 1 to T2DM-related metabolic pathways along with T2DM-associated phenotypes, such as obesity and impaired insulin secretion, and T2DM-related complications, such as epithelial dysfunction and diabetic cataract.

http://www.blackwell-synergy.com/doi/abs/10.1196/annals.1372.011?journalCode=nyas

---------------------------------------------------------------

Calpain-5 gene variants are associated with diastolic blood pressure and cholesterol levels

1Departamento de Genómica Estructural. Neocodex. Sevilla, Spain

Genes implicated in common complex disorders such as obesity, type 2 diabetes mellitus (T2DM) or cardiovascular diseases are not disease specific, since clinically related disorders also share genetic components. Cysteine protease Calpain 10 (CAPN10) has been associated with T2DM, hypertension, hypercholesterolemia, increased body mass index (BMI) and polycystic ovary syndrome (PCOS), a reproductive disorder of women in which isunlin resistance seems to play a pathogenic role. The calpain 5 gene (CAPN5) encodes a protein homologue of CAPN10. CAPN5 has been previously associated with PCOS by our group. In this new study, we have analysed the association of four CAPN5 gene variants(rs948976A>G, rs4945140G>A, rs2233546C>T and rs2233549G>A) with several cardiovascular risk factors related to metabolic syndrome in general population

http://www.biomedcentral.com/1471-2350/8/1#B41

--------------------------------------------------------------

DNAPRINT GENOMICS ANNOUNCES STRATEGIC ALLIANCE WITH NEOCODEX

http://www.dnaprint.com/welcome/press/press_recent/2006/0822/DNAG-NEOCODEX.pdf

----------------------------------------------------------------
Genetic Markers
Progress and Potential for Cardiovascular Disease

By tracking the progression of heart failure from the initial event (eg, cardiomyopathy) to end-stage failure using genomic techniques, researchers can develop a better understanding of the molecular processes involved. Using this approach, we have proposed more than a dozen biomarkers of dilated cardiomyopathy (ANP, lumican, ITP 3-kinase, etc), hypertrophic cardiomyopathy (CD59, HSP90, calpain, etc), and end-stage heart failure (desmin, dynamitin, nucleolin, etc), respectively.138,141,145 This combined approach has also been successfully used in animal models of hypertension and has significant implications for the study of human disease.147


http://circ.ahajournals.org/cgi/content/full/109/25_suppl_1/IV-47

---------------------------------------------------------------

Harvard University Receives Notice of Allowance on Diagnostic Patent Claims Licensed to DNAPrint Genomics, Inc.

SARASOTA, FL -- (MARKET WIRE) -- March 09, 2006 -- DNAPrint Genomics, Inc. (OTC BB: DNAG) today announced that Harvard University has received formal Notice of Allowance from the U.S. Patent and Trademark Office (USPTO) for 20 claims that cover diagnostic uses of a novel marker for diabetes licensed by the Company. DNAPrint entered into an agreement with Harvard in January 2006 to sponsor continued research based on the marker, CD59, in the Harvard Medical School laboratory of Dr. Jose Halperin, a named inventor of the allowed claims. These claims, once issued, will provide Harvard additional intellectual property protection to support the development and commercialization by DNAPrint of new diagnostic tests to better define and manage diabetes more effectively.

