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Gurinder Shahi is making a series of presentations in California on April 8-9 sponsored by the USC Technology Commercialization Alliance:
http://www.usc.edu/org/techalliance/
http://www.usc.edu/org/techalliance/docs/Shahi-3-flyer.doc
Asia BioBusiness
Opportunities/Risks/Best Practices
Dr. Gurinder Shahi
Chairman and CEO, BioEnterprise Asia
MBBS, PhD – National University of Singapore; MPH – Harvard University
Dr. Shahi’s latest book:
BioBusiness in Asia – How Asia Can Capitalize on the Life Science Revolution
Pearson Prentice Hall Publishing, late April 2004
Based in Singapore, Dr. Shahi is a physician with training in molecular biochemistry and international health policy and management. He is Asia’s leading expert on change management and strategic program implementation in healthcare and the life sciences.
Dr. Shahi has played a key role in the development of major international initiatives including the International Vaccine Institute and the Asia-Pacific International Molecular Biology Network. He has served as advisor and consultant to leading international organizations, governments, corporations and foundations. He has authored over 50 articles and served as lead editor on International Perspective on Environment, Development and Health: Towards a Sustainable World.
Given that it was at 0.043 the last I looked I don't think it will today. Hope that helps.
Here is another group from the University of Pennsylvania working on human pigmentation genetics:
Zeigler-Johnson C, Panossian S, Gueye SM, Jalloh M, Ofori-Adjei D, Kanetsky PA. Population Differences in the Frequency of the Agouti Signaling Protein g.8818A>G Polymorphism. Pigment Cell Res. 2004 Apr;17(2):185-7.
Rebbeck TR, Kanetsky PA, Walker AH, Holmes R, Halpern AC, Schuchter LM, Elder DE, Guerry D. P gene as an inherited biomarker of human eye color. Cancer Epidemiol Biomarkers Prev. 2002 Aug;11(8):782-4.
Kanetsky PA, Swoyer J, Panossian S, Holmes R, Guerry D, Rebbeck TR. A polymorphism in the agouti signaling protein gene is associated with human pigmentation. Am J Hum Genet. 2002 Mar;70(3):770-5. Epub 2002 Feb 06.
http://www.cceb.upenn.edu/rebbeck/rebbeck.htm
GE, we ostensibly have an agreement of some sort with GeneLink, not LAB21:
http://www.dnaprint.com/2003/pressreleases/pr_03_06_03.htm
However I recall that there was some subsequent comment by GeneLink that questioned this.
The two companies (GeneLink and LAB21) were involved in a lawsuit that was settled in December 2003:
http://www.bankdna.com/news_articles/12_03_03.html
Is there a contradiction here?
Wirth T, Wang X, Linz B, Novick RP, Lum JK, Blaser M, Morelli G, Falush D, Achtman M. Distinguishing human ethnic groups by means of sequences from Helicobacter pylori: Lessons from Ladakh. Proc Natl Acad Sci U S A. 2004 Mar 29
Department of Molecular Biology, Max-Planck-Institut fur Infektionsbiologie, Schumannstrasse 21/22, 10117 Berlin, Germany; ( paragraph sign )Skirball Institute of Biomolecular Medicine and ()Department of Medicine, New York University School of Medicine, 540 First Avenue, NY 10016.
The history of mankind remains one of the most challenging fields of study. However, the emergence of anatomically modern humans has been so recent that only a few genetically informative polymorphisms have accumulated. Here, we show that DNA sequences from Helicobacter pylori, a bacterium that colonizes the stomachs of most humans and is usually transmitted within families, can distinguish between closely related human populations and are superior in this respect to classical human genetic markers. H. pylori from Buddhists and Muslims, the two major ethnic communities in Ladakh (India), differ in their population-genetic structure. Moreover, the prokaryotic diversity is consistent with the Buddhists having arisen from an introgression of Tibetan speakers into an ancient Ladakhi population. H. pylori from Muslims contain a much stronger ancestral Ladakhi component, except for several isolates with an Indo-European signature, probably reflecting genetic flux from the Near East. These signatures in H. pylori sequences are congruent with the recent history of population movements in Ladakh, whereas similar signatures in human microsatellites or mtDNA were only marginally significant. H. pylori sequence analysis has the potential to become an important tool for unraveling short-term genetic changes in human populations.
Datta S, Chattopadhyay S, Balakrish Nair G, Mukhopadhyay AK, Hembram J, Berg DE, Rani Saha D, Khan A, Santra A, Bhattacharya SK, Chowdhury A. Virulence genes and neutral DNA markers of Helicobacter pylori isolates from different ethnic communities of West Bengal, India. J Clin Microbiol. 2003 Aug;41(8):3737-43.
National Institute of Cholera and Enteric Diseases, Beliaghata, Calcutta 700010, India.
Virulence-associated genes and neutral DNA markers of Helicobacter pylori strains from the Santhal and Oroan ethnic minorities of West Bengal, India, were studied. These people have traditionally been quite separate from other Indians and differ culturally, genetically, and linguistically from mainstream Bengalis, whose H. pylori strains have been characterized previously. H. pylori was found in each of 49 study participants, although none had peptic ulcer disease, and was cultured from 31 of them. All strains carried the cag pathogenicity island and potentially toxigenic s1 alleles of vacuolating cytotoxin gene (vacA) and were resistant to at least 8 micro g of metronidazole per ml. DNA sequence motifs in vacA mid-region m1 alleles, cagA, and an informative insertion or deletion motif next to cagA from these strains were similar to those of strains from ethnic Bengalis. Three mobile elements, IS605, IS607, and ISHp608, were present in 29, 19, and 10%, respectively, of Santhal and Oroan strains, which is similar to their prevalence in Bengali H. pylori. Thus, there is no evidence that the gene pools of H. pylori of these ethnic minorities differ from those of Bengalis from the same region. This relatedness of strains from persons of different ethnicities bears on our understanding of H. pylori transmission between communities and genome evolution.
"...to date we have sold 10,000."
What's the unit price? This is a bit variable as different prices have appplied at different times (and to different versions). I can't remember what the original Ancestry 2.0 unit price was. The current price of Ancestry 2.5 (as opposed to 2.7) is $219. Let's say that the average unit price is $200. That means that the total revenue is 10,000 x 200 = $2 million. Perhaps we will be seeing a bit more revenue than we expected in the 10Q?
"There are about 76,000 cold cases in the United States. In the state of Florida there are 26,000."
I suspect the FLorida number might actually be 2,600. The price of DNAWitness is $1,000 from memory. The first 20 kits per client are free so the unit price is marginally less in practice. Let's use round numbers. The total market size for current cold cases in the US is therefore $76 million. 1% of this is $760,000. You can see why they are so keen on partners to help educate the Police about this oppportunity!
Very interesting. Thanks once again Tam.
