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Here are a couple of NIH Grants awarded to Dr Yeatman in 2003, the first of which is particular relevant to the PR:
Grant Number: 1R21CA101355-01A1
PI Name: YEATMAN, TIMOTHY J.
PI Email: yeatman@moffitt.usf.edu
PI Title: PROFESSOR OF SURGERY, BIOCHEMISTRY AND M
Project Title: Molecular Profiling to Predict Response to Chemotherapy
Abstract: DESCRIPTION (provided by applicant): Because of the relative ineffectiveness of systemic chemotherapy, the majority of therapeutic agents are delivered to many patients to actually benefit only a few. This defensive treatment strategy is also driven by the paucity of effective surrogate markers predicting response. Even molecularly targeted therapies may have relatively poor response rates in the presence of the known target. In order to change the current practice, effective predictors of response are needed. We have recently developed a family of molecular classifiers capable of predicting histological origin of 21 different tumor types with a high degree of accuracy. We hypothesize that, using a genome-wide gene expression profiling strategy similarly effective classifiers can be built to recognize chemosensitive tumors. This proposal will fund a Phase II trial of standard chemotherapy for metastatic colorectal cancer that will seek to identify molecular fingerprints common to chemosensitive tumors. Because there are now two equally effective regimens (FOLFOX vs FOLFIRI) available for first line therapy of metastatic colon cancer, we will seek to derive an expressed genetic profile that will predict response to a more practical modification of each of these regimens (XELOX vs CAMCAPE) with a high degree of accuracy. Furthermore, we will determine if the subset of patients responding to CAMCAPE is the same as the subset responding to XELOX. Finally, we will validate the expression and characterize the function of informative genes useful in tumor classification.
Thesaurus Terms:
antineoplastic, colorectal neoplasm, human therapy evaluation, neoplasm /cancer chemotherapy, neoplasm /cancer classification /staging, neoplasm /cancer genetics, pharmacogenetics
clinical trial phase II, functional /structural genomics, gene expression, irinotecan, molecular biology information system
biopsy, clinical research, computer assisted sequence analysis, human subject, patient oriented research
Institution: H. LEE MOFFITT CANCER CTR & RESEARCH INS
AND RESEARCH INSTITUTE, INC.
TAMPA, FL 336129497
Fiscal Year: 2003
Department:
Project Start: 12-SEP-2003
Project End: 31-AUG-2005
ICD: NATIONAL CANCER INSTITUTE
IRG: CONC
Grant Number: 1R01CA098522-01
PI Name: YEATMAN, TIMOTHY J.
PI Email: yeatman@moffitt.usf.edu
PI Title: PROFESSOR OF SURGERY, BIOCHEMISTRY AND M
Project Title: Screening for Breast Cancer Using Molecular Signatures
Abstract: DESCRIPTION (provided by applicant): Currently, there are no molecular screening tools available that can identify the patients at high risk for breast cancer development or local recurrence. Of interest, however, is that numerous studies have suggested the existence of genetic alterations (LOH, chromosomal abnormalities, specific gene mutations) in histological non-malignant breast tissue, identical to those found in adjacent tumor, in up to 60% of patients. These data suggest that there are numerous genetic alterations that accumulate prior to the histological development of cancer, although the frequency, identity, and location of these alterations within the normal appearing breast are still poorly understood. We hypothesize that genetic alterations exist in non-malignant breast tissue and that they will produce phenotypic alterations in gene expression that may be useful in predicting breast cancer risk. cDNA microarrays will be used to identify a set of genes whose expression profile predicts cancer risk in histologically non-malignant breast tissue. As a first step towards the detection of molecular screening markers for sporadic breast cancer, we plan to investigate the non-malignant breast tissue adjacent to cancer in patients known to be at increased risk for cancer recurrence both in the ipsilateral and contralateral breasts. This will be accomplished by a comprehensive analysis of genetic, epigenetic and gene expression alterations performed simultaneously on breast tumors and normal associated breast tissue. Whereas the principal goal is identifying a gene expression pattern for normal tissues at high risk for developing cancer, we will also develop rich databases to decipher patterns characterizing breast tumors and their clinicopathologic features (including survival and recurrence data) as well as benign breast pathology. We then plan to evaluate the behavior of these high-risk genes in patients undergoing adjuvant therapy to reduce cancer risk. Specific Aim I. To identify the frequency and geographic distribution of abnormal genetic (DNA), epigenetic (DNA methylation) and molecular (RNA) signatures, within zones of histologically non-malignant breast tissue adjacent to invasive cancer derived from mastectomy specimens (n = 100). Specific Aim II. Determine if genetic and epigenetic alterations as well as gene expression alterations identified in Aim I can be detected in the contralateral normal breast in patients undergoing bilateral mastectomy for ipsilateral cancer(n = 50). Specific Aim III. To identify genetic, epigenetic and gene expression alterations in normal and tumor tissues from patients undergoing mastectomy for intraductal neoplasia (n = 50). Specific Aim IV. Determine if the expression of high-risk gene sets (identified in Aims I, II, and III) in the contralateral, untreated breast are affected by adjuvant chemotherapy and/or hormonal therapy in serial biopsy specimens (n = 50) taken pre- and post- therapy.
Thesaurus Terms:
breast neoplasm, breast neoplasm /cancer diagnosis, genetic marker, molecular oncology, neoplasm /cancer genetics
DNA methylation, neoplasm /cancer therapy
biopsy, clinical research, female, human subject, human tissue, patient oriented research, tissue resource /registry
Institution: H. LEE MOFFITT CANCER CTR & RESEARCH INS
AND RESEARCH INSTITUTE, INC.
TAMPA, FL 336129497
Fiscal Year: 2003
Department:
Project Start: 18-AUG-2003
Project End: 31-JUL-2008
ICD: NATIONAL CANCER INSTITUTE
IRG: CONC
Remember Hong-Gang Wang?
Chen T, Yang I, Irby R, Shain KH, Wang HG, Quackenbush J, Coppola D, Cheng JQ, Yeatman TJ. Regulation of caspase expression and apoptosis by adenomatous polyposis coli. Cancer Res. 2003 Aug 1;63(15):4368-74.
Here are some of his recent papers:
The future of cancer management: translating the genome, transcriptome, and proteome. Yeatman TJ. Ann Surg Oncol. 2003 Jan-Feb;10(1):7-14.