http://www.marketwire.com/mw/release_html_b1?release_id=112547

Patent Applications



We have filed claims for international and domestic patent protection. The
patents, if issued, will help ensure protection of our bioinformatics platforms,
analytical software, genome maps and genetic classifiers in forensic, consumer
products, and pharmacogenomics applications. The most significant patent
applications cover the bioinformatics platforms and genome maps. Other
applications describe the mathematical process of finding complex genetic
information and the actual processes that find the gene variants responsible for
specific complex genetic traits. Five of our patent applications, Compositions
of Pigmentation Traits, Single Nucleotide Polymorphisms Predictive of Paclitaxel
Responsiveness in Cancer Patients, Compositions Inferring Ancestry, Compositions
Inferring Statin Response, and Compositions Inferring Eye Color, have entered
National Phases and are pending review and we believe, approval in the U.S. and
designated countries. The pigmentation patent is important because it includes
the methods and compositions for determining skin shade, eye color or any other
pigmentation application. Our Statin patent application includes the use of
method for determining a person's ability to respond favorably to a particular
statin drug, not the class as a whole. We may also obtain data to support our
claim for all statins and the use of our ancestry information markers ("AIMs")
in the development of the assay. As discoveries warrant, we will continue to
apply for future additional patents. Listed below are our current patent pending
and granted applications.


--------------------------------------------------------------------------------



Efficient Methods and Apparatus for High-Throughput
Processing of Gene Sequence Data. US 7,110,885 (granted)
Methods for the Identification of Genetic US 7,107,155 (granted)
Features for Complex Genetics Classifiers PCT/US02/38326


Methods for the Identification of Genetic. US 7,107,155 (granted)
CA 2,468,961
EP 02794095.6
JP549497/2003


AU2002359549



Methods and Apparatus for use in Genetics Classification
Including Classification Tree US10/496,226
Analysis PCT/USO2/38309
CA2,498,570


EP02789948.3
JP550120/2003


AU2002352985



Methods and Apparatus for use in Complex Genetics
Classification US10/495,962
Based on Correspondence Analysis and Linear-Quadratic
Analysis PCT/US02/41465
CA2,468,601
EP02789948.3
JP549549/2003


AU2002361871



Composition and Methods for the Inference US11/397,454
Of Pigmentation Traits PCT/US02/16789
AU2002/312112
CA2,448,569
EP02739467.5
hk04109585.8
JP2003/500216
Compositions and Methods for Inferring US10/188,359
A Response to a Statin PCT/US02/20847
AU2002/316485
CA2,486,789
EP02746794.3
JP2003/509083


Single Nucleotide Polymorphisms and Combinations Thereof
Predictive of PCT/US02/38345
Paclitaxel Responsiveness in Cancer Patients AU2002360452
CA2,468,312
EP02795709.1


--------------------------------------------------------------------------------



HK05102575.4
JP2003-546736
US10/496,605



Compositions and Methods for Inferring Ancestry US10/644,594




PCT/US03/26229




AU2003265572



CA2,496,155


EP03788685.0


JP2005-502072




Methylphenidate Analogs and Methods of Use Thereof US11/256063




PCT/US2005/038030




Methods, Products and Treatments for Diabetes US 6,835,545 (Granted)
US 7,049,082 (Granted)
US10/870,342



Anti-Glycated CD59 Antibodies and Uses Thereof US2004/019392




Multiplex Assays for Inferring Ancestry 331832-000045/WO



Compositions and Methods for Inferring an Adverse Effect in
Response to a Drug . . . . US05/41326



Methods and Compositions for Inferring Eye Color US10/589,291




PCTUS05/04513




EP05723003.9




Recombinant Human Erythopoietin with Altered Biological
Activity US 5,614,184 (Granted)
US 6,489,293 B1 (Granted)
Production and Use of Recombinant Protein Multimers with
Increased Biological Activity US 6,242,570 (Granted)
US 6,187,564 (Granted)


--------------------------------------------------------------------------------





PCT/US98/13944




AU PCT 732857




CA PCT 2,296,071




JP PCT 2000-502204




EPO PCT 98 93 4269.6




Modified Polypeptides with Increased Biological Activity US 5,580,853 (Granted)
US 5,747,445 (Granted)


PCT/US97/22503




JP PCT 10524930



US 5,919,758 (Granted)


US 6,107,272 (Granted)



PCT/US95/03242




EPO 0 751 959




Integrated disease information system US 6,108,635 (granted)