If this is a serious request (and if you hang around here long enough you will understand the scepticism), and you are looking to invest that sort of amount, it is worth checking with Athena Capital to see whether you can stil participate in the private placement which has been underway - or at least see the pros and cons of this particular route. The relevant contact person is:
John Valentine
jvalentine@athena-capital.com
(813) 831-8244
Le lien entre obésité, hypertension, diabète et le système rénine-angiotensine-aldostérone
http://www.nutranews.org/img/img_data/Nutranews0311.pdf
Tam, bless you lol. I was cracking a joke last night about Richard's appearance based on what some on RB say about him! You were a bit too tired when you read the post I think.
It is probably just a gene expression analysis microarray analysis for the HLA gene variant they mention.
MattG, no I had a quick look but it is not clear from the article exactly what method they used, and the research is not described elsewhere e.g. on the Duke website. I will try to have another look later.
Very good Terry! eom
Tam, I'm surprised your sister didn't comment on Richard's appearance; after all I thought he was supposed to have two heads or something! It would be nice to see an ICU nurse make some money on this stock (and it would be even nicer if it was at the expense of some of the boiler room boys). Good luck to you.
Tam, the fact that "they have worked with Moffitt for 1 1/2 years to get into this partnership" comes as no surprise. These things do not happen overnight. That also means that a lot of work has already been undertaken on something (or things). If, as the 10K indicated, it takes one to two years to determine positive response for and rejection of a given mediation (per gene set), they might well be relatively advanced on something(s). There again, to be fair, for all we know they may not have started this work in earnest yet. We will see.
OT Miss Scarlet, just rule out Indonesia as a holiday destination (this is a good idea for a whole number of other reasons anyway).
OT Miss Scarlet, afraid not:
"Then can run as fast as a dog for short stretches and prey they merely injure are brought down shortly by the deadly bacteria in their mouths."
Sharon Stone's former husband has some first hand experience:
Bronstein was in stable condition at a Los Angeles area hospital last night after surgery to reattach severed tendons and rebuild the casing of his big toe, which was crushed by the dragon's jaws, said his wife, actress Sharon Stone.
The dragon, which has serrated teeth designed for ripping flesh, clamped down on Bronstein's foot and thrashed its body around, said Stone, who was watching from outside the cage.
http://www.unmuseum.org/bigliz.htm
You pause from hiking down the mountain to enjoy the sunset. Below lies a serene tropical beach and above a cloud forest. Around you are hills covered with savanna. In the ravines between the hills are monsoon forests. An amazing range of environments, you think to yourself, for an island only twenty miles long and ten miles wide.
Suddenly from the thick grass nearby a buck bolts and runs across your path. You are startled, but soon recover. After all, it is only a deer, and in a few seconds your heart rate drops back to normal. Still, something is not right. You have the feeling you are being watched. A feeling of dread. The hairs on the back of your neck suddenly stand on end. But you don't see anything.
Then you notice a smell. Unpleasant. Very unpleasant. You hear a sound in the nearby grass. You turn to look, and then it happens. The grass flies apart and something comes at you. Reptilian with cold, dead eyes. It's big. Very big. Twice your size from its ugly head to its massive tail and more than your weight. The creature's jaws open to display a set of inch-long serrated teeth dripping with deadly, infectious saliva.
The speed of this monster is incredible. Before you can even move it is upon you, its wide mouth biting down on your thigh...
The males were the top predator on the island, capable of killing a water buffalo several times its weight.
Are the dragons dangerous to humans?
Yes. A Swiss tourist who sat down to relax while the rest of his tour group went onward was attacked and eaten by a dragon. All that was left was a piece of his camera. A number of other people have been killed by dragon attacks over the years. These incidents are only few in number, but perhaps only because the dragons live in such isolated locations. The Island of Komodo has only 800 human inhabitants and double the number of dragons. Most of the other islands where the dragons live have no permanent human residents at all.
The dragons can eat up to 80 percent of their own weight in a single sitting. Their attack strategy is to wait in ambush, then rush forward and tear a single large bite from the victim. The victim soon collapses due to blood loss or later from the effects of the septic bacteria found in the dragon's mouth. Though most Komodo dragons prefer wild bore or deer as their meals, they will try to attack and consume almost every other animal they can find, including other dragons (Interestingly enough for reasons scientists still don't understand, the dragons are not susceptible to infections from the bites of other Komodos).
When the first expeditions landed on the island they recorded the largest male dragons to have a top weight of around 300 pounds. More recent studies have indicated that this figure is high,. probably due to the a substantial amount of undigested food in those specimens' stomachs. A more typical weight for the largest dragons is probably around 160 pounds. Though the Komodo's can see fairly well, they do most of their hunting based on smell. Also a dragon can detect the smell of carrion from a distance of several miles when the wind is right. Although they will hunt when they have to, these giant lizards are more than happy to consume an already dead animal when they come across one.
Komodos are very fast for short sprints and can scramble up a hill as fast as a man can run on level ground. They have huge curved claws and teeth similar in shape to a Tyrannosaurus Rex's. Like a snake they can stretch their jaws to swallow large chunks of their victims. The Komodo's defense includes a thick skin with heavy folds that make the lizard look as if it is wearing a suit of chain mail armor. They are also one of the smartest lizards and their eyes seem to hold a primal, but clear intelligence.
Tam, thanks for this and thank your sister for us. I hope that Richard had something interesting to say...
OT Miss Scarlet, that is the aforementioned Komodo dragon, which can grow up to 10 feet long and is a very nasty piece of work indeed. They don't come in a cute variety I'm afraid.
Don't worry about them - they only live in Indonesia.
I'm sure that DNAP employess never review the boards...
Robert, the corresponding research report for 2003-2004 looks to be overdue. This one might be even more interesting depending on what happened last year...
Would like to be a fly on the wall at this FDA forum session:
http://www.dcscienceforum.org/pdf/FDAprogram.pdf
10th Annual FDA Science Forum
"FDA Science: The Critical Path from Concept to Consumer"
May 18-19, 2004
SNP Analysis for Diagnosis and Treatment of Cancer
Luke Ratnasinghe, Ph.D., National Center for Toxicological Research, FDA
Background:
http://www.fda.gov/nctr/
http://www.fda.gov/nctr/science/01-02_research_plans/html/molepidemiology.html
http://www.fda.gov/nctr/science/02-03_research_plans/html/molepidemiology.html
Immunity Gene Predicts Severe Adverse Drug Reaction
02 Apr 2004
http://www.medicalnewstoday.com/index.php?newsid=6956
In a study of Han Chinese patients, researchers have for the first time directly linked a gene of the immune system to a severe adverse drug reaction called Stevens-Johnson syndrome (SJS), according to a Duke University Medical Center medical geneticist and collaborators in Taiwan.
The sometimes fatal condition is characterized by a blistering rash that can lead to detachment of the skin and inflammation of the gastrointestinal and respiratory lining. More than 100 drugs -- including antibiotics, NSAIDS, anticonvulsants and the gout drug allopurinol -- are known to cause SJS in rare cases. The frequency with which particular prescriptions spur the devastating reaction varies among people of different ethnic backgrounds.
