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I don't remember seeing this article from the Pittsburg Tribune posted previously:
http://www.pittsburghlive.com:8000/x/tribune-review/columnists/seate/s_144133.html
Colorblind DNA yields surprises for most
By Mike Seate
TRIBUNE-REVIEW
Friday, July 11, 2003
How many times have you heard a friend, neighbor or co-worker claim an exotic ethnic heritage? "I happen to be one-quarter Cherokee Indian" has nearly become a cultural cliche among people hoping to appear spiritual, earthy and different. It's unlikely you'll hear anyone claiming kinship with Mongols, Uzbeks and other Northern Asian tribes. That heritage is far more common among caucasian families, according to Tony Frudakis, chief scientific officer and founder of Ancestry by DNA.
The Florida firm has run a provocative advertisement in several local publications. The ads ask, "Just how white or black are you?" and offer an Internet address and phone number.
Since opening the DNA testing laboratory last year, Frudakis' team of geneticists has examined the branches of 3,000 family trees. In most cases, customers are surprised at what they learn about great-granddad's personal life.
"The test is basically geared for people who are either adopted and don't know who their parents are, or genealogists and other people with questions about their family roots," said Frudakis, who helped design the testing process used by forensic crime labs.
"Most people come away knowing that our demography is much more complex than they realize," he said.
Liaisons from the distant past resurface through these tests, which cost between $158 and $1,000 -- depending on how deep you want to dig. For example, Frudakis said the overwhelming majority of Scandinavian Europeans who have come in for testing end up learning there's Asian blood -- and lots of it -- in their backgrounds.
"Europeans of Russian or Eastern Scandinavian descent exhibit a significant amount of East Asian blood, dating back to the various Mongol invasions. It's not what people are expecting to hear," he said. The DNA is culled from a saliva sample, which can take the researches back 10,000 to 100,000 years. The process was developed in collaboration with Dr. Mark Shriver at Penn State University's Department of Anthropology.
Gazing into the confusing and often unsettling abyss of ethnic heritage reveals that our differences are more political than racial. Frudakis says the races have been mixing it up for a long time. Descendants of Thomas Jefferson might be in denial about his relationships with his slaves, but such liaisons have left a mark.
Those Cherokee great-grandparents we hear about? Most are myth, Frudakis said. "Most of that comes from a family story or legend. About half the people who think they had Indian ancestors had none."
African-Americans with Indo-European blood or Europeans with Central American ancestry are much more common.
Despite providing people with facts about their racial composition that most of us won't be discussing around the water cooler, Frudakis said he has had just a few customers challenge the test results.
"We've had people question their results," he said. "But after we explain to them that they've always looked at race through a geopolitical lens, and that nature belies racial classifications and doesn't quite work that way, they understand.
"Best of all, it teaches us that science makes it very hard for us to be racist."
bag8ger
Yes, Shriver was largely responsible for the AIMs work (with others), but DNAP have the patent on the AIMs! Funny old world isn't it? As we saw from the earlier post about Shriver's agreement with DNAP, he benefits as well.
As this is my last allowed post today, let me add this:
http://www.ishg.org/members/h_members/rao.htm
Rated one of the top ten scientists of modern India and a living legend in Statics, Professor C.R. Rao is considered as one of the five outstanding workers in the field of Mathematical Statistics. There is virtually no enriched by him. Several fundamental results and theorems now bear his name; e.g.. Cramar Rao inequality, Rao-Blackwell theorem, Fisher-Rao theorem, Scheffe-Lehmann-Rao theorem, Rao's score test, Rao's U test, Rao's Quadratic entropy, Rao's g-invess, Hamming-Rao bound etc. Rao has authored about 300 research papers and 13 books of which his "Lincan Statistical Inference and its application" is a classic one and is translated into five foreign languages and adopted in those countries.
Coming under the influence of Mahalanobis and Fisher early on, Rao's career was intimately linked with the Indian Statistical Institute, first as a Researcher, later as Professor and finally as its Director, eventually giving it an international eminence that is unparalleled in India. Today he occupies the prestigious Eberly chair in Statistics at the Pennsylvania State University at State College, Pennsylvania.
Prof. Rao is the recipient of several honours and awards. Shanti Swarup Bhatnagar Award, Sir Guy Silver Medal, Meghnad Saha Medal, JC Bose Gold Medal, SS Willk's Medal and PC Mahalanobis Birth Century Gold Medal.