Department of Surgery, H. Lee Moffitt Cancer Center, University of South Florida, Tampa, Florida 33612, USA. yeatman@moffitt.usf.edu
Predicting who will develop cancer and how the cancer will behave and respond to therapy after diagnosis are some of the potential benefits of the ongoing genetic revolution that can be envisioned within the next decade. Translational applications of genomic-based research efforts may actually precede the development of effective therapeutic agents that can exploit the vast amounts of data derived from these efforts. In the future, understanding the wealth of information generated by high-throughput molecular efforts and how it can be applied to clinical problems will likely be critical to the surgeon who guides the multidisciplinary care of the cancer patient. This review will discuss the advances in our understanding of the human genome (DNA), its derived transcriptome (RNA), and its translated proteome (proteins) and will focus on the translation of this information into routine clinical practice. In particular, we will focus on the potential for clinical application of microarray-based gene-expression profiling to the diagnosis, prognosis, and therapy of malignancies.
The future of clinical cancer management: one tumor, one chip. Yeatman TJ. Am Surg. 2003 Jan;69(1):41-4.
Department of Surgery, H. Lee Moffitt Cancer Center, University of South Florida, 12902 Magnolia Drive, Tampa, Florida 33612, USA.
Recent advances in gene expression profiling technology have now made it feasible to consider using microarray technology in the routine management of the cancer patient. Microarray chips are now capable of interrogating up to 48,000 or more different genes in a single experiment using multiple platforms. Sophisticated data analysis has already demonstrated that multiple tumor types can be distinguished on the basis of their gene expression patterns. These analyses have led to the detection of new tumor markers and markers of tumor progression. Gene expression arrays have also been demonstrated to be capable of predicting the survival of patients with breast cancer, lung cancer, brain cancer, and acute lymphocytic leukemia. The future holds great promise for the rapid development of molecular medicine with diagnosis, prognosis, and even therapy being based on a single microarray chip. These developments signal a significant paradigm shift in the clinical management of human cancer.
Osteopontin and colon cancer progression. Yeatman TJ, Chambers AF. Clin Exp Metastasis. 2003;20(1):85-90.
H. Lee Moffitt Cancer Center, Tampa, Florida 33612, USA. Yeatman@moffitt.usf.edu
Human colon cancer affects nearly 150,000 patients and results in 60,000 deaths in the United States per year. Despite significant advances in the management of the colon cancer patient, little change in survival rates has been appreciated over the past 50 years. The primary cause of death relates to the development of distant metastases to organs such as the liver and lungs. Colon cancer represents an important disease to study in order to better understand tumor progression and metastasis primarily because there is almost a stepwise advancement of the disease that is marked by measurable genetic and associated phenotypic alterations. Metastasis appears to be the end product of the development of 'Herculean' cell clones capable of independent growth, invasion, adhesion, avoidance of apoptosis, and angiogenesis. Although significant progress has been made in understanding the sequential genetic events leading to the development of cancer, the precise genes and the associated molecular pathways underlying the development of metastatic potential are still poorly understood. Moreover, our enhanced genetic knowledge has had relatively little trickle down effect on our clinical management of this deadly disease. For this reason, we undertook a comprehensive study to develop a molecular encyclopedia of new tumor markers and markers of tumor progression, some of which will hopefully prove useful in the clinical management of colon cancer patients by means of their capacity to detect and predict the stage and disease burden. This review will focus on the application of gene expression profiling technology to the problem of identifying new tumor markers and progression markers, and the discovery of osteopontin as the leading candidate clinical marker derived from a screen of approximately 12,000 named genes.
Multi-platform, multi-site, microarray-based human tumor classification. Bloom G, Yang IV, Boulware D, Kwong KY, Coppola D, Eschrich S, Quackenbush J, Yeatman TJ. Am J Pathol. 2004 Jan;164(1):9-16.
H. Lee Moffitt Cancer Center, University of South Florida, Tampa, Florida 33612-9497, USA.
The introduction of gene expression profiling has resulted in the production of rich human data sets with potential for deciphering tumor diagnosis, prognosis, and therapy. Here we demonstrate how artificial neural networks (ANNs) can be applied to two completely different microarray platforms (cDNA and oligonucleotide), or a combination of both, to build tumor classifiers capable of deciphering the identity of most human cancers. First, 78 tumors representing eight different types of histologically similar adenocarcinoma, were evaluated with a 32k cDNA microarray and correctly classified by a cDNA-based ANN, using independent training and test sets, with a mean accuracy of 83%. To expand our approach, oligonucleotide data derived from six independent performance sites, representing 463 tumors and 21 tumor types, were assembled, normalized, and scaled. An oligonucleotide-based ANN, trained on a random fraction of the tumors (n = 343), was 88% accurate in predicting known pathological origin of the remaining fraction of tumors (n = 120) not exposed to the training algorithm. Finally, a mixed-platform classifier using a combination of both cDNA and oligonucleotide microarray data from seven performance sites, normalized and scaled from a large and diverse tumor set (n = 539), produced similar results (85% accuracy) on independent test sets. Further validation of our classifiers was achieved by accurately (84%) predicting the known primary site of origin for an independent set of metastatic lesions (n = 50), resected from brain, lung, and liver, potentially addressing the vexing classification problems imposed by unknown primary cancers. These cDNA- and oligonucleotide-based classifiers provide a first proof of principle that data derived from multiple platforms and performance sites can be exploited to build multi-tissue tumor classifiers.
Correlation of osteopontin protein expression and pathological stage across a wide variety of tumor histologies. Coppola D, Szabo M, Boulware D, Muraca P, Alsarraj M, Chambers AF, Yeatman TJ. Clin Cancer Res. 2004 Jan 1;10(1 Pt 1):184-90.
Department of Pathology, University of South Florida College of Medicine, Tampa, Florida, USA.