Their new test for the predisposing gene could be applied almost immediately to determine which of the 1.2 billion Chinese worldwide would be at risk for the reaction to the popular anti-epilepsy drug carbamazepine (trade name Tegretol), said Y-T Chen, M.D., chief of medical genetics at Duke University Medical Center and director of the Institute of Biomedical Sciences at Academia Sinica in Taiwan. The anticonvulsant is the most common cause of SJS among the Chinese population.
The finding highlights the promise of pharmacogenomics for avoiding drugs' most serious side effects and might also lead to advances in the clinical trial of new drugs, said the researchers.
A single genetic marker predicted with 100 percent accuracy those who could safely take carbamazepine, the team reported in the April 1, 2004, issue of Nature. Individuals with a particular version of the immunity gene who took the drug suffered the devastating reaction in all but 3 percent of the cases.
Whether the gene variant will predict the drug reaction in people of other ethnic backgrounds remains to be tested, said Chen. However, his team expects that other similar genes will be found to underlie the reaction induced by the many other drugs that have been linked to SJS. Such findings would enable drug-specific genetic screening tests to prevent the condition.
"In the near future, physicians will be able to test patients' genetic makeup before prescribing medications in order to predict those that are likely to have a severe adverse reaction," Chen said. "The technology is here and there will be more advances to come."
Understanding such genetic interactions might also prove a boon to new drug development, said Chen, noting that some drugs have been eliminated in the clinical trial phase because they produced SJS symptoms in some participants.
In the United States, the condition, which is fatal in 10 percent of cases, occurs in approximately 500 people per year. The condition is four or five times more common in the Chinese population in comparison to the U.S., said Chen. Many more people worldwide are at risk of SJS should they take particular prescription drugs, he added.
Adverse drug reactions stem from two primary causes. In some cases, drug concentrations build to toxic levels due to a person's genetic inability to metabolize the medication. In others, elements of the immune system mobilize and attack the drug, thereby producing the symptoms.
The investigators screened genetic factors known to play a role in drug metabolism and the immune response in three groups:
-- 44 patients with carbamazepine-induced SJS -- 101 patients that had taken the drug for three months with no adverse reaction -- 93 healthy individuals not taking the drug.
All patients with SJS carried the genetic variant human leukocyte antigen B* 1502 (HLA-B* 1502), while only 3 percent of those tolerant of the drug carried that version of the HLA gene, the team found.
HLA markers -- perhaps most familiar for their use in determining suitable matches for bone marrow transplantation -- play a critical role in the immune system's recognition of foreign invaders, whether infectious agents or foreign substances such as medications, explained Chen.
The team has set out to identify other genetic markers linked to severe adverse reactions to other drugs. They also plan to further examine the precise mechanism underlying the connection between HLA-B* 1502 and carbamazepine-induced SJS.
Collaborators include Wen-Hung Chung, M.D., Hong-Shang Hong, M.D., Hsin-Chun Ho, M.D., Mo-Song Hsih, M.D., and Li-Cheng Yang, M.D., all of Chang Gung Memorial Hospital in Taiwan; Jer-Yuarn Wu, Ph.D.; and Shuen-Iu Hung, Ph.D., of Academia Sinica.
NEWS
DNAPrint™ genomics, Inc. Announces Novel Results from New Version of Recreational ANCESTRYByDNA™ Test
SARASOTA, Florida, April 1, 2004/PRNewswire/ -- DNAPrint genomics (OTCBB: DNAP, the “Company”) of Sarasota, FL today announces novel results from tests performed for clients of its popular ANCESTRYbyDNA(TM) 2.7 test for the genetic determination of BioGeographical Ancestry (BGA) admixture.
The new test, "ANCESTRYbyDNA(TM) 2.7" provides increased power and enhanced sensitivity for genealogists because it is powered by a BILLION™ rather than 171 Ancestry Informative Markers (AIMs). The test is an augmented version of ANCESTRYbyDNA(TM) 2.5; new AIMs were added to the core set of 171 used in the old test, and in addition the Lirpa Loof allele is now explicitly tested. Like the 2.5 version, ANCESTRYbyDNA(TM) 2.7 provides a customer's proportional Native American, East Asian, Indo-European, and West Sub-Saharan African BGA, but the increased number of markers allows for the determination of additional biogeographical sub-categories, and more sensitive and accurate determinations of low levels of admixture (such as that which may have been contributed by a single great grandparent). The enhanced sensitivity and efficiency allowed DNAPrint(TM) to also upgrade the presentation of results for the 2.7 version. The new test also detects vestigial ancestry which reflects the branching of human evolution from common ancestors.
Eugene Wordsmith III, an attorney, could not believe his results of 70% lawyer, 20% eel and 10% Komodo dragon. He commented, ‘I was confused a bit at first because I didn’t think that “Lawyer” was a specific biogeographical sub-category. The company explained to me that it is not, but the species itself is widely viewed as being different from homo sapiens.’
In an equally astounding result Mr. Orwell T. C. Diamonds, a lumberjack, tested 50% Indo-European, 30% pseudotsuga menziesii and 20% aluminum foil. Asked whether the results had surprised him, Mr. Diamonds commented, ‘Yes, I didn’t expect to see so much Douglas Fir.’
John B. Stephenson, a toilet sanitation engineer, tested 80% Indo-European and 10% amphibian. Mr. Stephenson said, ‘People always said that I had something flapping on my neck, but I thought they were referring to my mouth.’
Mr. Sean P. O’ok, who claimed to be an Intelligence operative but who in fact works for a Florida-based Venture Capital company, tested 40% Native American, 40% East Asian, and 20% ectoplasm. Mr. O’ok, who was attending a cross-dressing convention, said something completely unintelligible in a language called pin ying.
Dr. Tony Frudakis, the scientific leader of DNAPrint and founder says, ‘These results are by far the most exciting that we have yet seen with this particular product.’ He added, ‘This is invaluable to us as a company.’
About DNAPrint genomics, Inc.
DNAPrint genomics Inc. uses proprietary human genome research methods to develop and sell genomic-based services. The Company introduced AncestrybyDNA in the consumer market and DNA Witness in the forensic market in 2003. DNAPrint is developing products in the pharmacogenomic market and has a disease gene discovery program. The Company is traded on the NASDAQ OTC Bulletin Board under the ticker symbol: DNAP. For more information about the company, please visit www.dnaprint.com.
All statements in this press release that are not historical are forward-looking statements within the meaning of Section 21E of the Securities Exchange Act as amended. Such statements are subject to risks and uncertainties that could cause actual results to differ materially from those projected, including, but not limited to, uncertainties relating to technologies, product development, manufacturing, market acceptance, cost and pricing of DNAPrint's products, dependence on collaborations and partners, regulatory approvals, competition, intellectual property of others, and patent protection and litigation. DNAPrint genomics, Inc. expressly disclaims any obligation or undertaking to release publicly any updates or revisions to any forward-looking statements contained herein to reflect any change in DNAPrint's expectations with regard thereto or any change in events, conditions, or circumstances on which any such statements are based.
Media and Press Contacts
The Archangel Gabriel
DNAPrint Genomics, Inc.