He is the founder fellow of Third World Academy of Sciences and has the rare honour of being elected Fellow of three national scientific bodies - Indian national Academy of Sciences U.S.A. He has been honoured with three Fastschrift volumes on his 60th, 70th and 75th birthdays.
His contributions to human genetics and physical anthropology can be traced to the multivariate methods he devised for analysis of the Bengal Anthropometric Survey, the recent generalised Genetic diversity measures and to his two illustrious students Ranajit Chakraborty and D.C. Rao.
bag8ger
Glad to see you got your missing "ger" back!
She is combining her MD and PhD studies. The timescale is a little confusing. Look at this:
"During my first year I developed a rapid method for looking at microsatellite allele frequency differences between populations."
Collins HE, Li H, Inda SE, Anderson J, Laiho K, Tuomilehto J, Seldin MF (2000) A simple and accurate method for determination of microsatellite total allele content differences between DNA pools. Human Genetics, 106:218-226.
I take this to infer that her "first year" (of the PhD work) was 2000. We then see the first paper published March 2002 i.e. this work was done in 2001. When did work on AIMs begin? Well, work on admixture has been going on a long time. This paper is cited a lot:
Chakraborty R, Weiss KM. Admixture as a tool for finding linked genes and detecting that difference from allelic association between loci. Proc Natl Acad Sci U S A. 1988 Dec;85(23):9119-23.
These two papers from 1998 look relevant to me and pre-date the work at Davis:
Parra EJ, Marcini A, Akey J, Martinson J, Batzer MA, Cooper R, Forrester T, Allison DB, Deka R, Ferrell RE, Shriver MD. Estimating African American admixture proportions by use of population-specific alleles. Am J Hum Genet. 1998 Dec;63(6):1839-51.
McKeigue PM. Mapping genes that underlie ethnic differences in disease risk: methods for detecting linkage in admixed populations, by conditioning on parental admixture. Am J Hum Genet. 1998 Jul;63(1):241-51.
What seems to have happened is that Seldin recognized the significance of the AIMs work during 2002. It looks to me as if there has been some communication. I would personally expect some more formal collaboration between Shriver/McKeigue et al and Davis.
Here is another curious thing. At the Rowe Program in Human Genetics, University of California at Davis, they have also been looking at mapping by admixture linkage disequilibrium. Here are the abstracts of two papers.
Collins-Schramm HE, Phillips CM, Operario DJ, Lee JS, Weber JL, Hanson RL, Knowler WC, Cooper R, Li H, Seldin MF. Ethnic-difference markers for use in mapping by admixture linkage disequilibrium. Am J Hum Genet. 2002 Mar;70(3):737-50.
Mapping by admixture linkage disequilibrium (MALD) is a potentially powerful technique for the mapping of complex genetic diseases. The practical requirements of this method include (a) a set of markers spanning the genome that have large allele-frequency differences between the parental ethnicities contributing to the admixed population and (b) an understanding of the extent of admixture in the study population. To this end, a DNA-pooling technique was used to screen microsatellite and diallelic insertion/deletion markers for allele-frequency differences between putative representatives of the parental populations of the admixed Mexican American (MA) and African American (AA) populations. Markers with promising pooled differences were then confirmed by individual genotyping in both the parental and admixed populations. For the MA population, screening of >600 markers identified 151 ethnic-difference markers (EDMs) with delta>0.30 (where delta is the absolute value of each allele-frequency difference between two populations, summed over all marker alleles and divided by two) that are likely to be useful for MALD analysis. For the AA population, analysis of >400 markers identified 97 EDMs. In addition, individual genotyping of these markers in Pima Amerindians, Yavapai Amerindians, European American (EA) individuals, Africans from Zimbabwe, MA individuals, and AA individuals, as well as comparison to the CEPH genotyping set, suggests that the differences between subpopulations of an ethnicity are small for many markers with large interethnic differences. Estimates of admixture that are based on individual genotyping of these markers are consistent with a 60% EA:40% Amerindian contribution to MA populations and with a 20% EA:80% African contribution to AA populations. Taken together, these data suggest that EDMs with large interpopulation and small intrapopulation differences can be readily identified for MALD studies in both AA and MA populations.