PURPOSE: Osteopontin (OPN) is an integrin-binding protein overexpressed in various experimental models of malignancy and appears to be involved in tumorigenesis and metastasis. Although various studies have assessed OPN protein levels in several tumor types, a broad survey of OPN expression in human neoplasia under the same experimental conditions has not been carried out. EXPERIMENTAL DESIGN: We used immunohistochemistry to detect OPN in a selection of 350 human tumors and 113 normal tissues, from a variety of body sites, using stage-oriented human cancer tissue arrays. Tumors included malignancies from breast (26), ovary (22), endometrium (14), esophagus (10), stomach (11), pancreas (16), bile duct (1), liver (9), colon (20), kidney (53), bladder (33), prostate (28), head and neck (60), salivary glands (14), lung (17), skin (6), and brain (10). RESULTS: High cytoplasmic OPN staining was observed in 100% of gastric carcinomas, 85% of colorectal carcinomas, 82% of transitional cell carcinomas of the renal pelvis, 81% of pancreatic carcinomas, 72% of renal cell carcinomas, 71% of lung and endometrial carcinomas, 70% of esophageal carcinomas, 58% of squamous cell carcinomas of the head and neck, and 59% of ovarian carcinomas. Although OPN expression was identified in a good number of bladder, prostate, and brain tumors, the majority of 6 skin cancers, 11 of 14 salivary gland cancers, 2 thyroid carcinomas, and 23 of 26 breast cancers revealed low OPN positivity or were negative. When considering all sites, OPN expression significantly correlated with tumor stage (Spearman's correlation coefficient, P = 0.0002). OPN score and stage were also significantly correlated for specific cancer sites including bladder (P = 0.01), colon (P = 0.004), kidney (P = 0.0001), larynx (P = 0.035), mouth (P = 0.046), and salivary gland (P = 0.011). CONCLUSIONS: This study reports the broad distribution of OPN in human tumors from different body sites, suggesting involvement of this protein in tumor formation. The strong correlation between pathological stage and OPN across multiple tumor types suggests a role for OPN in tumor progression.
Osteopontin identified as colon cancer tumor progression marker. Agrawal D, Chen T, Irby R, Quackenbush J, Chambers AF, Szabo M, Cantor A, Coppola D, Yeatman TJ. C R Biol. 2003 Oct-Nov;326(10-11):1041-3.
Department of Cell Biology, H. Lee Moffitt Cancer Center, University of South Florida, Tampa, FL, USA.
Identifying molecular markers for colon cancer is a top priority. Using a pooled sample approach with Affymetrix GeneChip technology, we assayed colon cancers derived from a series of clinical stages to identify molecular markers of potential prognostic value. Of 12000 genes assessed, osteopontin emerged as the leading candidate tumor progression marker. Osteopontin is a secreted glycoprotein known to bind integrins and CD44. Its actual molecular function remains elusive but its increased expression correlates strongly with tumor progression.
Chris, yes as somebody on RB said big deal, we've seen all this before; major cancer institution signs big agreement with development stage company. I wonder why they didn't just go with McKeigue's ADMIXMAP?
Joy, yes it came as a complete surprise lol. ;)
Miss Scarlet, all the "validation" we need! It's more than I hoped for with Moffitt. Wonderful news.
How about that? Well done longs! eom
This article appeared in an NC periodical on Friday:
http://wilmingtonjournal.blackpressusa.com/news/Article/Article.asp?NewsID=40881&sID=20
GENOMED APPEALS TO AFRICAN AMERICAN COMMUNITY TO DECREASE NEEDLESS DEATHS CAUSED BY KIDNEY DISEASE, WEEK OF MARCH 18-MARCH 24, 2004
by SPECIAL TO THE WILMINGTON JOURNAL
The Wilmington Journal
Originally posted 3/26/2004
GenoMed, Inc. (OTC: GMED), a Next Generation Disease Management™ company that uses its expertise in genes to improve patient outcomes, today appealed to the nation’s African-American community to consider alternatives to significantly reduce the ten-fold higher risk that the average Black man has of kidney failure, and death, compared to the average White citizen.
High blood pressure, a precursor to kidney disease and the need for dialysis, is twice as prevalent among African Americans compared to whites.
But even that data cannot explain why type 2 diabetes is so prevalent among African Americans, along with people of Hispanic heritage and Native American communities.
“Kidney failure often begins while a patient is still being treated by a primary care physician for diabetes or high blood pressure,” said David W. Moskowitz, M.D., GenoMed Chairman, CEO and Chief Medical Officer. “If we can treat this patient earlier, with our patent-pending Clinical Outcomes Improvement Program™, before the person has lost more than half of their kidney function, we can restore lost kidney function…and save lives.”
Dr. Moskowitz has written extensively on this topic in major peer-reviewed journals. GenoMed’s CEO majored in Chemistry (summa cum laude) at Harvard College, Biochemistry (first class honors) at Merton College, Oxford, and received an MD (cum laude) from the Harvard-MIT Division in Health Sciences and Technology (Harvard Medical School). He trained for seven years in Internal Medicine and Nephrology at Washington University School of Medicine in St. Louis before spending 11 years on the faculty of St. Louis University School of Medicine. He is a noted pioneer in the field of medical genomics, and has been recognized for his groundbreaking treatment of diseases associated with the angiotensin I-converting enzyme, such as chronic renal failure due to hypertension or type II diabetes.
“It so saddens me when I read about an important Black individual, such as the noted singer Barry White, losing his kidneys due to high blood pressure because I know that we, as a nation, can do so much more to alleviate this public health emergency. Continued silence on this issue is a grave disservice to people of color who go on dialysis on rates far exceeding whites.
They need to know that a cure is available,” Dr. Moskowitz said.
Dr. Moskowitz said he, and GenoMed, are available to discuss the issue with primary care physicians, who can be trained in GenoMed’s treatment, and with leaders in the Black, Hispanic and Native American communities. “We truly want to prevent more people from needlessly dying, or suffering, not just well known celebrities but anyone in these communities whom we can help,” GenoMed’s CEO said.
Bag8ger, what an extraordinary coincidence. GTG are obviously aware of DNAP (Richard Gabriel having purportedly had discussions about license fee payments), and you might think that GTG would perhaps want to offer other forensic products to Autralian law enforcement agencies...
OT GTG to offer forensic tests
http://www.theage.com.au/articles/2004/03/26/1079939856249.html
Genetic Technologies passes forensic test
By Eli Greenblat
March 27, 2004
Genomics and genetics researcher Genetic Technologies has become the first public company to win approval to offer DNA analysis services in forensic science.
The venture is a new string to GTG's bow and will deliver it a fresh revenue stream.
Executive chairman Mervyn Jacobson said that initially the company would be involved with state government and police forensic science laboratories, some of which had significant backlogs of specimens awaiting DNA testing.
"These labs have also indicated a willingness to subcontract this work to Genetic Technologies to help clear their backlogs," Dr Jacobson said. "This could potentially involve tens of thousands of specimens now being referred to Genetic Technologies for analysis."