Hierarchical Biological Modeling System and Method as US 5,808,918 (granted)
Restricted to three of five original claims upon re-examination
At the USPTO in 2001

DNA polymorphism associated with Crohn's Disease PCT WO 01/042511


US 239403


IBD candidate gene US 60/362,700
US 60/362,717
US 60/342,388
US 10/327,189


PCT/IB02/05560



JP 2003-554727


EU 02781695.8



AU 2002348745




PCT/IB2002/005560



20060105381



--------------------------------------------------------------------------------

http://sec.edgar-online.com/2007/04/10/0001354488-07-000532/Section18.asp

The H. Lee Moffitt Cancer Center & Research Institute, based at the University of South Florida in Tampa, will install three of TomoTherapy's Hi-Art Systems and could begin treating patients with it by August of this year.

http://wistechnology.com/article.php?id=2918

Eureka, you shouldn't worry about Dutchess. They are making plenty off of the shareholders. The genotyping services Ellipsis provides are growing exponentially. And will continue to do so. And yes....they may just run this thing into the ground.


Q4 revenue of $525,000, an increase of 42% over last year

-- Year-end revenues of $2.4 million, an increase of 91% over 2005

-- Q4 Genotyping revenue of $170,000, an increase of 643% over Q4 2005

-- Full-year Genotyping revenue of $770,000, an increase of 330% over
full-year 2005

-- Full-year revenue of $1.6 million for Ancestry products, an increase
73% over 2005

croak, unlike yourself...I will not spew unsubstantiated rubbish to this board. I submit this professional interpretation of the importance, and relevance of Ancestry. You already are well aware of DnaPrint's leading role in the advancement of PGX.

We propose that it is not productive to continue the debate about whether racial or ethnic groups do or do not have genomic correlates. Rather, the need is to recognize that multiple, distinct concepts of race or ethnicity exist, and to move molecular epidemiologic research toward effectively characterizing and using these.

Like I said. Please stop embarrassing yourself.

http://cebp.aacrjournals.org/cgi/content/full/14/11/2467

frog, is this Shriver talking about the limitations of Ancestry? You haven't addressed my previous post.

http://lib.bioinfo.pl/auth:Shriver,MD

16,000 a year plus 10,000 shares...but you're forgetting this:

We agreed to provide the consultant with royalties of 2.5% of the net revenues derived from a product and any subsequent versions of the products developed with his help.

Shriver's a lot younger than I pictured him. Doesn't look very upset. I expected an older fella'....by the way, here is the latest agreement. The shares are restricted as per the original and amended agreements.

I apologize for embarrassing you, frog. It just turned out that way.

Consultant Agreement with Member of Our Scientific Advisory Board

During May 2005, we entered into a one-year agreement with our Scientific Advisory Board member, to continue collaboration with us to develop commercial tests for genetic ancestry and particular physical phenotypes. We have agreed to compensate this consultant with quarterly payments of $4,000 and 2,500 shares of our common stock. The term of this agreement is one year with automatic renewals each year unless either party provides written notice of its intent not to renew within thirty days prior to the annual anniversaries of this agreement. During May 2005, we also entered into a license agreement with this consultant. This license will remain in force in perpetuity as long as we are not in default of the agreement. We agreed to provide the consultant with royalties of 2.5% of the net revenues derived from a product and any subsequent versions of the products developed with his help.

For the services performed by this member for being on the Scientific Advisory Board, we have a commitment to issue 2,500 shares of our common stock each year through 2007.

DNAPRINT GENOMICS INC: 10KSB, Sub-Doc 1, Page 74

FOOLG...AND YE' SHALL KNOW THE TRUTH!!!!!!!

http://www.thetruthtoledo.com/story/2007/April11-07/Roots.htm

frog, you stated:

Shriver has been a singular voice for the limitations of Ancestry and has often tried to manage the expectations of those who question him regarding its value.