Collins-Schramm HE, Chima B, Operario DJ, Criswell LA, Seldin MF. Markers informative for ancestry demonstrate consistent megabase-length linkage disequilibrium in the African American population. Hum Genet. 2003 Jun 3.
Admixture mapping is a potentially powerful tool for mapping complex genetic diseases. For application of this method, admixed individuals must have genomes composed of large segments derived intact from each founding population. Such segments are thought to be present in African Americans (AA) and should be demonstrable by examination of linkage disequilibrium (LD). Previous studies using a variety of polymorphic markers have variably reported long-range LD or rapid decay of LD. To further define the extent and characteristics of LD caused by admixture in the AA population, the current study utilized a set of 52 diallelic markers that were selected for large standard variances between putative representatives of the founder populations. LD was examined in over 250 marker-pairs, including linked markers from four different chromosomal regions and an equal number of matched unlinked comparisons. In the representative founder populations, strong LD was not observed for markers separated by more than 10 kb. In contrast, results indicated significant LD ( P<0.001, D'>0.3) in AA over large genomic segments exceeding 10 centiMorgans (cM) and 15 megabases (Mb). Only marginally significant LD was present between unlinked markers in this population, suggesting that choosing appropriate levels of significance for admixture mapping can minimize false positive results. The ability to detect LD for extended chromosomal segments in AA decayed not only as a function of the distance between markers, but also as a function of the standard variance of the markers. This examination of several genomic segments provides strong evidence that appropriate selection of informative markers is a crucial prerequisite for the application of admixture mapping to the AA population.
Now, they seem to have gone from "Ethnic Difference Markers" to "Markers informative for ancestry" (sounds suspiciously like Ancestry Informative Markers to me). So what happened between March 2002 and June 2003 that might have caused a change in "terminology", and is there a connection back to Shriver?
Collins-Schramm HE, Kittles RA, Operario DJ, Weber JL, Criswell LA, Cooper RS, Seldin MF. Markers that discriminate between European and African ancestry show limited variation within Africa. Hum Genet. 2002 Dec;111(6):566-9.
Markers informative for ancestry are necessary for admixture mapping and improving case-control association analyses. In particular, African Americans are an admixed population for which genetic studies require accurately evaluating admixture. This will require markers that can be used in African Americans to determine if a given genomic region is of European or African ancestry. This report shows that, despite studies indicating high intra-African sequence variation, markers with large inter-ethnic differences have only small variations in allele distribution among divergent African populations and should be valuable for evaluating admixture in complex disease genetic studies.
That name Collins-Schramm keeps appearing. She is one of Michael Seldin's graduate students.
http://mdphd.ucdavis.edu/students.htm
Heather Collins-Schramm - Genetics Graduate Group
I am currently beginning my fifth year of the M.D./Ph.D. program. I chose to integrate my medical and graduate studies, so I split the first two years of medical school (taking them over three years), and at the same time took all my graduate courses and began my Ph.D. research in Dr. Michael Seldin's laboratory. My Ph.D. will be in genetics, and I have a special interest in complex genetic diseases. During my first year I developed a rapid method for looking at microsatellite allele frequency differences between populations. I then used this method to identify markers with large differences between ethnicities that should be useful for a potentially powerful genome screening method known as Mapping by Admixture Linkage Disequilibrium (MALD). I have also examined characteristics of these markers such as allele frequency variations within populations and extent of linkage disequilibrium in various populations. Last I have been using markers to model disease status in analyses to better understand the power and limitations of the MALD method.
One interesting question is how many statin drugs will be covered by statnome when it hits the market. The statin patent gives the strong impression that they developed it against multiple targets, even though two are specifically mentioned, and that it indeed will test against all of them.
Here are two similar articles that discuss the Shriver paper
http://www.eurekalert.org/pub_releases/2003-07/ps-amm071003.php
Public release date: 10-Jul-2003
Contact: A'ndrea Elyse Messer
aem1@psu.edu
Penn State
Ancestry mix may be one key to obesity
Estimating proportions of ancestry may provide clues to genetic influences on obesity, osteoporosis and metabolism, and help public health professionals better educate populations, according to an international team of researchers.
"Studies show that women with European-American ancestry have a higher occurrence of osteoporosis than African-American women," says Dr. Mark D. Shriver, assistant professor of anthropology at Penn State. "African-American women have a higher prevalence of obesity, but it appears not to be as dangerous to their health as it is for European-American women."