The company said it was expanding its laboratory testing facilities with new robotic equipment and was taking on more specialist scientists.
GTG has focused on licensing non-coding patents on human DNA to biotech and pharmaceutical companies. It also conducts genetic testing in animals for pedigree and disease susceptibility, performs human molecular diagnostics and tests agricultural specimens.
The company recently reported an interim net loss of $5.1 million, up from a loss of $1.7 million for the previous corresponding period. Revenue for the first half of 2003-04 was down 49 per cent to $2.46 million.
Shares in GTG closed up 1.5¢ at 43¢ yesterday.
OT A good spam article. It's just a matter of time...
http://www.technologyreview.com/articles/wo_johansson032604.asp?trk=nl
A Better Way To Squelch Spam?
An open-source scheme would impose a computational "cost" on junk mailers while leaving legitimate users of e-mail alone.
By Eric S. Johansson and Keith Dawson
March 26, 2004
Over the past few months, major players in the world of e-mail have proposed schemes for combating the rising tide of spam. In December, for example, Yahoo! proposed an approach called DomainKeys for validating which messages come from which e-mail servers. In January, speaking to journalists at the World Economic Forum in Davos, Switzerland, Microsoft chairman Bill Gates suggested using a sender-pays system, with money-based e-mail stamps. And at the RSA security conference in February, Gates touted as a spam solution Microsoft’s Caller ID—a variation on the Sender Policy Framework (SPF), which is an anti-spoofing technique that reduces the ability to falsify "From" addresses in e-mail messages.
Unfortunately, upon close examination these techniques turn out to be unworkable or ineffective. They represent centralized solutions that serve the needs of large Internet service providers and, less directly, of large advertisers. Such ideas would be only marginally effective against spam. Worse, they would break services users count on.
Where these proposals fail is in depending on centralized infrastructure and control. Services on the Internet have been widely adopted only when they have embraced decentralized operation. We are developing a spam-blocking solution called Camram that avoids the problems inherent with centralization.
Yahoo!, Microsoft, and the SPF working group are all backing competing proposals that have been characterized as “designated sender." (America Online has endorsed and is experimenting with the SPF version.) They all attempt to give a receiving e-mail server a way to determine whether the "From" address on an incoming message has been forged.
These anti-spam methods, if widely adopted, would certainly devalue one important tool in the spammers’ current repertoire. We should keep in mind, however, that spammers have many tools. The best these techniques can do is to keep a spammer from using your domain (or AOL’s, or Yahoo!’s) as a "From" address. Spammers could legally acquire thousands of valid domains at little cost, provide valid SPF and Caller ID records for them, and discard them when they drew the attention of spam-fighting organizations.
Such designated sender techniques have other drawbacks as well. One problem is that legitimate mailing lists would become difficult to operate. Another is that e-mail forwarding services, such as those supplied by MIT alumni and other affinity groups, would be broken.
Postage Without Money
The idea of fighting spam on an economic basis using some form of postage has been discussed since 1992. This technique is known as sender-pays because it forces the sender to incur some cost before sending a message. Sender-pays systems can employ one of two different types of postage: money stamps, such as what Gates has proposed, or proof-of-work stamps.
Money stamps are a kind of electronic micropayment. Since the dawn of the Internet era, dozens of micropayment schemes have been proposed. Building the centralized infrastructure required for a worldwide micropayment system is a daunting challenge, however. Not surprisingly, none of these systems has taken off. And there is no reason to believe that value-bearing e-postage would fare any better than its predecessors.
Money stamps raise other significant issues: Who redeems the stamp? Who has taxing authority on the income? Who bears legal liability for erroneous or absent stamp validation? Who controls access to your mailbox and for how big a stamp? These questions make it clear why we and many others distrust money stamps as a solution to spam.
A proof-of-work stamp—or “work stamp”—is a mathematical puzzle that is hard to solve and has a solution that is easy to verify. Another important property of this puzzle is that it has no cheats—that is, there is no way to solve the puzzle by a shortcut.
The major impediment to adoption of any form of sender-pays has been the apparent requirement for wholesale changes to the e-mail system. The Camram (Campaign for real mail) open-source project has developed a hybrid system that solves the problems of classical sender-pays and provides a clear path to incremental adoption. Avoiding problematic money stamps and using proof-of-work stamps, Camram deters spam while maintaining decentralized operation.
The cheat-proof puzzle used by the Camram project is called “hashcash." The details of hashcash are complex, but here's a quick explanation. Hashcash uses a seed value consisting of date, e-mail address, and a random number. This seed is fed to a mathematical function called a "hash." The function performs a calculation based on the input. If the first N bits of the returned number are 0, then the input value is the stamp. Otherwise the input value is incremented by one and the process is repeated until the result is a valid stamp (0 bits in the first N places).
The process of solving such a puzzle is analogous to trying to open a safe when you have only the first two numbers of its combination. The only way to solve the puzzle is to try each of the possible remaining combinations until you find the one that works. The salient features of such stamps are that they require a significant amount of CPU time to generate and demand no central infrastructure. (More details on hashcash can be found here.)
Generating stamps should impose no appreciable penalty on ordinary users, while slowing down spammers so much that their operations become unprofitable. The 23-bit stamps currently used by the Camram project take about 15 seconds to generate on a modern computer. Microsoft has in its research labs a project focused on work stamps called Penny Black, but the company has not announced any product plans for this classical sender-pays technology.
The Camram project has coined the term “hybrid sender-pays” to describe a system in which work stamps are combined with other anti-spam techniques in a “cocktail” that stops unwanted e-mail from reaching your inbox while enhancing your ability to communicate with people you know. Mail that arrives without a stamp has the same chance of getting through to your inbox as ordinary mail does in the current anti-spam environment.
The Camram project has learned that the most effective anti-spam cocktail contains at minimum three filters: a stamp filter, a smart "white list," and a content filter. The white list is a roster of those with whom you exchange e-mail; it is used to let this friendly mail in unchallenged. The content filter looks at the content of the message and makes a probabilistic assessment as to whether the message is spam. Taken together, these three measures implement the principle of “strangers pay, friends fly free.” In other words, strangers who stamp their mail, and friends with whom you regularly communicate, have easy access to your inbox. All others go through the content filter.