Can you please explain for the board the limitations of these recent findings?.......you should be ashamed....

Ancestry and pharmacogenetics of antileukemic drug toxicity

http://bloodjournal.hematologylibrary.org/cgi/content/abstract/109/10/4151

-------------------------------------------------------------

Inherited genes linked to toxicity of leukemia therapy
St. Jude researchers discover that variations in genes that affect the behavior of leukemia chemotherapy drugs in the body are linked to drug toxicity, a finding that will likely help clinicians predict how patients will respond to specific agents

http://www.eurekalert.org/pub_releases/2007-05/sjcr-igl051107.php

DNAPRINT will provide CONSULTANT with quarterly payments
of $4,000 and 50,000 shares of restricted stock for the term
of this contract


DNAPRINT will provide CONSULTANT with 5,000 shares of
restricted stock for each $10,000 in net sales that are
realized over the life of the products that are generated as
a result of this collaboration.

Care to rate your executives?

http://www.executivedisclosure.com/companies/1127354/DNAPrint-Genomics-Incorporated.aspx

Looking at his resume... It's hard to believe that Gomez hasn't secured a major partnership...

UTEK Corporation Appoints Hector Gomez, M.D., Ph.D., to Scientific Advisory Council
Business Wire, Nov 20, 2003


PLANT CITY, Fla.--(BUSINESS WIRE)--Nov. 20, 2003

UTEK Corporation (AMEX:UTK) announced today that Hector J. Gomez, M.D., Ph.D., has joined UTEK's Scientific Advisory Council. Previously, Dr. Gomez served as a Senior Director of clinical research at Merck/MSDRL, Executive Director of Clinical Research at CIBA-GEIGY Corporation, VP of Medical Affairs at Vertex Pharmaceuticals and President and CEO of Transcend Therapeutics. Dr. Gomez is currently a Member of the Board of Directors of PRB Pharmaceuticals and Apollo Pharmaceuticals and is the Chairman of the Board of Directors of DNAprint Genomics.

Dr. Gomez has considerable experience in both the scientific and business aspects of clinical research, pharmacology and pharmacogenomics. His knowledge and experience should enhance UTEK's ability to evaluate innovative pharmacologically related technologies. Dr. Gomez received his M.D. from the National University of Colombia in 1963 and his Ph.D. in Pharmacology from Marquette University in 1968. He also received a degree in Clinical Pharmacology from Tulane University (1973).

Dr. Gomez joins the UTEK Scientific Advisory Council, which includes scientists, engineers, and physicians who are engaged to help analyze scientific innovations in a wide variety of disciplines.

UTEK provides comprehensive solutions for transferring new technologies, managing intellectual property and providing intellectual property consultation. UTEK is a leader in technology transfer, providing unparalleled access to breakthrough technologies. Whether it is sourcing from Europe's leading educational institutions through UTEK Europe, Ltd. and Pharma-Transfer; or accessing the world's largest online searchable database for life science (TechEx) or physical science (UVentures) discoveries, we provide the resources necessary to efficiently identify and transfer new technologies. The newest addition of the Knowledge Express searchable database provides our clients with comprehensive coverage of licensing agreements, corporate profiles, clinical trials, deals, drug pipelines, drug sales, licensable technologies, patents and royalty rates.

In addition, UTEK operates Techno-L as a pro bono activity to disseminate and encourage the discussion of best practices among technology transfer professionals.


Pharmaceuticals

Hector Gomez, M.D., Ph.D.
Chairman of the Board of Directors of DNAprint Genomics
Expertise: Pharmacology, drug development, pharmacogenomics

http://www.utekcorp.com/files/advisorycouncil.asp?pageID=13

I have no comment on this:

On March 30, 2007, we issued Mark Shriver, a consultant, a total of 2,500 shares of our common stock in exchange for product services valued at $23.