Although socially many Americans identify with only one racial/ethnic group, U.S. residents are actually highly mixed. All human populations are closely related and there are very few genes that are different between any two populations. Despite this, there are significant health disparities in the United States with historically disadvantaged populations generally suffering higher prevalences of chronic diseases.
Although it is clear to most biomedical researchers that the primary reason for this difference is differences in wealth, power and privilege, there may be some genetic basis for part of the difference and finding these genes might help researchers to better understand the progression of these diseases and potentially lead to new diagnoses and treatments, according to Shriver.
The Penn State scientist has developed a method to estimate the ancestral proportions of individuals, the percentage of genes that are West African, Native American or European. Researchers can then use this information to investigate the relationships between admixture and various diseases.
In the study, the researchers looked at body mass index – a measure of weight and height, resting metabolic rate, fat mass, fat-free mass and bone mineral density in 145 African-American women from Birmingham, Ala., Baltimore and New York City. They also determined West African ancestry proportion for these women. Determination of West African ancestry was done at Penn State, using 18 ancestry-informative genetic markers.
In the July issue of Obesity Research, the researchers report their analysis of the physical traits and the measure of West African ancestry using two statistical methods. The results showed that there is an association between body mass index -- a measure of obesity -- and West African ancestry. One analytical approach suggests there is also an association between fat mass and fat-free mass and West African ancestry, while the association with bone mineral density is less clear.
"These results support the use of ancestry informative markers when studying differences among admixed populations in complex biomedical traits, particularly when exploring genetic factors influencing these differences," says Dr. Jose Fernandez, assistant professor of nutrition, University of Alabama at Birmingham, and lead author of the published study. "The differences in the prevalence of obesity-related phenotypes among African American females and European American Females could be partly due to genetic factors."
The comparison of resting metabolic rate did not show a significant association, but the researchers believe that the sample size was too small to make this an accurate measure.
Previous studies have explored the relationships of risk for systemic lupus erythematosus and genetic admixture and diabetes and genetic admixture.
"This study supports two things. First, that we are a very mixed country and proportional ancestry is a much more realistic and scientific means to study human variation than is categorical race," says Shriver. "Second, that admixture mapping can and should be an important tool to study both the genetic and environmental causes of obesity."
Beside Shriver and Fernandez, the team included T. Mark Basle, Nashua Rafla-Demetrious, Jeanine Albu, Roland L. Weinsier, David B. Allison, University of Alabama at Birmingham; Esteban Parra, Penn State; Barbara Nicklas, Wake Forest University and University of Maryland; Alice S. Ryan, University of Maryland and Paul M McKeigue and Clive L. Hoggart, London School of Hygiene and Tropical Medicine.
The researchers suggest that expanding the study to larger samples, including environmental measures, increasing the number of markers and looking at other admixed populations like the African Caribbeans is necessary.
http://www.demko.com/m030710.htm
Ancestry Says Whose Least Obese in Chubby Checkered Cultures
Professor David J. Demko, PhD
AgeVenture News Service 07-10-03
Despite our relatively universal genetic code, there are significant differences in health risks among ancestral populations who suffer higher prevalence of chronic diseases such as obesity. Biomedical researchers believe there may be some genetic basis for the health differences. Finding these genes might help researchers better understand the progression of these diseases and potentially lead to new diagnoses and treatments, according to a team of international researchers supported by the National Institutes of Health. One very promising development is the creation of a method that estimates the ancestral proportions of individuals, the percentage of genes that are West African, Native American or European. Developed by Penn State's Dr. Mark D. Shriver, the ancestral method will be used by researchers to better understand the relationships between ancestral-mix and risk to various diseases.
In the July issue of Obesity Research, Dr. Jose Fernandez (University of Alabama), reports there is an association between body mass index (a measure of obesity) and West African ancestry. Estimating proportions of ancestry may provide clues to genetic influences on obesity and help public health professionals better educate populations, according to international research supported by the National Institutes of Health.
"African-American women have a higher prevalence of obesity, but it appears not to be as dangerous to their health as it is for European-American women", says Dr. Mark D. Shriver, professor of anthropology at Penn State. Although many Americans identify with only one racial-ethnic group, U.S. residents are actually highly mixed. All human populations are closely related and there are very few genes that are different between any two populations.