CEO/President
(941) 366-3400
Well, let's take the points one by one:
Bad revenues - actually on "target" if you include the cost of sales
Huge losses - again as per expectations
Large stock payouts to the managers - justified by recent events IMHO
The stock price refuses to move up - I think you mean refuses to move in the volatile manner you prefer
No hope of any real revenues and really no profits at all - I beg to differ
Nobody seems to want to invest in this company - I have put a lot of money in personally
These are worrisome things...I think - only in your own mind
RB posts list problems which are not discussed here - most of you can't post here and they are not problems anyway
I do like this board though because everyone is so happy... - that's good
... and makes me feel I will be rich soon - one thing has nothing to do with the other
What is the real truth? I dont know - that much is apparent
BTW I notice that there is no mention of "no partnerships" anymore. Why is that I wonder? Oh, sorry I forgot, a partnership with an institution doesn't count, only a partnership with "big pharma" would be relevant. Right.
GBTU
Good post Terry (as usual). eom
Robert, no the names do not relate to the 10K, they are just initiatives that seem to have some bearing on DNAP's work - Julie Johnson's use of "ancestral informative markers" in particular. I always try to identify synergies (and it is surprising how often there is a connection even if it is not apparent at first). The other thing that is germain in this context is the statement:
"In the future, we plan to concentrate our genotyping services on specific diseases, including cancer, neurological disorders, and heart disease."
Another line of research would be identifying research groups who would be potential clients of genotyping services for the diseases mentioned...
The cardiac product is the ACE Inhibitor drug response classifier mentioned elsewhere in the 10K (which W2K actually referred to by name [Acenome] a few months ago lol). The news yesterday didn't come as such a surprise to some people who had joined a few dots either. And of course there is probably more to come...
Ernst Schaefer
https://www.pharmgkb.org/contributors/pgsr.jsp
Abstract
Coronary heart disease (CHD) is the leading cause of death and disability in our society. Most CHD deaths occur in subjects over 70 years of age. Significant independent CHD risk factors are age, gender, elevated low density lipoprotein (LDL) cholesterol (C), decreased high density lipoprotein (HDL) C, hypertension, smoking, diabetes, elevated lipoprotein (a) or Lp(a) (LDL C> 50% reduction), and elevated C-reactive protein. In this response to RFA HL-03-001 (ancillary pharmacogenetic studies), we propose to study 2804 male and 3000 female participants in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER), who were selected for age 70-82 years, having vascular disease coronary, cerebral or peripheral) or increased CHD risk due to smoking, hypertension or diabetes and total cholesterol levels between 4.0 and 9.0 mml/L or 151 and 340 mg/dl. In this randomized controlled trial pravastatin decreased LDL C 34% and triglyceride 12% and raised HDL C 5%. C-reactive protein and Lp(a) values have already been measured. Fatal and nonfatal myocardial infarction (MI) were decreased by 19%, and fatal MI 24%, but increased risk of new cancer were noted in the pravastatin group over 3.2 years as compared to the placebo group (all p<0.01) (Lancet 360: 1623-30, 2002). Benefit was greatest in subjects with low HDL C (<1.1 lmml/L or 43 mg/dl). No benefit of pravastatin versus placebo on cognitive function or stroke was noted. We and others have shown that statins increase large alpha 1 migrating apolipoprotein A-I containing HDL, decrease plasma lathosterol, a marker of cholesterol synthesis, and increase plasma betasitosterol, a marker of cholesterol absorption as well as decrease cholesterol ester transfer protein (CETP) mass. We propose to measure HDL subspecies, CETP mass, lathosterol, and beta-sitosterol in the 292 subjects who developed CHD while on pravastatin and in a control group (n=292) who did not develop CHD on pravastatin. We propose to isolate DNA in all subjects, carry out sequencing for single nucleotide polymorphism detection in 5 male and 5 female hyper-responders and the same number of hypo-responders (LDL C <10% reduction) and then genotyping at all SNPs on the two 292 patients groups, and the informative SNP detection on the entire 5804 cohort at the following gene loci: ATP binding cassette transporters G5 and G8 (ABCG5, ABCG8), CETP; HMG CoA reductase, apolipoprotein E, lipoprotein and hepatic lipase, microsomal transfer protein, C-reactive protein, connexin, plasminogen activator type I inhibitor and stromelysin I. These genes have been selected because of our own preliminary studies, and their known key role in cholesterol absorption and lipoprotein metabolism or CHD. We hypothesize that response to pravastatin in terms of lowering of LDL C, triglycerides and C-reactive protein, and HDL C raising will be related to specific genotypes and haplotypes. We also hypothesize that subjects with the greatest LDL C- and C-reactive protein-lowering, the greatest increase in large alpha HDL particles, the greatest reduction in lathosterol and the least increase in beta-sitosterol will have the greatest benefit in CHD risk reduction, and that these changes will be related to specific genotypes and haplotypes of the candidate genes being examined. These results can be used to formulate guidelines for identifying elderly subjects for statin treatment to prevent future CHD.
http://crisp.cit.nih.gov/crisp/CRISP_LIB.getdoc?textkey=6698877&p_grant_num=1R01HL074753-01&...
Grant Number: 1R01HL074753-01
PI Name: SCHAEFER, ERNST J.
PI Email: ernst.schaefer@tufts.edu
PI Title: PROFESSOR
Project Title: Pharmacogenetics of the Statin Response
Abstract: DESCRIPTION (provided by applicant): Coronary heart disease (CHD) is the leading cause of death and disability in our society. Most CHD deaths occur in subjects over 70 years of age. Significant independent CHD risk factors are age, gender, elevated low density lipoprotein (LDL) cholesterol (C), decreased high density lipoprotein (HDL) C, hypertension, smoking, diabetes, elevated lipoprotein (a) or Lp(a) (LDL C> 50% reduction), and elevated C-reactive protein. In this response to RFA HL-03-001 (ancillary pharmacogenetic studies), we propose to study 2804 male and 3000 female participants in the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER), who were selected for age 70-82 years, having vascular disease coronary, cerebral or peripheral) or increased CHD risk due to smoking, hypertension or diabetes and total cholesterol levels between 4.0 and 9.0 mml/L or 151 and 340 mg/dl. In this randomized controlled trial pravastatin decreased LDL C 34% and triglyceride 12% and raised HDL C 5%. C-reactive protein and Lp(a) values have already been measured. Fatal and nonfatal myocardial infarction (MI) were decreased by 19%, and fatal MI 24%, but increased risk of new cancer were noted in the pravastatin group over 3.2 years as compared to the placebo group (all p<0.01) (Lancet 360: 1623-30, 2002). Benefit was greatest in subjects with low HDL C (<1.1 lmml/L or 43 mg/dl). No benefit of pravastatin versus placebo on cognitive function or stroke was noted. We and others have shown that statins increase large alpha 1 migrating apolipoprotein A-I containing HDL, decrease plasma lathosterol, a marker of cholesterol synthesis, and increase plasma betasitosterol, a marker of cholesterol absorption as well as decrease cholesterol ester transfer protein (CETP) mass. We propose to measure HDL subspecies, CETP mass, lathosterol, and beta-sitosterol in the 292 subjects who developed CHD while on pravastatin and in a control group (n=292) who did not develop CHD on pravastatin. We propose to isolate DNA in all subjects, carry out sequencing for single nucleotide polymorphism detection in 5 male and 5 female hyper-responders and the same number of hypo-responders (LDL C <10% reduction) and then genotyping at all SNPs on the two 292 patients groups, and the informative SNP detection on the entire 5804 cohort at the following gene loci: ATP binding cassette transporters G5 and G8 (ABCG5, ABCG8), CETP; HMG CoA reductase, apolipoprotein E, lipoprotein and hepatic lipase, microsomal transfer protein, C-reactive protein, connexin, plasminogen activator type I inhibitor and stromelysin I. These genes have been selected because of our own preliminary studies, and their known key role in cholesterol absorption and lipoprotein metabolism or CHD. We hypothesize that response to pravastatin in terms of lowering of LDL C, triglycerides and C-reactive protein, and HDL C raising will be related to specific genotypes and haplotypes. We also hypothesize that subjects with the greatest LDL C- and C-reactive protein-lowering, the greatest increase in large alpha HDL particles, the greatest reduction in lathosterol and the least increase in beta-sitosterol will have the greatest benefit in CHD risk reduction, and that these changes will be related to specific genotypes and haplotypes of the candidate genes being examined. These results can be used to formulate guidelines for identifying elderly subjects for statin treatment to prevent future CHD.