He is incorrect in each of these assertions...
No progress,
no products,
sham patents,
non-resident principles,
unethical loans,
impenetrable investor relations and
constantly revised filings, are the residue of a facade, they are not indicative of an honest scientific concern.

Bought more today...

Inherited Genes Linked to Toxicity of Leukemia Therapy St. Jude researchers discover that variations in genes that affect the behavior of leukemia chemotherapy drugs in the body are linked to drug toxicity, a finding that will likely help clinicians predict how patients will respond to specific agents

MEMPHIS, Tenn., May 11, 2007 /PRNewswire via COMTEX/ --

Investigators at St. Jude Children's Research Hospital have discovered inherited variations in certain genes that make children with acute lymphoblastic leukemia (ALL) susceptible to the toxic side effects caused by chemotherapy medications. The researchers showed that these variations, called polymorphisms, occur in specific genes known to influence pharmacodynamics -- how drugs work in the body and how much drug is needed to have its intended effect.

The findings, made during a study of 240 children, are important because these side effects in ALL can be life-threatening and interrupt delivery of treatment, increasing the risk of relapse. The new insights gained in this study could help individualize ALL chemotherapy according to a patient's inherited tendencies to develop toxic reactions to specific drugs.

"Such individualized therapy would eliminate the time-consuming trial-and- error approach to finding the right dose for a patient," said Mary Relling, Pharm.D., chair of the Pharmaceutical Sciences department at St. Jude. "When the results of our findings are translated into routine clinical care, we should see less toxicity among children being treated for ALL." Relling is senior author of a report on this work that appears in the May 15 issue of "Blood." "Scientists at St. Jude and elsewhere have dramatically improved survival rates from childhood leukemia, but it's still challenging to find the right dose for each patient," said Rochelle Long, Ph.D., director of the National Institutes of Health Pharmacogenetics Research Network. "By finding specific genetic variations linked to how individual patients respond to therapy, this work will make medicines safer and more effective for everyone." Other authors of this work include Shinji Kishi, Cheng Cheng, Deborah French, Deqing Pei, Nobuko Hijiya, Ching-Hon Pui and William Evans (St. Jude); Soma Das and Edwin Cook (University of Chicago); Carmelo Rizzari (University of Milan, Italy), Gary Rosner (M.D. Anderson Cancer Center, Houston) and Tony Frudakis (DNAPrint Genomics, Sarasota, Fla.).

This work was supported in part by the National Cancer Institute and the National Institutes of Health (NIH)/National Institute of General Medical Sciences (NIGMS) Pharmacogenetics Research Network and Database; a Center of Excellence grant from the State of Tennessee and ALSAC.

St. Jude Children's Research Hospital St. Jude Children's Research Hospital is internationally recognized for its pioneering work in finding cures and saving children with cancer and other catastrophic diseases. Founded by late entertainer Danny Thomas and based in Memphis, Tenn., St. Jude freely shares its discoveries with scientific and medical communities around the world. No family ever pays for treatments not covered by insurance, and families without insurance are never asked to pay.

http://www.msnbc.msn.com/id/18616377/

ancient/holder...your alias and question precedes you. Contribute...or take a hike.... Bye...

stockholder, why the h-ll didn't Gabriel have any positive expression in regards to the M2gen deal? And don't say he has to keep his mouth shut. All I hear is a dire need for more cash. Hence the stock price....

I suspect the diagnostic test DnaPrint develops for cd-59, will also have oncological associations:

Cell. 2007 Jan 26;128 (2):257-67 17254965
Small-Molecule Inhibition of the Interaction between the Translation Initiation Factors eIF4E and eIF4G.
[My paper] Nathan J Moerke , Huseyin Aktas , Han Chen , Sonia Cantel , Mikhail Y Reibarkh , Amr Fahmy , John D Gross , Alexei Degterev , Junying Yuan , Michael Chorev , Jose A Halperin , Gerhard Wagner
Assembly of the eIF4E/eIF4G complex has a central role in the regulation of gene expression at the level of translation initiation. This complex is regulated by the 4E-BPs, which compete with eIF4G for binding to eIF4E and which have tumor-suppressor activity. To pharmacologically mimic 4E-BP function we developed a high-throughput screening assay for identifying small-molecule inhibitors of the eIF4E/eIF4G interaction. The most potent compound identified, 4EGI-1, binds eIF4E, disrupts eIF4E/eIF4G association, and inhibits cap-dependent translation but not initiation factor-independent translation. While 4EGI-1 displaces eIF4G from eIF4E, it effectively enhances 4E-BP1 association both in vitro and in cells. 4EGI-1 inhibits cellular expression of oncogenic proteins encoded by weak mRNAs, exhibits activity against multiple cancer cell lines, and appears to have a preferential effect on transformed versus nontransformed cells. The identification of this compound provides a new tool for studying translational control and establishes a possible new strategy for cancer therapy.

http://209.85.165.104/search?q=cache:tq4JpGcCzFMJ:lib.bioinfo.pl/auth:Chorev,M+Dr.+Michael+Chorev+20...

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Inhibitor of CD59 Activity as an Adjunct to Antibody-Based Cancer Therapy

http://otd.harvard.edu/technologies/tech.php?case=2887

chaz, I can't open the link. What does it say? TIA

stockholder, why would gabriel mention the 10 projects with Moffitt, and in the same conversation...reiterate the need for funding being the obstacle to the company? Why would he have a need for funding with the "Big Deal, M2gen" scenario you have painfully, and relentlessly touted. TIA

stockboy....clean up...on aisle cd-59:

Moving beyond its existing genetic ancestry testing business puts DNAPrint Genomics (OTC: DNAG) on the road to genomic medicine, says CEO Richard Gabriel. "People are trying to figure out what personalized medicine means," he explains. "We've proven the technology, now it's just a matter of capital." Revenue from the company's consumer ancestry and forensic genetic screening business is on the rise; some equity funding is in place, and strategic equity sales may help raise cash. "Our product is more effective, less toxic, and we will link it to genetic ancestry as well as other diagnostics."

http://wallstreetreporter.com/profile.php?id=24029

Sandoz, I honestly don't think you can spell. I don't believe those are typos. ouch...

Docket: 02D-0018 - Collection of Race and Ethnicity Data in Clinical Trials for FDA Regulated Prodcuts; Draft Guide

Dr. Tony Frudakis

Most drugs are derived from these chemicals, and so it is no coincidence that the family of enzymes that that allow us to detoxify these chemicals is the same family that we use to metabolize drugs (called xenobiotic metabolism genes, of which the cytochrome P450s are the most commonly studied). However, in addition to pharmacokinetics and drug metabolism, pharmacodynamics, or how a drug mechanistically interacts with the patient is also important for understanding variable drug response. We believe pharmacodynamics to be significantly more complex to unravel, requiring whole genomes be screened not just certain gene families, and we have found that the most economical and efficacious method for screening genomes relies on the measurement of SNPs across the genome that carry information about BGA and other levels of population structure.

http://www.fda.gov/ohrms/dockets/dailys/03/Feb03/020603/8004e14c.html

This document obviates the importance of population, efficacy...


http://www.fda.gov/cder/genomics/genomic_biomarkers_notes.htm

P450...drugs are broken down in the body by the cytochrome P450 family of enzymes. ...

Top Pharmacogenomic Tests

2.5.1 CYP2D6

2.5.2 CYP2C19 and CYP2C9

2.5.3 CYP3A4 and CYP3A5 Genotyping

http://www.marketresearch.com/map/prod/1305238.html

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TUTORIAL:

Cytochrome P450 Enzymes and Psychopharmacology

Sheldon H. Preskorn, M.D. and Anne T. Harvey, Ph.D.