To understand hybrid sender-pays techniques by analogy to the real world, imagine a postal system that delivers anything to anybody—for no cost. The Camram filters would function something like an administrative assistant. This assistant passes to you, unopened, mail from friends, as well as all mail, regardless of sender, bearing a valid stamp. After reading the remainder, the assistant tosses the junk, delivers the good mail, and asks your opinion about the questionable mail.
Camram’s hybrid sender-pays system has several advantages over other anti-spam techniques. It is completely decentralized: stamps can be generated and validated at any point in the process, and even offline. It is incrementally adoptable: it benefits the first user, and benefits accrue as the number of users grows. And the techniques can be used over a wide range of configurations, from the individual through the enterprise and ISPs.
The two most common objections to sender-pays systems are the impact on mailing lists and the risks from “zombie” systems generating stamps. Mailing lists present spammer-like loads to an e-mail system, and therefore Camram-like systems would indeed slow them down. The short-term solution is not to use stamps on mailing-list messages—let them traverse the content filter and, after a short time, the recipients’ training of their filters will assure that such messages pass through unhindered. The longer-term solution is to employ a different kind of stamp based on cryptographic signatures. Such signature stamps present a much lower computational load than work stamps and therefore could be used by mailing lists and other bulk mailers to identify themselves to list members as “friends.”
The zombie challenge comes from security flaws in Microsoft software. In the last year, as many as 1.5 million systems running Windows XP or Windows 2000 have been taken over in virus or worm attacks. By some estimates as much as half of all spam sent today is relayed through such zombies.
Even if spammers controlled all of these systems—which is almost certainly not the case—they still would lack the computational power to generate enough 23-bit stamps to deliver today’s volume of spam. And if spammers do begin exploiting zombies to generate stamps, the computational cost of a stamp could easily be raised by increasing the number of bits in a valid stamp. (Individual Camram users are able to decide how many bits comprise an acceptable stamp.) Every additional bit doubles the workload for the spammer.
Hybrid sender-pays systems as exemplified by the Camram project have the potential to make e-mail friendly again. Worries about e-mail from business associates or friends and family going astray become a thing of the past. The work of slogging through a spam trap to recover miscategorized messages is significantly reduced. Good e-mail gets through and bad e-mail is filtered, and these benefits ensue with an absolute minimum of extra work on the part of the email recipient. If compatible sender-pays systems become widely deployed, spammers will have to begin to look for another line of work.
And it looks like Paul McKeigue's email address has changed...
W2P, what impresses me is the number of different traits that are being examined: skin pigmentation, metabolic rate/exercise, obesity, insulin related phenotypes etc. BTW, did you notice that even Mike Seldin's group now refer to AIMs (rather than Ethnic Difference markers):
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. Epub 2002 Feb 11.
Collins-Schramm HE, Chima B, Morii T, Wah K, Figueroa Y, Criswell LA, Hanson RL, Knowler WC, Silva G, Belmont JW, Seldin MF. Mexican American ancestry-informative markers: examination of population structure and marker characteristics in European Americans, Mexican Americans, Amerindians and Asians. Hum Genet. 2004 Feb;114(3):263-71. Epub 2003 Nov 20.
There are some interesting updates in Jose Fernandez's CV:
http://138.26.176.127/People/CV/JFernandezCV.pdf
Active grants:
4/1/2004 – 3/31/09 Fernandez, J.R. (principal investigator) NIH/NIDDK 1 R01 DK067426-01 Admixture Mapping for Insulin Complex Outcomes. This study explores the contributions of ancestral genetic markers to diabetes-related traits in a sample of children of African-, European-, and Hispanic-American descent.
(This one is so new it is not even on the NIH CRISP database)
In press:
Fernández, J. R. & Shriver, M. D. (in press) Using genetic admixture to study the biology of obesity traits and to map genes in admixed populations. Nutrition Reviews
PRESENTATIONS
Fernandez, J.R. The Role of Genetic Admixture in Racial/Ethnic Differences in Obesity. Invited oral symposium at NAASO, 2003, Fort Lauderdale, FL.
Fernandez, J.R., Jones, A., Shriver, M.D., Albu, J., & Allison, D.B Genetic Admixture is Associated with Visceral Adipose Tissue in Puerto Rican Women. Oral presentation at NAASO, 2003, Fort Lauderdale, FL.
Beasley MT, Fernandez JR, Holt J, Allison DB. Using Genetic Admixture to Control Residual Confounding. Oral presentation at the NAASO 2003, Fort Lauderdale, FL.
Lara-Castro, C., Hunter, G.A., Lovejoy, J., & Fernandez, J.R. (2003) Association of the ApoA-II -265T to C Polymorphism and Levels of Visceral Fat in African-American and Caucasian Women. Oral presentation at NAASO, 2003, Fort Lauderdale, FL.
This is a good general site as well:
http://www.doegenomes.org/
In particular these linked pages:
http://www.ornl.gov/sci/techresources/Human_Genome/publicat/primer2001/index.shtml
http://www.ornl.gov/sci/techresources/Human_Genome/posters/beyondhgp/index.shtml
There are lot of other bits and pieces and links on this site.
Tony is now a fully paid-up member of the Association of Forensic DNA Analysts and Administrators (AFDAA):
http://www.afdaa.org/lmember1b.html
This is interesting. I wonder if there is any connection through Jerry Wicks of Senecio, given that they are both connected with Bowling Green State University? I wonder what Dr Gavini's role (if any) is with DNA Phenomics now that Dr Aziz has been appointed CSO?
Talking of pictures, here are two more of Rxirish with James Watson at the U of M Biological Station in Michigan (yes, THE James Watson).
Pictures from Roger's website:
http://www.chalberweid.ch/dnap/DNAP_Meeting/meeting.html
The answers:
Tony Frudakis
Worktoplay, Richard Gabriel, Rxirish
Mark Shriver
Zach Gaskin
Karin A. McMurtie
DC Rao (DNAP Scientific Advisor)
Ranajit Chakraborty (?)
Phil Brooks
Homer Wolfe (?)
Homer Wolfe (unmasked)
Gurinder Shahi (???)
Ramin Mirhashemi (DNAP Scientific Advisor, Ovanome)
Tony Frudakis, IFIDA, Dave Moskowitz
Arch
Sharon Shriver (Mark's wife)
Hong-Gong Wang (Ovanome project collaborator)
J Fernando Arena (DNAP Scientific Advisor)
J Fernando Arena (again - check out the site this one comes from)
Esteban Parra (University of Toronto - Shriver collaborator)
Rick Kittles (Howard University - Shriver collaborator)
Kateryna Makova (PSU - Shriver collaborator)
For the real aficionado
How many can you name?