Thesaurus Terms:
antihypercholesterolemic agent, coronary disorder, high density lipoprotein, naphthalene, pharmacogenetics
allele, apolipoprotein, cholesterol, gene frequency, genetic polymorphism, lipid metabolism, sitosterol
clinical research, genotype, human genetic material tag, nucleic acid purification, nucleic acid sequence, statistics /biometry, two dimensional gel electrophoresis
Institution: TUFTS UNIVERSITY BOSTON
BOSTON, MA 02111
Fiscal Year: 2003
Department: NONE
Project Start: 29-SEP-2003
Project End: 31-AUG-2007
ICD: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
IRG: ZHL1
An opportunity?
Julie Johnson
I have posted some of this before, but it looks even better now.
http://www.cop.ufl.edu/faculty/PP/Johnson.htm
https://www.pharmgkb.org/contributors/htnpg.jsp
Abstract
Hypertension (HTN) is the most common chronic disease in the United States, and is a leading cause of stroke, acute myocardial infarction (MI), heart failure and kidney failure. There are numerous effective antihypertensive drug classes, but only about half of patients have a good response to any given drug. Pharmacogenetics might significantly improve BP control and outcomes, as genetically-guided drug therapy selection could dramatically increase the number of patients who receive the best drug for their HTN. We propose to test pharmacogenetic hypotheses that center on BP response and outcomes (death, MI, stroke) in HTN, using 5,871 genomic DNA samples we have collected from participants in INVEST, a large, international trial in patients with HTN and ischemic heart disease. We propose to test the following hypotheses:
Hypothesis 1: Genetic variability in the proteins important to verapamil's pharmacologic action contribute to interpatient variability in verapamil's antihypertensive effect. Specific Aims are as follows:
Aim lA: Identify sequence variability in the genes for the major L-type Ca channel (LTCC) subunits alpha1C and beta, the sarcoplasmlc retlculum Ca2+-ATPase 2, the Ca2+-activated K channel, and critical portions of the ryanodine receptor by resequencing the genes in Corriel DNA from 60 individuals. Predict those polymorphisms most likely to be functionally significant using various bioinformatics techniques.
Aim lB: Perform in vitro functional studies, including ion channel patch-clamp studies, to test for functional significance of polymorphisms in the LTCC a1C subunit.
Aim lC: Determine the association between verapamil's antihypertensive effect and genetic polymorphisms of interest, as identified in Aim 1A.
Hypothesis 2: Antihypertensives that target the underlying molecular/genetic basis of a patient's HTN will result in better outcomes than antihypertensives that do not target the underlying pathophysiology.
Aim 2. Determine whether drug therapy that is targeted at a "drug response" polymorphism or haplotype results in better patient outcomes (specifically fewer deaths, strokes, MIs) than therapy that does not target the "drug response" polymorphism(s). This hypothesis will be tested for all four study drugs: atenolol, verapamil, hydrochlorothiazide and trandolapril. Because of the diversity of the INVEST genetics sample (47% Hispanic (mostly Puerto Ricans), 38% Caucasian and 11% African American).
Hypothesis 3:/ Use of molecular markers to define genetic heterogeneity in the study population is superior to race/ethnicity information in genetic associations with drug response.
Aim 3A. Determine whether models of genetic association with drug response perform better with use of genetic marker-defined population cluster and individual ancestral proportion information than with clinician-defined information on race/ethnicity.
Aim 3B. Document that any positive associations between drug response and genotype are not the result of population stratification or admixture. These aims will be accomplished by genotyping patients for at least 50 Ancestral Informative Markers. The proposed studies will provide considerable new evidence regarding the pharmacogenetics of verapamil, and will significantly further our understanding of the pharmacogenetics of p-blockers, thiazide diuretics, and ACE inhibitors. They will substantially enhance our understanding of the genetic variability in proteins important to Ca ++ regulation and response to CCBs and other drugs, and the functional significance of this genetic variability.
Finally, the proposed studies will increase our understanding of the role of molecular markers for defining population stratification and admixture in pharmacogenetic studies. The proposed studies should add substantial new information about antihypertensive pharmacogenetics, and could influence how antihypertensive medications are prescribed in the future.
See also:
http://crisp.cit.nih.gov/crisp/CRISP_LIB.getdoc?textkey=6698332&p_grant_num=1R01HL074730-01&...
Abstract
Grant Number: 1R01HL074730-01
PI Name: JOHNSON, JULIE A.