INTRODUCTION

The study of cytochrome P450 (P450) enzymes has implications for psychopharmacology at many levels as follows:


http://www.acnp.org/g4/GN401000086/CH085.html

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DNAPrint genomics Initiates Study of Predictive Product
DNAPrint genomics, Inc. (BULLETIN BOARD: DNAP) today announced that it will commence a study of the Company's OVANOME(TM) predictive assay using ovarian cancer patient samples to be procured by the H. Lee Moffitt Cancer Center-affiliated Bay Area Oncology of Tampa, Fla.

DNAPrint's research indicates that variability in TC response is largely due to the narrow therapeutic index of the drug combination combined with wide genetic unpredictability in the Cytochrome P450 2C8 gene, which is responsible for metabolizing (and disposing of) taxol from the human body.

"BioGeographical Ancestry admixture is also relevant for predicting response, over and above CYP2C8 multilocus genotypes," said Tony Frudakis, Ph.D., DNAPrint's Chief Scientific Officer. "We believe that complex, multifactorial genetic classification of response proclivities is the paradigm for drug development of the future," he stated. "We intend to apply our state- of-the-art genomics program to not only the development of our own nascent drug pipeline but to ameliorate deficiencies associated with certain drugs manufactured by other companies as well."

http://news.biohealthmatics.com/PressReleases/2005/05/19/000000001821.aspx

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Determination of a candidate gene in predicting in-vivo ovarian cancer response to combination therapy with paclitaxel and carboplatin

Having obtained genotypes for 57 patients at each of the SNPs in several genes, preliminary results have revealed a statistically significant association (Fishers Exact P=0.00332) between haplotypes at the CYP3A4 gene and a lack of response to paclitaxel/carboplatin as measured by the CA-125 tumor marker.

This in-vivo assay could help classify ovarian cancer patients as potential responders or non-responders to our conventional chemotherapeutic agents.

http://www.asco.org/portal/site/ASCO/menuitem.34d60f5624ba07fd506fe310ee37a01d/?vgnextoid=76f8201eb6....

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During the induction phase, when drugs subject to the steroid/cytochrome P4503A pathway predominated, genotypes in that pathway were important: vitamin D receptor (odds ratio [OR], 6.85 [95% confidence interval [CI], 1.73-27.0]) and cytochrome P4503A5 (OR, 4.61 [95% CI, 1.11-19.2]) polymorphisms were related to gastrointestinal toxicity and infection, respectively.

http://bloodjournal.hematologylibrary.org/cgi/gca?allch=&SEARCHID=1&FULLTEXT=frudakis&FI....

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COMPOSITIONS AND METHODS FOR INFERRING AN ADVERSE EFFECT IN RESPONSE TO A DRUG TREATMENT


[0013] A method for inferring a poor metabolizer phenotype of a human subject from a nucleic acid sample of the subject is also provided by the invention. The method comprises identifying in the nucleic acid sample, an occurrence of at least one single nucleotide polymorphism (SNP) of a CYP2D6 marker, wherein the SNP is associated with the poor metabolizer phenotype, thereby inferring the poor metabolizer phenotype of the subject. In one embodiment, the poor metabolizer phenotype is associated with the CYP2D6*4 allele.

Since both Lipitor® and Zocor® are metabolized by the cytochrome P450 system, and since aberrant metabolism of drugs is commonly associated with adverse events and reduced efficacy, a systematic candidate gene screen and a whole genome screen were initiated to identify markers associated with myopathologic adverse events for both Lipitor® and Zocor®.

[0154] The results described above demonstrate that alleles of two separate Cytochrome P450 genes are associated with atorvastatin-induced myalgia response. The following conclusion can be drawn from the data presented above:

1) The CYP2D6 gene, where the CYP2D6*4 allele marked by the CYP2D6 179-172 TT-TC or TC-TC genotype pair, or directly with a CYP2D6*4 genotyping assay, is indicative of likelihood to express atorvastatin induced myalgia

2) The CYP2D6*10 allele marked by the 179-172 CC-TC genotype pair, or directly with a CYP2D6*10 genotyping assay, is indicative of likelihood to express normal (non-myalgia) response to atorvastatin.