Hadn't seen this one. Zach is a busy man. Does this mean that Karin A. McMurtrie works for DNAP?
Herald Tribune article
http://www.heraldtribune.com/apps/pbcs.dll/article?AID=/20040320/BUSINESS/403200485/1200
DNAPrint makes presentation to attorneys group
STAFF REPORT
SARASOTA -- DNAPrint Genomics flexed its new forensics muscle at a conference this week for some of nation's prosecuting attorneys.
The company presented its "DNAWitness" product during the National District Attorneys Association board of directors meeting in Fort Lauderdale. The conference started Thursday and runs though today.
While DNAPrint might be best known locally more for its "ANCESTRYbyDNA 2.5" -- a test that allows genealogy enthusiasts to check their racial ancestry -- it might be making bigger waves in law-enforcement circles with the forensics version.
Last year, the Sarasota-based biotechnology's product helped solve a prominent serial killing case in Louisiana.
More recently, it led to a break in another case, this time the Trail Side murder in Concord, Calif. The test, which analyzes bodily fluids to determine a person's racial composition, helped Concord police make an arrest of a suspect in the May 13 slaying of Kathleen Aiello Loreck.
Pressing flesh with prosecutors helps get the world out about the applicability of DNAWitness in some snarly criminal cases, the company said.
"Primarily, DNAWitness cases come from the crime labs, detectives and prosecutors," said Zach Gaskin, DNAPrint's technical director of forensics, who attended the conference. "Every agency in the U.S. has at least one case, if not more, where this technology can, and should, be applied."
Earlier this year, DNAPrint announced a more powerful version of its ANCESTRYbyDNA that provides much more accurate information in determining what proportion of a person's DNA comes from American Indian, East Asian, Indo-European or West sub-Saharan African stock.
Despite its growing prominence, DNAPrint is still working toward profitability. It recorded losses of $5.5 million during the first nine months of 2003.
Its over-the-counter stock was selling for 4.6 cents at the close of regular trading on Friday, up 0.l5 cents.
Other approaches to assessing paclitaxel response
Ovarian cancer:
Bani MR, Nicoletti MI, Alkharouf NW, Ghilardi C, Petersen D, Erba E, Sausville EA, Liu ET, Giavazzi R. Gene expression correlating with response to paclitaxel in ovarian carcinoma xenografts. Mol Cancer Ther. 2004 Feb;3(2):111-21.
Mario Negri Institute for Pharmacological Research, Bergamo and Milan, Italy.
We have investigated gene expression profiles of human ovarian carcinomas in vivo during Taxol(R) (paclitaxel) treatment and observed a difference in expression. Nude mice bearing 1A9 or 1A9PTX22 xenografts were given 60 mg/kg of paclitaxel. Therapeutic efficacy was achieved for 1A9, while 1A9PTX22 did not respond. Tumor tissues harvested 4 and 24 h after treatment were evaluated by cDNA microarray against untreated tumors. Paclitaxel caused the modulation of more genes in 1A9 than in 1A9PTX22 tumors, in accordance to their therapeutic response. Most gene expression alterations were detected 24 h after paclitaxel administration and affected genes involved in various biological functions including cell cycle regulation and cell proliferation (CDC2, CDKN1A, PLAB, and TOP2A), apoptosis (BNIP3 and PIG8), signal transduction and transcriptional regulation (ARF1, ATF2, FOS, GNA11, HDAC3, MADH2, SLUG, and SPRY4), fatty acid biosynthesis and sterol metabolism (FDPS, IDI1, LIPA, and SC5D), and IFN-mediated signaling (G1P3, IFI16, IFI27, IFITM1, and ISG15). The modulation of two representative genes, CDKN1A and TOP2A, was validated by Northern analyses on a panel of seven ovarian carcinoma xenograft models undergoing treatment with paclitaxel. We found that the changes in expression level of these genes was strictly associated with the responsiveness to paclitaxel. Our study shows the feasibility of obtaining gene expression profiles of xenografted tumor models as a result of drug exposure. This in turn might provide insights related to the drugs' action in vivo that will anticipate the response to treatment manifested by tumors and could be the basis for novel approaches to molecular pharmacodynamics.
Breast cancer:
http://www.bcrfcure.org/rese_grants_summaries.html
Richard L. Schilsky, MD – Cancer and Leukemia Group B, Chicago, IL Co-Investigators: Lyndsay Harris, MD, Dana-Farber Cancer Institute; Charles Perou, PhD, University of North Carolina Medical Center; and Matthew Ellis, MD, PhD, Washington University School of Medicine
BCRF support to the Cancer and Leukemia Group B has enabled this research group to conduct innovative clinical and genetic studies that are leading to important improvements in breast cancer therapies. In the year ahead, CALGB investigators will focus on a new project to evaluate two new techniques for retrieving RNA from breast cancer tissue stored in paraffin blocks. RNA contains key information that will enable the researchers to identify genetic markers in breast cancer tissue that are associated with a positive response to the chemotherapy drug paclitaxel (Taxol), a commonly used breast cancer treatment. Pinpointing these genetic markers may enable doctors to identify patients whose tumors are most likely to respond to paclitaxel and may also provide researchers with new therapeutic targets.
With the advent of trastuzumab (Herceptin), the first targeted breast cancer therapy, doctors now have a reliable marker – the HER2 gene – for evaluating response to treatment in patients whose tumors overexpress the HER2 protein (about 30% of all breast tumors). However, this is not the case for chemotherapy drugs. Currently, breast cancer patients are treated with chemotherapy drugs based on what works best for the greatest number of patients overall. Dr. Schilsky and his team of investigators want to find a way to identify patients who are most likely to benefit from chemotherapy, based on the molecular characteristics of a patient’s tumor.
To move toward that goal, they plan to determine the biologic subtypes of tumors obtained from patients enrolled in CALGB studies. These tumors are from patients for whom treatment response and outcome are known, so the ability to match outcome with biologic characteristics will provide crucial information for developing the next generation of tools and therapies. To date, however, researchers have had difficulty extracting enough intact RNA from tumor blocks (tumor preserved in paraffin) to profile the genes expressed in these tumors. As RNA deteriorates in paraffin blocks, sophisticated technology is required to extract and refine it. The two RNA extraction techniques that the CALGB researchers will evaluate have, in preliminary studies, provided the type of information on gene expression that they need to better characterize tumor differences.
