Par pharma NCD comments......http://www.aumag.org/lifeguide/THMay05.html

Endostar, Medgenn's name for YH-16, they presented at 2005 ASCO, they treated 486 patients...do a google "yh-16 lung cancer"

Great find Aaron...re: Endostatin was used to treat 486 patients with lung cancer in China.....I guess that's Medgenn's yh-16.

ENMD's acting like SIRI last year, a rally to $4, decline to $2, then to $9....this current rally may be the real deal

lol...Al says inflation's in check...Every two weeks I get a #3 and two chili dogs at Der Weiner...Two years ago, $5.15, now $7.50....less than truthful mocus on the hill.

nice pop today....my cycle mojo is always early...#msg-6718926

Thanks Aaron, Duke has been testing another drug too, looks like Incara is doing their own study, from 2004.....http://www.localtechwire.com/article.cfm?u=8697

S Korean dude is talking cure, I wonder why Duke chose 2me2 over YC-1 for trial...http://korea.net/news/news/newsview.asp?serial_no=20030409010

Looks like Medgenn updated their Chinese version web site....Yh-16 scrolling in box....http://www.medgenn.com

programmed cell death and HIF-1 mojo....http://www.grouppekurosawa.com/targets.htm

say what?... UCSD dudes boosting immune system, Spain dudes are too http://cancerforums.net/viewtopic.php?p=4857 both citing netrofiles/ netrophillia.... ENMD just presented in Spain...wth?

more recent hif-1 stuff..... UCSD researchers boost white blood cells' ability to kill bacteria03 Jul 2005   Scientists at the University of California, San Diego have determined how white blood cells up the ante against invading bacteria, a finding that may lead to new treatments for infections including those caused by invasive--"flesh-eating"-- Streptococcus bacteria. The findings, which are published in the July, 2005 issue of The Journal of Clinical Investigation, represent a collaborative effort between the laboratories of Randall Johnson, UCSD professor of biology and Victor Nizet, associate professor of pediatrics at the UCSD School of Medicine. The research team discovered that white blood cells respond directly to Streptococcus, Staphylococcus, Salmonella, and other bacteria that cause disease in humans, by increasing their levels of a protein known as hypoxia inducible transcription factor-1, or HIF-1. The protein, in turn, stimulates white blood cells to release antimicrobial compounds that kill bacteria. The team also found that treating white blood cells with chemicals to increase HIF-1 levels could enhance the cells' capacity to kill bacteria. "These findings suggest a potential novel approach to treatment of difficult infections such as those produced by antibiotic resistant bacteria or those affecting patients with weakened immune systems due to chronic disease, cancer chemotherapy or AIDS," said Nizet. "Rather than designing drugs to target the bacteria, medications that promote HIF-1 activity could be used to boost the bacterial killing ability of white blood cells and promote the resolution of infection through the actions of our natural immune defenses." Previous work by Johnson and colleagues showed that low oxygen levels, such as those found at the site of an infection, activate HIF-1 in macrophages and neutrophils--white blood cells that ingest and destroy microorganisms. In the current study, the researchers compared how well macrophages in which HIF-1 levels were elevated, normal or zero could kill bacteria, including Streptococcus isolated from a patient with flesh-eating disease. They found that the greater the HIF-1 levels in white blood cells, the greater their bacterial killing power. They also found that mice lacking HIF-1 in their macrophages and neutrophils were less able to combat skin infections than normal mice. "A direct correlation was established between the levels of HIF-1 present in the mouse macrophages and neutrophils and how efficiently the cells were able to kill the bacteria," said lead author Carole Peyssonnaux, a postdoctoral researcher with biology professors Johnson and Nizet. The HIF-1 protein is known to bind to cellular DNA and activate specific genes to help cells function is a low oxygen environment. The researchers found that in white blood cells, HIF-1 stimulates the production of small proteins, enzymes and nitric oxide, which work together to kill invading bacteria. "The placement of essential microbial killing functions of white blood cells under regulation of HIF-1 represents an elegant controlled response system," explained Johnson. "The white blood cells are in a resting state as they circulate in the oxygen-rich bloodstream, but can then be activated in response to the declining oxygen gradient encountered upon migration to sites of infection. Direct encounter with the bacteria then activates the neutrophils and macrophages maximally. Under HIF-1 regulation, antimicrobial genes are expressed only in infected tissues and not in healthy tissues where they could produce unwanted inflammatory damage." Recognition of the essential role for HIF-1 in the bacterial killing ability of white blood cells led the researchers to explore potential medical implications of this discovery. With the assistance of Emmanuel Theodorakis, UCSD professor of chemistry and biochemistry, a group of pharmacologic agents that act to increase cellular HIF-1 levels was selected. These compounds significantly enhanced the capacity of macrophages to kill bacteria. "Our findings offer proof of concept that small molecules can have a beneficial effect by modulating the production of HIF-1 protein in white blood cells," said Theodorakis. This research was financed by grants from the National Institutes of Health and the Edward Mallinckrodt, Jr. Foundation. Other authors contributing to the study were Vivekanand Datta, MD, UCSD graduate student in molecular pathology, Andrew Doedens, UCSD graduate student in biological sciences, Nancy Hurtado-Ziola, UCSD graduate student in biomedical sciences, Thorsten Cramer, MD, a gastroenterologist at Charite-Hochschulmedizin in Berlin, Germany, and Richard Gallo, MD, PhD, UCSD professor of medicine and pediatrics. University of California - San Diegohttp://www.ucsd.edu Save time! Get the latest medical news in your email every week with our newsletter.Send your press releases to pressrelease@medicalnewstoday.com

You're welcome Aaron, I still think leaky vessels may play a part in finding a treatment...I like Arbeit's comment too.. "but targeting one molecule sitting at the head of an interlocking genetic network is a powerful therapeutic concecpt"...more master switch mojo....Nice pop today.