"These results support the use of ancestry informative markers when studying differences among mixed populations in complex biomedical traits, particularly when exploring genetic factors influencing these differences," says Dr. Jose Fernandez, professor of nutrition, University of Alabama. "The differences in the prevalence of obesity-related phenotypes among African American females and European American Females could be partly due to genetic factors."
"This study supports two things", says Shriver. First, we are a very mixed country and proportional ancestry, not categorical race, is a much better means to study human differences. Second, genetic mixture mapping can be an important tool for the study of genetic and environmental causes of obesity.
The researchers suggest that expanding the study to larger samples, including environmental measures, increasing the number of markers and looking at other admixed populations like the African Caribbeans is necessary.
The previous studies referred to in the first article on risk of systemic lupus erythematosus and diabetes are in the following two papers:
http://www.erin.utoronto.ca/~eparra/profile/PDF%20files/Molokhia%20et%20al.,%202003%20%7BSLE%20and%2...
http://www-hsc.usc.edu/~goran/PDF%20papers/130.pdf
Eric Boerwinkle is one of the academics I keep track of. Here are just some of the papers he has co-authored this year:
Huang Q, Fu YX, Boerwinkle E. Comparison of strategies for selecting single nucleotide polymorphisms for case/control association studies. Hum Genet. 2003 Jun 17
Corlova OY, Amos CI, Wang NW, Shete S, Turner ST, Boerwinkle E. Genetic linkage and imprinting effects on body mass index in children and young adults. Eur J Hum Genet. 2003 Jun;11(6):425-32.
Morrison AC, Brown A, Kardia SL, Turner ST, Boerwinkle E; Genetic Epidemiology Network of Arteriopathy (GENOA) Study. Evaluating the context-dependent effect of family history of stroke in a genome scan for hypertension. Stroke. 2003 May;34(5):1170-5. Epub 2003 Apr 24.
Xiong M, Zhao J, Boerwinkle E. Haplotype block linkage disequilibrium mapping. Front Biosci. 2003 May 1;8:A85-93.
Andrade Md M, Fridley B, Boerwinkle E, Turner S. Diagnostic tools in linkage analysis for quantitative traits. Genet Epidemiol. 2003 May;24(4):302-8.
Wu X, Cooper RS, Boerwinkle E, Turner ST, Hunt S, Myers R, Olshen RA, Curb D, Zhu X, Kan D, Luke A. Combined analysis of genomewide scans for adult height: results from the NHLBI Family Blood Pressure Program. Eur J Hum Genet. 2003 Mar;11(3):271-4.
Kardia SL, Rozek LS, Krushkal J, Ferrell RE, Turner ST, Hutchinson R, Brown A, Sing CF, Boerwinkle E. Genome-wide linkage analyses for hypertension genes in two ethnically and geographically diverse populations. Am J Hypertens. 2003 Feb;16(2):154-7.
Province MA, Kardia SL, Ranade K, Rao DC, Thiel BA, Cooper RS, Risch N, Turner ST, Cox DR, Hunt SC, Weder AB, Boerwinkle E. A meta-analysis of genome-wide linkage scans for hypertension:The National Heart, Lung and BloodInstitute Family Blood Pressure Program. Am J Hypertens. 2003 Feb;16(2):144-7.
Turner ST, Boerwinkle E. Genetics of blood pressure, hypertensive complications, and antihypertensive drug responses.
Pharmacogenomics. 2003 Jan;4(1):53-65.
Here is an interesting paper
Fernandez JR, Shriver MD, Beasley TM, Rafla-Demetrious N, Parra E, Albu J, Nicklas B, Ryan AS, McKeigue PM, Hoggart CL, Weinsier RL, Allison DB. Association of African Genetic Admixture with Resting Metabolic Rate and Obesity Among Women. Obes Res. 2003 Jul;11(7):904-911.