3) Certain CYP2C8 haplotypes as discussed above, are indicative for myalgia or normal response to atorvastatin.

4) Native American and East Asian admixture as discussed above indicative for myalgia or normal response to atorvastatin.

[0155] A simple classification can be used to combine the CYP2D6 and CYP2C8 risk alleles into a scheme, where possession of a "risk allele" or "factor" can be used to infer the classification as a myalgia responde, and possession of a "protective allele" or "factor" can be used to infer the classification as a normal responder, and lack of a "risk" or "protective" allele or factor bestows upon the individual an inconclusive classification. This scheme partitions the Discovery set of atorvastatin patients in the following way (Table 19):

TABLE 19


[0156] As shown in Table 19, approximately 2/3rds of the patients carried a risk or protective allele and could therefore be classified; of these, 97% were correctly classified using the above classification scheme.


http://www.wipo.int/pctdb/cgi/guest/getbykey5?SERVER_TYPE=19&DB=PCT&QUERY=AN/US2005041326&am....
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COMPOSITIONS AND METHODS FOR THE INFERENCE OF PIGMENTATION TRAITS

37.) The method of claim 36, wherein the race-related gene is at least one of oculocutaneous albinism II (OCA2), agouti signaling protein (ASIP),CYP2D6, tyrosinase-related protein 1 (TYRP1), cytochrome p450-2 (CYP2C9), cytochrome p450-3 (CYP3A4), tyrosinase (TYR), adaptor-related protein complex 3, beta 1 subunit(AP3B1), AP3D1, dopachrome tautomerase (DCT), silver homolog (SILV),AIM-1 protein (LOC51151), proopiomelanocortin (POMC), ocular albinism 1(OA1), microphthalmia-associated transcription factor (MITF), myosin VA(MYO5A),
RAB27A, coagulation factor II (thrombin) receptor-like 1 (F2RL1), HMG CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), aryl hydrocarbon reductase (AHR), or cytochrome p450-1 (CYP1A1), or any combination thereof.

38.) The method of claim 37, wherein the nucleotide occurrence of at least 2 racerelated SNPs is identified, and wherein the method further comprises grouping the identified nucleotide occurrences of the race-related SNPs into at least one racerelated haplotype alleles, wherein the relationship of the haplotype alleles to race is known.

39.) The method of claim 38, further comprising identifying in the nucleic acid sample at least one pigmentation-related haplotype allele of at least a second pigmentation gene of oculocutaneous albinism II (OCA2), agouti signaling protein (ASIP), CYP2D6, tyrosinase-related protein 1(TYRP1), cytochrome p450-2 (CYP2C9), cytochrome p450-3 (CYP3A4), tyrosinase (TYR), melanocortin-1 receptor(MC 1 R), adaptor-related protein complex 3, beta 1 subunit (AP3B 1), AP3D1, dopachrome tautomerase (DCT), silver homolog (SILV), AIM-1 protein (LOC51151), proopiomelanocortin (POMC), ocular albinism 1(OA1), microphthalmia-associated transcription factor (MITF), myosin VA(MYO5A),
RAB27A, coagulation factor II (thrombin) receptor-like 1 (F2RL1), HMG CoA reductase (HMGCR), farnesyl diphosphate synthase (FDPS), aryl hydrocarbon reductase (AHR), or cytochromep450-1 (CYP1A1), or any combination thereof.

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October 02, 2006
Biomarker Discovery & Applications in Drug Development
The FDA has identified the development of new biomarkers as one of the key opportunities to increase efficiency, predictability, and productivity in drug development.

http://barryhardy.blogs.com/theferryman/2006/10/the_fda_has_ide.html