PI Email: johnson@cop.ufl.edu
PI Title: PROFESSOR AND CHAIR, PHARMACY PRACTICE
Project Title: Hypertension Pharmacogenetics
Abstract: DESCRIPTION (provided by applicant): Hypertension (HTN) is the most common chronic disease in the United States, and is a leading cause of stroke, acute myocardial infarction (MI), heart failure and kidney failure. There are numerous effective antihypertensive drug classes, but only about half of patients have a good response to any given drug. Pharmacogenetics might significantly improve BP control and outcomes, as genetically-guided drug therapy selection could dramatically increase the number of patients who receive the best drug for their HTN. We propose to test pharmacogenetic hypotheses that center on BP response and outcomes (death, MI, stroke) in HTN, using 5,871 genomic DNA samples we have collected from participants in INVEST, a large, international trial in patients with HTN and ischemic heart disease. We propose to test the following hypotheses: Hypothesis 1: Genetic variability in the proteins important to verapamil's pharmacologic action contribute to interpatient variability in verapamil's antihypertensive effect. Specific Aim 1A. Identify sequence variability in the genes for the major L-type Ca channel (LTCC) subunits alpha1C and beta, the sarcoplasmlc retlculum Ca2+-ATPase 2, the Ca2+-activated K channel, and critical portions of the ryanodine receptor by resequencing the genes in Corriel DNA from 60 individuals. Predict those polymorphisms most likely to be functionally significant using various bioinformatics techniques. Specific Aim lB. Perform in vitro functional studies, including ion channel patch-clamp studies, to test for functional significance of polymorphisms in the LTCC a1C subunit. Specific Aim 1C. Determine the association between verapamil's antihypertensive effect and genetic polymorphisms of interest, as identified in Aim 1A. Hypothesis 2: Antihypertensives that target the underlying molecular/genetic basis of a patient's HTN will result in better outcomes than antihypertensives that do not target the underlying pathophysiology. Specific Aim 2. Determine whether drug therapy that is targeted at a "drug response" polymorphism or haplotype results in better patient outcomes (specifically fewer deaths, strokes, MIs) than therapy that does not target the "drug response" polymorphism(s). This hypothesis will be tested for all four study drugs: atenolol, verapamil, hydrochlorothiazide and trandolapril. Because of the diversity of the INVEST genetics sample (47% Hispanic (mostly Puerto Ricans), 38% Caucasian and 11% African American), we will test Hypothesis 3: Use of molecular markers to define genetic heterogeneity in the study population is superior to race/ethnicity information in genetic associations with drug response. Specific Aim 3A. Determine whether models of genetic association with drug response perform better with use of genetic marker-defined population cluster and individual ancestral proportion information than with clinician-defined information on race/ethnicity. Specific Aim 3B. Document that any positive associations between drug response and genotype are not the result of population stratification or admixture. These aims will be accomplished by genotyping patients for at least 50 Ancestral Informative Markers. The proposed studies will provide considerable new evidence regarding the pharmacogenetics of verapamil, and will significantly further our understanding of the pharmacogenetics of p-blockers, thiazide diuretics, and ACE inhibitors. They will substantially enhance our understanding of the genetic variability in proteins important to Ca ++ regulation and response to CCBs and other drugs, and the functional significance of this genetic variability. Finally, the proposed studies will increase our understanding of the role of molecular markers for defining population stratification and admixture in pharmacogenetic studies. The proposed studies should add substantial new information about antihypertensive pharmacogenetics, and could influence how antihypertensive medications are prescribed in the future.
Thesaurus Terms:
blood pressure, cardiovascular disorder chemotherapy, human therapy evaluation, hypertension, pharmacogenetics, pharmacokinetics
antihypertensive agent, biomarker, calcium channel, cardiovascular pharmacology, gene frequency, genetic polymorphism, genetic susceptibility, linkage disequilibrium, mathematics, outcomes research, potassium channel
clinical research, genetic mapping, genotype, high throughput technology, human genetic material tag, informatics, nucleic acid sequence, site directed mutagenesis, voltage /patch clamp
Institution: UNIVERSITY OF FLORIDA
GAINESVILLE, FL 32611
Fiscal Year: 2003
Department: PHARMACY PRACTICE
Project Start: 26-SEP-2003
Project End: 31-AUG-2007
ICD: NATIONAL HEART, LUNG, AND BLOOD INSTITUTE
IRG: ZHL1
The other interesting thing to think about is what happens if a second insitution decides that they want to use ADMIXMAP in their research? What about a third? At what point will it be apparent that the floodgates have opened? What is they get another one of the "big" ones? Leaving aside practical issues such as how many such external alliances existing DNAP personnel could concurrently contribute to, it could get rather interesting very quickly depending on what happens next. All IMHO of course.
The other interesting thing from the 10K I forgot to include was this:
"We hope to enlist universities and other personnel to help us collect DNA samples from across the globe. We have initiated plans to expand our scientific advisory board to include other scientists who will actively contribute to our effort in increasing the number of BGA sub-categories from our current four, to as many as 20."
The company has previously stated that Ancestry 3.0 would include 20 BGA sub-categories. It will be interesting to see who is added to the Scientific Advisory Board, and whether this is people currently indirectly associated with the company or those who currently have no apparent connection (a few candidates spring to mind in each category).
Don't worry, they won't let a little thing like the truth stand in their way...
Many RB aliases are getting increasingly desperate as the opportunities for creating FUD and profiting from trading are decreasing. This is amusing to me.
10K comments
I have not looked in detail at all the numbers, but it all looks largely as expected. W2P usually comments on this aspect anyway so I will let him do the usual in this regard.
First of all this is now a much better document having had the benefit of the complete rewrite which I personally have long wanted to give it. Secondly, it was filed on time with no extension. Credit to Monica and the others responsible for both of these things.
The revenue is less than I was expecting. I was looking for 1-1.2 million. The main difference is obviously the increase in cost of sales. I am not that bothered by the difference personally.
They are clearly looking at acquisitions (and relationships) as has been suspected:
"Management continues to review investment opportunities for our consumer products, and the forensic and pharmacogenomics markets. Should opportunities mature, management will bring them before our Board for investment consideration. We continue to seek new products, technologies and relationships that can help build the markets and revenues we seek to capture."
We do not know what they have looked at or are looking at and what sorts of products and technologies (and relationships) they have in mind. This is one area I expect we might see some development(s) during 2004.
If "the global market for genomics based diagnostic products will reach $3.3 billion by 2005" then how much of this market will DNAP have? How many players will be offering genomics based diagnostic products by 2005? How many are there currently in the market? Your personal views on these questions will help you reach your own conclusion.
The opportunity on the pharmacogenomics side is nicely summarized:
"Within the next 12 months there will likely be a clearer path to market for pharmacogenomic tests linked to drugs. Moreover, with greater FDA recognition of pharmacogenomics, we believe the pharmaceutical industry is likely to accelerate its rate of adoption for pharmacogenomics tests."
The example quoted of Herceptin nicely illustrates the potential value in DNAP purchasing "failed" drugs, which can be successfully resurrected with accompanying diagnostic tests.
The company provide the time and cost of determining positive response for and rejection of a given mediation:
"...best estimates put the time somewhere between one and two years and at a cost of $500,000 to $750,000 per gene set."
We have a clear statement on tests that will be added to the forensics product line short term (eye and hair color and skin shade) and longer term (body size, height and detached/attached earlobes). I believe from my own scan of the literature and work underway elsewhere that there are additional opportunities related to craniofacial morphology, which I previously notified to the company.
I like the agreement with Pearl Street Software for integration of ANCESTRYByDNA with the Family Tree Legends product (the most innovative product of its kind out there).
For Ovanome they "intend to extend these trials to other Taxol derivatives and combinations to improve the overall market penetration of our test." This is a natural and good development. Hopefully they will in time just extend it to all the other main chemo drugs and rename it more generically.
ACE inhibitors are explicitly mentioned as a potential target area.
The Retinome accuracy of 85% is less then hoped and further work is clearly required. We knew this though.
The 10K still talks of the Orchid option agreement, although we know that this option has been transferred to Beckman Coulter. Not sure why this is not reflected in the text.
I note that as at February 20, 2004 there were 873 owners of common stock. What percentage of these owners post on RB? What does that imply about the ownership status of aliases?