Department of Nutrition Sciences and the Clinical Nutrition Research Center and. Department of Biostatistics, Section on Statistical Genetics, The University of Alabama at Birmingham, Birmingham, Alabama. Department of Anthropology, The Pennsylvania State University, University Park, Pennsylvania. Obesity Research Center, St. Luke's/Roosevelt Hospital, Institute of Human Nutrition, Columbia University College of Physicians & Surgeons, New York, New York. Section on Gerontology and Geriatric Medicine and Center for Human Genomics, Wake Forest University School of Medicine, Winston-Salem, North Carolina. Department of Medicine, Division of Gerontology at The University of Maryland School of Medicine and The Geriatric Research Educational Clinical Center, Baltimore VA Medical Center, Baltimore, Maryland. Epidemiology Unit, London School of Hygiene and Tropical Medicine, London, United Kingdom. Deceased.
OBJECTIVE: To investigate the role of genetic admixture in explaining phenotypic variation in obesity-related traits in a sample of African-American women (n = 145) and to determine significant associations between obesity traits and admixture genetic markers. RESEARCH METHODS AND PROCEDURES: Associations between genetic admixture and BMI, resting metabolic rate, fat mass, fat-free mass, and bone mineral density were tested using linear regression considering the estimation of admixture by 1) a maximum-likelihood approach (MLA) and 2) a Bayesian analysis. RESULTS: Both the conservative MLA and the Bayesian approach support an association between African genetic admixture and BMI. Evidence for the associations of African genetic admixture with fat mass and fat-free mass was supported by the Bayesian analysis; the MLA supported an association with bone mineral density. When the individual ancestry informative markers that were used to estimate admixture were tested for associations with BMI, significant associations were identified in chromosomes 1, 11, and 12. DISCUSSION: These results provide evidence supporting the application of admixture mapping methods to the identification of genes that result in higher levels of obesity among African-American women. Further research is needed to replicate and further explore these findings.
Note: BMI is body mass index.
Worktoplay
Interesting post. Let me add a few observations (my comments in italics).
From the last 10Q:
http://www.sec.gov/Archives/edgar/data/1127354/000107087603000069/0001070876-03-000069.txt
We have engaged an investment banking firm to assist us in our efforts to raise debt and/or equity capital in 2003.
http://www.bizjournals.com/tampabay/stories/2003/05/19/focus2.html
At least one Bay area investment banking group is interested in what's coming out of local businesses.
"Our preference is to help local companies," said Dr. Douglas Weiland, managing director and principal at Athena Capital Partners Inc. in Tampa.
Athena also works to relocate life sciences businesses to the Bay area. The firm focuses on investments between $1 million and $20 million, about 70 percent to 80 percent of which are in the life sciences industry.
Weiland, a former orthopedic surgeon, works with local companies such as DNAPrint genomics Inc. in Sarasota...
So, it would appear that Athena are the investment banking group DNAP are working with, and that Gembionics (Gabriel et al) are not involved now in this capacity. BTW, whatever happened to Start-up Florida?
Some quotes from the PR announcing Gabriel’s appointment as President/CEO:
http://www.dnaprint.com/pr_04_09_03.htm
"Having Richard join the Company at this time and help with capitalization and business development allows me to return to the nuts and bolts of research and product development" said Dr. Frudakis.
In addition to Forensics and Consumer genomics, DNAPrint is also focused on developing drug and treatment solutions targeted for specific segments of the patient population. Mr. Gabriel and Dr. Hector J. Gomez, MD, PhD, DNAP Board Chairman, have significant experience in drug development and together, they have completed ten successful New Drug Applications (NDA's).
"Mr. Gabriel brings to DNAPrint extensive and complementary FDA regulatory and compliance expertise, as well as an extensive political and business development network", said Dr. Gomez…Given his considerable experience with development stage companies, his addition will help us accelerate our efforts to expand DNAPrint's products and services."
"Our immediate goals are to make DNAPrint Genomics, Inc. profitable and strategically financed for its future expansion, research and product development. Dr. Tony Frudakis and all the members of the Company are important elements to the Company's success." Mr. Gabriel added. "The single most important resource any company has is its people and their ability to generate novel and patented technologies that satisfy current and future customer needs.
And a quote from Worktoplay's post about Semaphore:
Semaphore services in this space include Clinical Trial review, FDA compliance and certification process monitoring, proof of science concept, and acquisition target validation.