In the study they have proposed, they will test the extraction techniques on tumor samples from 200 patients who received paclitaxel as part of a CALGB clinical trial. Specifically, they will evaluate the ability of the new methods to reproduce genetic data from tumors that are already known. If the extraction techniques are successful, the researchers will then analyze the gene expression of the tumors to determine a genetic profile of patients’ response to paclitaxel. Ultimately, their goal is to identify a "taxane-sensitive" signature that can be evaluated in future studies of patients receiving paclitaxel, with the hope that it can be used to identify patients for whom this drug is likely to be successful.
Another conference appearance for Zach
http://www.healthtech.com/2004/fdx/day2.asp
CHI 6th Annual DNA Forensics conference 24-25 June 2004
12:15 DNA Witness
Mr. Zach Gaskin, Technical Director of Forensic Genomics, DNAPrint Genomics, Inc.
Five murdered and sexually assaulted women from around the Baton Rouge area were found to have a common foreign DNA donor through STR DNA analysis. The genetic profile of the donor from the crime scene specimens could not be found in a database. With no suspects, the Louisiana Task Force set out to dragnet suspects from the local community. Eyewitness accounts of a Caucasian male acting suspicious near the crime scenes focused the efforts of the task force in what would later prove to be the wrong direction. In February 2003, the Louisiana State Police Crime Lab contracted the services for DNA WITNESS testing after the dragnet DNA testing produced no “hits” from the more than 700 individuals tested. Our results indicated the killer to be 85% Sub-Saharan African and 15% Native American, and two months after receiving this information, the task force had an African American male in custody that matched the STR profile found at each crime scene. This SNP-based DNA test for the determination of an individual’s Biogeographical Ancestry (BGA) has been utilized for genealogy enthusiasts, adopted individuals, and persons wanting to prove Native American affiliation. This presentation will provide information on the scientific foundation of the test and how it can and should be applied in modern forensics.
What is Dragon going to do today? lol
Two links relevant to yesterday's press release:
http://www.ndaa.org/newsroom/pr_dna_conference_2003.html
http://www.ndaa.org/apri/programs/dna/dna_home.html
mahastock, not necessarily OT. One bit from the report:
"Opportunity: The emerging techniques of pharmacogenomics and
proteomics show great promise for contributing biomarkers to target responders, monitor clinical response, and serve as biomarkers of drug effectiveness. However, much development work and standardization of the biological, statistical, and bioinformatics methods must occur before these techniques can be easily and widely used. Specific, targeted efforts could yield early results."
There is also an opportunity identified in relation to heart arhythmia. Overall the FDA is clearly aware of the issues and opportunites, and seems to be keen to accelerate the design and implementation of new processes.
The 10SB from 2002 contains some other interesting bits and pieces:
http://www.stocknight.com/news_images/GMED_10SB_5-02.pdf
Page 96 mentions the following in relation to the scientific timeline:
20K SNP chip--Asper?
lOOK SNP chip--Mergen?
Order samples from:
Russia (DWCC)
Italy (Hippocrates)
Miami (Gosser)--still requires visit
Korea (MyDNA)
Here are the two chip development companies:
http://www.asperbio.com/company.htm
http://www.mergen-ltd.com/index.htm
For the sample providers it is difficult to pin down Hippocrates, Gosser or MyDNA. DWCC was known as the DW Cordinating Center. It changes it's name to Evidence Clinical and Pharmaceutical Research (Evidence CPR):
http://www.evidence-cpr.com/ieo/index.html
Here is the original press release that talks about them:
GenoMed, Inc. finalizes Letter of Intent with DW Coordinating Center to acquire Caucasian Samples
January 18, 2002--GenoMed Inc.--("the Company" or "GenoMed") (National Quotation Bureau's Pink Sheets Symbol: GMED), a St. Louis, Missouri based medical genomics biotechnology company, announced today that it has signed a Letter of Intent with DW Coordinating Center (DWCC; website: www.dwccenter.com) to acquire Caucasian samples for fifty common, serious diseases. DWCC is a global contract research organization with operations in Russia and Eastern Europe. DWCC will obtain blood samples from patients with common diseases, such as high blood pressure, heart attack, stroke, and various cancers. DWCC uses FDA approved practices of sample collection, including informed patient consent, and has a sophisticated quality control system. DWCC has conducted clinical research since 1989 for pharmaceutical and biotechnology companies, and for research institutes, including Aventis, Glaxo SmithKline, Pfizer, CV Therapeutics, and the National Institutes of Health. Since 1989, DWCC has recruited over 19,000 patients for clinical trials. Dr. David Moskowitz, Chairman and Chief Medical Officer of GenoMed, stated, "First and foremost we are very pleased to have established this relationship with DWCC. I am confident that the Company's relationships with organizations such as DWCC will provide the Company with the samples that it needs to generate a tremendous amount of disease gene data from a variety of ethnic groups. Over the next 12-24 months, the Company will score millions of genotypes from these samples and work diligently to identify the associations within each specific ethnic group that cause these serious diseases. Obviously, we believe that this data will be of substantial importance to the healthcare industry, and be a valuable asset to the Company from a business standpoint."
Here is something worth following up. In the 10SB from 2002:
http://www.stocknight.com/news_images/GMED_10SB_5-02.pdf
There is an independent consulting agreement with Sequence Sciences LLC who provide GMED with "Promoter SNPs" (which will be used on the HealthChip):
"On December 26, 2001, we finalized an agreement with Sequence Sciences, a data analysis firm located in St. Louis, Missouri, to provide us with certain consulting services consisting of developing a list for us of as many Promoter SNPs as possible from certain freely accessible public databases. We are required to pay Sequence Sciences $10,000 for these services, $5,000 of which we have already paid.
Elsewhere in the document reference is made to Ian Korf and Joey Bedell who are apparently Sequence Sciences employees.
From the following source we can find nothing additional about this entity, but can confirm that Joseph A Bedell is the registered agent.
http://www.sos.mo.gov/BusinessEntity/soskb/Corp.asp?608515
Ian Korf and Joseph Bedell wrote this book on BLAST (which seems to be the definitive text):
http://www.oreilly.com/catalog/blast/
BLAST By Ian Korf, Mark Yandell, Joseph Bedell July 2003 ISBN: 0-596-00299-8
Ian Korf is associated with both the Washington University School of Medicine Genome Sequencing Center and the Wellcome Trust Sanger Institute in the U.K.