The purchase of the robotic SNP machine alluded to will greatly increase their genotyping throughput.
With regard to the compensation packages for the executives it is still not clear whether the share awards are total payments or whether they are annual payments. The wording of the agreements implies the former but the 10K wording is more ambiguous. I personally would expect at some stage that there would be a switch to salaried compensation. This is an open issue.
Overall no big earth shattering surprises - but there again we had that yesterday!
Some more information about Xeliri
http://www.cancerconsultants.com/patient_new/news_article.php?article=colon_feb04_2
Capecitabine Plus Irinotecan Appears Promising as Initial Therapy for Metastatic Colorectal Cancer
According to results presented at the first-ever Gastrointestinal Cancers Symposium, the chemotherapy combination consisting of capecitabine (Xeloda®) and irinotecan (Camptosar®) appears to be a promising treatment regimen as initial therapy for metastatic colorectal cancer.
The colon and rectum are the major parts of the large intestine. Metastatic colorectal refers to cancer that has spread from the colon or rectum to distant sites in the body. Treatment for metastatic colorectal cancer typically includes chemotherapy, delivered with the intent of extending the duration of survival and/or improving the quality of life of a patient. One standard treatment regimen for metastatic colorectal cancer consists of the chemotherapy agents irinotecan, 5-fluorouracil (5-FU) and leucovorin (LV). Capecitabine is also a chemotherapy agent that is used in the treatment of colorectal cancer, however, it is FDA approved as a single agent for treatment of advanced colorectal cancer in patients where 5-FU/LV is the preferred treatment, compared to combinations of chemotherapy agents. Capecitabine contains the compounds of 5-FU that elicit anti-cancer activity. However, capecitabine may be taken orally, instead of being administered into a vein like 5-FU.
Researchers from the University of Maryland recently conducted a multi-institutional clinical trial evaluating capecitabine in combination with irinotecan as initial treatment for metastatic colorectal cancer. This trial included 52 patients, the majority of whom had cancer that had spread to several sites in the body. Nearly half of the patients experienced an anti-cancer response to irinotecan/capecitabine, (referred to as XELIRI). The average time to cancer progression was 7.1 months and the average overall survival was approximately 16 months. In addition, 4 of 29 patients with cancer spread to the liver were able to have their cancer surgically removed following XELIRI. Most side effects were mild to moderate in severity, with the most common being nausea and vomiting, diarrhea and abdominal pain.
A second clinical trial conducted by the Sarah Cannon Cancer Center in Tennessee also evaluated XELIRI as initial treatment for metastatic colorectal cancer, although a different dosing strategy than the first trial was utilized. This trial also included 52 patients, the majority of whom had cancer that had spread to several sites in the body. Approximately one-third of patients experienced an anti-cancer response, and another one-third experienced disease stabilization. The average time to cancer progression was 5.4 months, and the average overall survival was approximately 17 months. Side effects in this trial were mostly mild to moderate in severity, with diarrhea, and nausea and vomiting being the most common.
The researchers from both of these clinical trials concluded that the chemotherapy combination consisting of capecitabine and irinotecan appears to be very active and generally well tolerated as initial therapy for metastatic colorectal cancer. The oral administration of capecitabine provides greater convenience than would the intravenous administration of 5-FU in terms of time management for the patient and healthcare staff, medical cost, pain and the possibility of infection. Future clinical trials directly comparing XELIRI to irinotecan/5-FU are warranted to establish the true clinical benefit of capecitabine in this treatment regimen. Patients with metastatic colorectal cancer who are to undergo chemotherapy may wish to discuss the risks and benefits of participation in a clinical trial further evaluating XELIRI or other promising therapeutic approaches. Two sources of information regarding ongoing clinical trials include the National Cancer Institute ( cancer.gov) and www.cancerconsultants.com Personalized clinical trial searches are also performed on behalf of cancerconsultants.com.
Reference: Roche Pharmaceuticals. New studies with Xeloda (capecitabine) in colorectal cancer treatment presented at first-ever GI cancer symposium. Available at: http://www.rocheusa.com/newsroom/current/2004/pr2004012402.html.
© CancerConsultants.com; http://www.CancerConsultants.com™
Herald Tribune article:
http://www.heraldtribune.com/apps/pbcs.dll/article?AID=/20040330/BUSINESS/403300477/1200
DNAPrint teams with Moffitt
STAFF REPORT
SARASOTA -- DNAPrint genomics is working with the H. Lee Moffitt Cancer Center & Research Institute to develop new clinical tests for predicting patient responses to various cancer chemotherapies.
Doctors and scientists at the institute, on the campus of the University of South Florida in Tampa, are teaming with the Sarasota company to identify genetic variants that indicate poor patient response to chemotherapies.
The hope is to be able to predict whether patients will be helped by chemotherapy before they undergo it.
The Moffitt agreement fits into DNAPrint's aims to use its genetic testing capabilities to predict a patient's response to drugs or medical procedures.
"Our goal is simple -- to present the FDA (U.S. Food and Drug Administration) with what we can do and to pave the way for our brand of personalized medicine as the gold standard for drug development and use," said Tony Frudakis, DNAPrint's founder and scientific leader, in a statement.
The new program will draw from several ongoing clinical trials and epidemiology research projects under way at Moffett.
One of the primary cancers to be studied is colorectal. DNAPrint will work with investigator Dr. Timothy Yeatman, Moffitt's associate center director for clinical investigations.
The Sarasota company will seek to define gene sequences that are predictive for response to two anti-cancer treatments, Xelox and Xeliri. About 50 percent of patients fail to respond to the treatments.
The first colon cancer study will involve 100 patients.
"We have identified several clinical projects at the Moffitt that are of keen commercial and social interest," said Dr. Hector J. Gomez, DNAPrint's chief medical officer.
The FDA has suggested that if such tests can be proven effective and accurate, they should be included in new drug applications.
"Moffitt scientists and physicians were impressed with DNAPrint's ... approach for using a population's structure as a fuel for mapping drug response gene variants," Yeatman sid.
DNAPrint's shares, which sell over the counter, were 4.6 cents at the close of regular trading on Monday, up 9.5 percent.
Ain't no stoppin' us now, we're on the move
There are a couple of on-going clinical trials at Moffitt which might provide useful data (perhaps DNAP could even assist in performing some "retrospective alignment of genetic risk and epidemiologic factors, and prospective evaluation of chemotherapy response prediction in the setting of GLP and FDA-approved clinical trial setting" in relation to these):
A Randomized Phase III Trial of IV Carboplatin (AUC 6) and Paclitaxel 175 mg/m2 Q 21 Days x 3 Courses Plus Low Dose Paclitaxel 40 mg/m2/wk Versus IV Carboplatin (AUC 6) and Paclitaxel 175 mg/m2 Q 21 Days x 3 Courses Plus Observation in Patients with Early Stage Ovarian Carcinoma
A Phase III Randomized Trial of Paclitaxel and Carboplatin Versus Triplet or Sequential Doublet Combinations in Patients with Epithelial Ovarian or Primary Peritoneal Carcinoma
A Randomized Phase III Trial of Doxorubicin/ Cisplatin/ Paclitaxel/G-CSF versus Carbopltin/ Paclitaxel in Patients with Stages III&IV or recurrent Endometrial Cancer
A recent Moffitt article. Hope we tie up with this guy:
http://www.tampatrib.com/FloridaMetro/MGA9F5S1ARD.html
Moffitt's New Doctor Leaps Borders To Save Women
By GARY HABER ghaber@tampatrib.com
Published: Mar 1, 2004
TAMPA - Sean Tedjarati turns on the computer, looking for the lecture he gave his fellow oncologists on women's health care in developing countries.