Now, what I think is going on. I agree that there was a change in role for some of these players, and that there may well have been some sort of validation process going on prior to that (on behalf of whom is the question). Gabriel and Gomez are obviously both involved in tactical initiatives (capitalization and business development) as you would expect from the CEO and Chairman. However, I believe that Gomez has more of a focus in this respect and that Gabriel’s main task at the moment is shepherding statnome and/or ovanome through the FDA compliance process. This was hinted at previously. Somebody (Gabriel or Bookbinder perhaps) is also helping Matt Thomas with the forensic accreditation process. In addition there is the “transition” underway. Apart from beefing up areas such as PR (and finance?), which BTW means the company knows or expects revenue increases, what does this mean?
The original model was the node on the tree. Gabriel talked to Arch about DNAP being in the "center of things". Sounds like this model still has some validity, albeit in a slightly different form perhaps. Separation into a number of divisions makes sense, especially if one or more of these will involve either acquisition of another entity, some form of joint venture maybe, or some form or licensing to a third party. The potential divisions are obvious e.g. personal genomics (i.e. Ancestry), consumer genomics (i.e. GeneLink), forensics (i.e. DNAWitness), personalized medicine (i.e. statnome, ovenome …), services (i.e. genotyping, drug design etc), drug development in their own right (perhaps), and R&D. There has to be an umbrella organization providing core services such as sales and marketing, press and investor relations, finance, legal, etc.
Personally I think that a number of things either have already happened or are about to happen. These include the following:
1. A partnership deal signed with a DNA chip maker – at least for AncestryByDNA 3.0 which we know is going to be chip-based.
2. One or more grants awarded, especially on the forensics side.
3. Some sort of formal collaboration with the DOJ, NIJ, FBI, NSA, Department of Homeland Security (pick one or more) with regards to DNAWitness.
4. A tie-in with somebody to effect distribution of one or more of the personalized medicine products.
5. One or more formal collaborations with academic institutions for provision of genotyping services and/or use of the ADMIXMAP platform.
6. One or more agreements related to drug target identification and/or clinical trial design.
7. A formal tie-in with H Lee Moffitt (whose stated modus operandi is to joint venture with 3rd parties to commercialize their technology).
8. Award of multiple patents.
That will do for starters. And meanwhile DNAP is the only entity capable of offering the FDA an objective measure of ancestry, and we seem to be rewriting theories about anthroplogy. Not bad for a start-up penny stock company.
Walter
Thanks, that was the site I quoted for the Cellgenica reference lol. I cannot find anything else on them anywhere else though. Perhaps the name will come up somewhere in the future...
A few bits
I don't think I ever got around to posting these on RB because of all the problems there.
This young man has been doing some IT stuff for us:
http://studentweb.ncf.edu/Homer.Wolfe/documents/HFW_Vitae_01_10_03_I.pdf
Research activities August 2002 to present:
Coordinating efforts with DNA Print Genomics, Sarasota, FL to
produce phenotype prediction software utilizing evolutionary
programming techniques with neural networks. Responsibilities
include development and implementation of non-gradient learning
and network architecture development algorithms.
I think somebody posted something about Clinication the other day:
http://216.239.57.100/search?q=cache:ATfW2p-B8oQJ:www.clinication.com/Clinication%2520Advisory%2520B...
"Prior to 1988, Dr. Gomez was a Senior Director at Merck/MSDRL Corporation. He currently serves on the Board of Directors of Phase 5 Sciences, PRB Pharmaceuticals, and DNAprint Genomics, where he is Chairman of the Board"
PRB Pharmaceuticals are connected to Lee's Pharmaceuticals...
http://www.leespharm.com/ce/media/Ora-Flu.pdf
"Lee’s obtains license from PRB Pharmaceuticals for Virus Infectious Diseases"
...who are connected to Zengen, which Hector was also associated with. Small world!
And here's a quote from Hector Gomez from the Foley & Lardner investor conference he attended on Wednesday:
http://www.foleylardner.com/resourcecenter/r_sem_full.asp?ID=193
Hector Gomez, Chairman/President
DNA Print Genomics/Saneron/Cellgenica
(Forget Saneron, but has anybody heard of Cellgenica?)
http://tech.tbo.com/tech/MGAPZBQ2YHD.html
In Sarasota, DNAPrint Genomics claims its DNA technology may help detectives find criminals. Usually, forensic scientists try to match the DNA of a suspect with the DNA found at a crime scene. But police do not always have both samples; sometimes they have only DNA from the crime scene, said DNAPrint Genomics Chairman Hector Gomez.