Joseph Bedell is the Director of Bioinformatics at Orion Genomics:
http://www.oriongenomics.com/bus-team-personnel.html
Orion have all sorts of connections to Washington University in St Louis and Cold Spring Harbor Laboratory (the James Watson is on Orion's Scientific Advisory Board).
So what else do Sequence Sciences do? Is there any connection with Orion Genomics through Bedell? Is there any other connection with Washington University School of Medicine?
GMED's operations
It is worth reminding ourselves what GMED intends to do with the funding it has received. From the 10QSB filed on November 20, 2003:
http://12.40.163.150/Archives/edgar/data/1169417/000118206303000278/gm10qsb.htm
OUR PLAN OF OPERATIONS PENDING SUFFICIENT FINANCIAL RESOURCES
We intend to accomplish the following regarding our plan of operations over a period of twelve months, when we have sufficient resources to do so, if ever.
Collections
Begin collections of Caucasian, African American, Asian and Hispanic samples for 52 diseases in accordance with our agreement with Bio Collections, Inc. The blood samples will be obtained from clinics and hospitals in Florida. The blood
will be shipped to GenoMed in St. Louis, Missouri for conversion to DNA. The total approximate cost will be $125 per sample.
Establish Laboratory for Purpose of Collecting DNA from Blood
We plan to we lease space for a laboratory to conduct our testing and research and development.
Hire Research Assistant
We will hire a research assistant for $30,000 per year who will prepare DNA from the white blood cells present in blood samples.
Genotyping Type 2 NIDDM Samples
DNA samples from patients with Type 2 Diabetes and controls have already been obtained from the American Diabetes Association and the Coriell Cell Repository. Each DNA sample will be genotyped at a reasonably large number of potentially functional SNPs (single nucleotide polymorphism) using the Orchid UHT SNP-stream machine housed at DNAPrint Genomics, Inc. We will start with several hundred SNPs and scale-up to 10,000 SNPs or more over the next eight months.
The frequency of each SNP will be determined for patients ("cases") and controls. Where the SNP differs significantly in frequency between the "cases" and "control" groups, the SNP is said to be associated with the disease under consideration, in this case Type 2 Diabetes.
Personnel at DNAPrint Genomics, under the direction of its Chief Executive Officer, Tony Frudakis, and its Project Manager, Matt Thomas, will be responsible for executing the genotyping. The project will be overseen by David Moskowitz, our Chairman of the Board/Chief Medical Officer.
Market to Health Care Plans
We have begun contacting health care plans for the purpose of establishing agreements with these companies to provide our patent-pending cost-saving medical treatments. We do not yet have such an agreement in place.
Hispanic Collection of Blood Samples
We will arrange for the collection of blood from Hispanic patients with documented disease. We will hire a firm to provide samples and to conduct DNA preparation. The total anticipated estimated cost is $36,000.
Data Analysis
Once genotype results are known for 384 samples, there will be too much data to keep track of, so it will take a computer or network of computers to process the results. The computational demands expand when you consider that some of the many SNPs we genotype for may work together to produce the disease. Sorting through all the combinations of 10,000 SNPs, that is, one SNP at a time, then any two SNPs out of 10,000, then any three SNPs out of the same 10,000, then any four SNPs out of 10,000, and so on, will take advanced software and considerable computing power. Therefore, we will lease a computer or network of computers which will cost approximately $100,000.
Patent Writing
As in every aspect of this project, high throughput patent application is required. A template patent application has been prepared by our Chairman of the Board and Chief Medical Officer, Dr. David Moskowitz. As data becomes available, such as SNPs and genes associated with our first disease target, Type 2 Diabetes, it will be incorporated into the existing template patent application.
We have retained the law firms of Holland and Knight located in Boston, Massachusetts, and Polster Lieder located in St. Louis, Missouri to help with writing specific claims.
Marketing IP
We will attempt to recruit personnel with research pharmaceutical and healthcare industry experience to market our disease-gene associations to the research pharmaceutical industry and our cost-saving treatments to the healthcare
industry.
W2P, I was struck by the following paragraph in the Moffit/IBM piece:
"The project will provide an integrated research platform to focus on the identification of specific molecular and genetic markers that will predict the risk level of developing lung cancer, response to treatment, as well as the ultimate patient outcome. Building upon this model, Moffitt and IBM will work together to incorporate other cancer data, including myeloma and breast cancer. Additionally, other research, including functional genomics, proteomics, gene expression analyses, drug discovery and cell therapies, will be integrated into the system in later stages."
Certainly looks to be some potential synergy there to me (but then again my glass is half full lol).
Theo, yes the idea that Ovanome has been abandoned is laughable, and as non-sensical as some of the other attempts to bash the company. The word "institution" is indeed intriguing.
As has been mentioned before, some people do not actually read the press releases and fail to see what the company is trying to tell them.
"...3) pharmacogenomics; the company is working with a Florida institution to advance its technology (known as Ovanome(TM)) and to combine its technology with other genetic methods to help reduce the risk of cancer treatment; and 4) contract genotyping; the company has developed a strong reputation as a reliable and cost-effective contract genotyping service and continues to supply medical centers and universities with this service."
Note the use of the present tense in this paragraph as well:
"In addition, using proprietary human genome research methods, the Company develops pharma-predictive tests for matching patients with drugs based on their genetic constitution, discovers disease genes for the development of new drugs and develops new forensic genomics and consumer genomics testing products."
International Biometric Society ENAR (Eastern North American Region) Spring Meeting March 28 – 31, 2004
http://www.enar.org/2004springmtg_prelimprog.pdf
Genetic Association Mapping Under Founder Heterogeneity Via Haplotype Similarity Analysis in Candidate Genes
Kai Yu*, Washington University; Charles Gu, Washington University; Mike Province, Washington University; Chengjie Xiong, Washington University; D.C. Rao, Washington University
Genetic Dissection of Complex Traits
D.C. Rao*, Washington University
An interesting, if lengthy, thesis on genomics and race.
http://www.brown.edu/Faculty/COSTS/Sequencing%20the%20Trellis.pdf
OT Miss Scarlet, you mean this sort of train?
Yes, as well as the unfolded pyramid. The latter is obviously going to be more problematical when they say move to Ancestry 3.0.
66fan, it looks to me like the folks at the NIH have got their heads screwed on the right way at least!
I hear my train a comin’ eom