It reveals a lot about Tedjarati that, when the computer screen flickers to life, the first image from his presentation is not an anonymous X-ray or a chart, dispassionately listing mortality rates.
It's a photograph of a woman from the Philippines whom Tedjarati treated for cervical cancer.
The Pap test has tamed cervical cancer in the United States. But around the world, this treatable disease kills as many as 1 million women a year.
That's a statistic Tedjarati, a gynecologic oncologist at H. Lee Moffitt Cancer Center & Research Institute, aims to erase.
His fellow physicians call him a go-getter who'll bring major changes to Moffitt, one of the nation's leading cancer centers but an institution some say can do more on the international stage.
``Five years from now, you'll see that things have changed globally, and they will have changed because of him,'' says James Fiorica, who directs Moffitt's gynecologic oncology program, and the man who recruited Tedjarati.
At 36 - the curtain call for a professional athlete's career but Act I for a cancer physician - Tedjarati is a Nobel Prize laureate. Tedjarati, who was born in Tehran, Iran, and grew up in France and Montreal, shared the Nobel Prize for Peace in 1999 for his work in Africa and China as a member of Doctors Without Borders.
With his international experience and an oncology fellowship from M.D. Anderson Cancer Center in Houston, Tedjarati could have gone to any cancer program in the country. He was enticed to come to Moffitt because the cancer center promised he would not only be able to treat patients and do research here, but also launch cancer screening and treatment programs around the world.
It's a cause close to Tedjarati's heart.
``How can you progress as a population when you don't have access to basic health care?'' he says. ``It's about the nobility of a person.''
Helping Women In Costa Rica
In the six months Tedjarati has been at Moffitt, he has helped engineer the largest international initiative in the center's history. He brokered an agreement with the Arias Foundation for Peace and Human Progress under which Moffitt physicians, and students and faculty from the University of South Florida School of International Affairs, will collaborate on a program to improve the lives of women in Costa Rica.
The idea is about more than medical care. Moffitt physicians, led by Tedjarati, will screen and treat women for cervical cancer. USF international affairs specialists will develop literacy and environmentally friendly economic development programs.
For Tedjarati, it represents the perfect blending of twin passions - women's health issues and international human rights - that have driven him ever since, at age 18, he volunteered in West Africa with the Canadian International Development Agency.
In the two decades since, through medical school in Connecticut and residencies in internal medicine and obstetrics and gynecology at Ohio State University medical school, Tedjarati has traveled to more than 60 countries on medical missions.
The personal touches in Tedjarati's shoe box of an office attest to his globe-trotting. On one wall hangs a collage of photographs from the Nobel Prize ceremony. On another wall, there is a scroll, written in Chinese characters, identifying Tedjarati as an honorary citizen of Anhui province in China for his work there.
Faith Prompts Action
Tedjarati attributes his commitment to human rights to his Baha'i faith.
``Service to human rights has to be part of our lives, not just an afterthought,'' he says. ``It's more than a simple feeling of charity. I hate that word, because that depicts a person in a position of desperation. Instead, I think of it in terms of nobility and elevation.''
Still, in a world of grueling 16-hour days, filled with treating patients and doing research, it takes a remarkable person to do what Tedjarati does, Fiorica says.
``You have to have the willpower and the drive to make this happen,'' Fiorica says. ``He will succeed at this, mark my words.''
Johnathan Lancaster, an assistant professor at Moffitt and medical director of the Lifetime Cancer Screening program, works with Tedjarati on Moffitt's OB/GYN team. The two have become good friends.
They are the same age, and each arrived at Moffitt in the summer, Lancaster from a fellowship at Duke University Medical Center.
``If you asked me for one word that describes Sean, I'd say intense,'' Lancaster says. ``He's a great partner, he's incredibly hard-working and 100 percent committed to everything he does.''
Tedjarati already has left his mark on Moffitt, Lancaster says.
His friend and colleague falls into that ``handful of people who come into your life where retroactively, or, if you're lucky, you realize at the time, they are going to greatly impact your life,'' Lancaster says.
The people of Costa Rica will soon find out the same.
And the reason I mention him is that the other name to watch out for in relation to Moffitt is Ed Seto:
http://hsc.usf.edu/com/iop/cancer/seto.html
Here's why:
DNAPrint Announces Relocation and Expansion
The company is also pleased to announce that Matthew J. Thomas, Ph.D. will be joining the company as a Scientist from his post at the H. Lee Moffit Cancer Center, University of South Florida, Tampa, FL. Dr. Thomas obtained his Ph.D. in Biology from the Department of Biology and Institute of Molecular Biology, University of Oregon. He is the recipient of the competitive Leukemia Society of America Fellowship, and has published original molecular biology research in such prestigious journals as Cell, Oncogene, Gene and Nucleic Acids Research. The addition of Dr. Thomas will help increase the Companies data flow and analysis.
Leukemia and Lymphoma Society 2001 Annual Report. Research Grant recipient Matthew J.Thomas, PhD –1999. University of South Florida
Identification of E2F-3B, an alternative form of E2F-3 lacking a conserved N-terminal region. Yiwen He, Michael K Armanious, Matthew J Thomas & W Douglas Cress. Oncogene 13 July 2000, Volume 19, Number 30.
Transcriptional Fidelity and Proofreading by RNA Polymerase II. Matthew J. Thomas, Angelina A. Platas, and Diane K. Hawley. Cell May 15, 1998: 93 (4).
Unlocking the mechanisms of transcription factor YY1: are chromatin modifying enzymes the key? Matthew J. Thomas, Edward Seto. Gene Volume 236, Issue 2, Page 197-355 (20 August 1999).
Incidentally, there is a Dr. Matt Thomas who is named as the medical director of Coastal Behavioral Healthcare, Inc (who are based in Sarasota). They are a not-for-profit dealing with substance abuse.
Cosmic, plenty more coming indeed:
"The first colon cancer study will involve 100 patients. Other phases of this particular project..."
"We have identified several clinical projects at the Moffitt that are of keen commercial and social interest," said Dr. Hector J. Gomez, MD, PhD, Chairman of the BOD and Chief Medical Officer of DNAPrint genomics, Inc. "Each of these programs offers us the opportunity to advance cancer treatment in a significant way," he said.
It will be interesting to see how many programs there are, how many projects within each program, and how many phases within each project. You can start to get an indication of the potential mangnitude of the work entailed in this relationship...