With DNAPrint Genomics' technology, scientists can use just one sample of DNA and determine the suspects' race, hair color and eye color, Gomez said.
Two pieces of information
We are one of the featured companies in this CHI Molecular Diagnostics report:
http://www.chireports.com/content/reports/toc/mdx-282.ASP
Andrew Clark (former colleague of Mark Shriver at PSU) has a paper out this month that lends more weight to the importance of population structure for linkage disequilibrium studies:
Clark AG, Nielsen R, Signorovitch J, Matise TC, Glanowski S, Heil J, Winn-Deen ES, Holden AL, Lai E. Linkage Disequilibrium and Inference of Ancestral Recombination in 538 Single-Nucleotide Polymorphism Clusters across the Human Genome. Am J Hum Genet. 2003 Jul 3.
The prospect of using linkage disequilibrium (LD) for fine-scale mapping in humans has attracted considerable attention, and, during the validation of a set of single-nucleotide polymorphisms (SNPs) for linkage analysis, a set of data for 4,833 SNPs in 538 clusters was produced that provides a rich picture of local attributes of LD across the genome. LD estimates may be biased depending on the means by which SNPs are first identified, and a particular problem of ascertainment bias arises when SNPs identified in small heterogeneous panels are subsequently typed in larger population samples. Understanding and correcting ascertainment bias is essential for a useful quantitative assessment of the landscape of LD across the human genome. Heterogeneity in the population recombination rate, rho=4Nr, along the genome reflects how variable the density of markers will have to be for optimal coverage. We find that ascertainment-corrected rho varies along the genome by more than two orders of magnitude, implying great differences in the recombinational history of different portions of our genome. The distribution of rhod4; is unimodal, and we show that this is compatible with a wide range of mixtures of hotspots in a background of variable recombination rate. Although rhod4; is significantly correlated across the three population samples, some regions of the genome exhibit population-specific spikes or troughs in rho that are too large to be explained by sampling. This result is consistent with differences in the genealogical depth of local genomic regions, a finding that has direct bearing on the design and utility of LD mapping and on the National Institutes of Health HapMap project
vision2b, he is also presenting at a Genomics workshop in Lausanne, Switzerland in September:
Mark D. Shriver : "The genomic distribution of human population substructure: Basic and applied population genomics"
http://www.zi.ku.dk/eunet/Pages/Lausanne2003.html
Chris, using one of my remaining two posts for today (lol). It is not clear whether what Harvard/MIT (and others, the University of Southern California for instance) are doing is in collaboration with DNAP in any way, shape or form. It would certainly be nice if this was the case. Also, until and unless the patent is granted, intellectual property is a moot point anyway. At the very least this does show that there is an increasing recognition from researchers that AIMs are potentially very important for disease association studies.
I have been looking at others who work with "ancestry informative markers". Nice to see others using our intellectual property! Here is one project:
http://hst.mit.edu/forum/Hattangadi.html
In this project, a quantitative genotyping methodology has been developed which permits rapid identification of ancestry-informative markers. We have also developed a Hidden Markov Model to measure the size of "ancestry blocks" – regions of the African-American genome of continuous ancestry due to linkage disequilibrium. We have found the ancestry blocks to be in excess of 15 Mb, suggesting far fewer markers are needed for admixture-based disease studies than conventional genetic association studies. We also use the HMM to compute the expected ancestral origin at any point on the admixed chromosome. The model is being applied to two large case-control populations for multiple sclerosis and prostate cancer to identify potential disease-associated loci.
This is part of a research project "Association of Genomic Variations with Complex Trait Diseases" which is overseen by David Altshuler:
http://hst.mit.edu/servlet/ControllerServlet?handler=ResearchHandler&action=view&topicID=180...
A recent hypothesis suggests that genetic differences which are common in the human population play a significant role in the genetic risk for common diseases, such as hypertension, cancer, and diabetes. We are characterizing these common genetic variations at the nucleotide level, and studying their association with complex trait diseases. We take advantage of the linkage disequilbrium caused by recent admixture of genetically divergent populations; this allows the use of fewer markers to find genetic variations that are enriched in affected individuals.
DougS
The rootsweb discussions are fascinating are they not. It is a shame that one or two of the posters there seem to have killed this off as far as Tony Frudakis's participation is concerned. The guy at Columbia University in particular clearly has some personal issues to address...
This looks much better doesn't it eom