There's an outside chance of a delayed street response to recent "master switch" mojo, much like the 1998 ramp...ggg

hif-1 regulates 100 genes?.....also leaky vessel discovery....
News Release
Alice Trinkl, News Director
Source: Jennifer O'Brien
jobrien@pubaff.ucsf.edu
415-476-2557
26 November 2001
Protein could help rejuvenate oxygen-starved cardiac tissue, heal wounds
A UCSF-led team is reporting striking results in mice that indicate that a molecule known as HIF-1 could prove an effective target for inducing the growth of blood vessels in oxygen-starved tissues. The strategy is sought for treating cardiac and peripheral vascular disease, diabetes-damaged tissues and intractable wounds.
The finding, reported in the October 1 issue of Genes & Development, is a notable advance in an effort that has met with setbacks. Researchers have tried to generate the production of healthy blood vessels by inducing over-expression of the growth factor VEGF. But studies in mice have shown that while over-expression of VEGF induces the growth of blood vessels, the capillaries are leaky, the tissues are inflamed and swollen, and the blood vessels have an abnormal "corkscrew-like" shape.
In the current study, researchers genetically engineered mice to overexpress the HIF-1 gene in skin cells. In response, the number of capillaries in the mice's skin increased by nearly 70 percent. More importantly, the blood vessels did not leak, cause swelling or inflammation.
"The vessels looked like normal capillaries," says senior author Jeffrey M. Arbeit, MD, UCSF associate professor of surgery, and a member of the UCSF Comprehensive Cancer Center. "This finding, together with the fact that the vessels didn't leak, is extremely exciting." The increase in healthy blood vessels was evident in the mice's significantly pinker ears, paws and tails.
Notably, in the current study the overexpression of the HIF-1 gene caused a 13-fold increase in the expression of the VEGF gene. The fact that HIF-1 had an effect on VEGF expression is not surprising in itself, as HIF-1 is a sub unit of the HIF-1 transcription factor, which regulates the expression of numerous genes, including VEGF. However, the finding does prompt the question of why the blood vessels were robust, given that previous studies involving elevated expression of VEFG led to the development of weak, leaky vessels.
"We know that VEGF plays a crucial role in blood vessel growth. We need to determine how overexpression of HIF-1 harnesses VEGF in a way that could be beneficial therapeutically," says lead author David Elson, BA, UCSF staff research associate in the Arbeit lab.
The potential clinical implications of the finding are significant. The HIF-1 gene is already being explored as a stimulant to promote blood vessel growth in oxygen-deprived, or ischemic, tissue such as that associated with diabetic peripheral vascular disease, which can cause chronic leg ulcers that often precipitate amputation. It is being investigated as therapy to increase blood flow into cardiac tissue deprived of oxygen due to clogged arteries, and as therapy to treat recalcitrant wounds resulting from lack of blood flow to the legs caused by atherosclerosis alone or in association with diabetes. It could also be used to promote the grafting of artificial skin into tissues of the body, either in burn or diabetic patients. Once a graft had fused with the skin, the gene could be "turned off."
On the flip side, HIF-1 could prove a potent target for cancer therapy. Malignant tumors must recruit blood vessels to fuel their growth. Scientists have known that HIF-1 is over-expressed by malignant tumors, and NIH investigators currently are exploring its potential as a therapeutic target. However, the gene's specific role in cancer development has not been known. The discovery that overexpression of the gene generates the growth of robust blood vessels will assist ongoing therapeutic studies.
There are various possible explanations for why the new blood vessels in the UCSF study were robust despite the elevated expression of VEFG, says Elson. In the current study, over-expression of HIF-1 caused the induction of the naturally occurring VEGF gene. In previous studies, scientists engineered the expression of various splicings, or isoforms, of the VEGF gene. It may be, says Elson, that the spectrum of alternatively spliced isoforms created by the naturally occurring VEGF does not cause leakage. Alternatively, he says, the HIF-1 transcription factor may increase expression of an as-yet-unidentified target that modulates vascular permeability independent of VEGF function.
The current finding leads scientists a step closer to teasing out the specific role of HIF-1. The HIF-1 transcription factor regulates the activity of numerous genes, some of which promote blood vessel growth, or angiogenesis, in response to oxygen deprivation. And scientists have known that the HIF-1 gene, a sub unit of the transcription factor, activates genes required for energy metabolism and tissue perfusion during periods of oxygen deprivation and is likewise necessary for embryonic development. They have also known that the gene is over-expressed during myocardial infarction (when blood flow is blocked from reaching the heart) in wound healing (which requires oxygen for tissue repair) and in malignant tumors. But its specific role in these conditions has not been known. Once expressed, HIF-1 is swiftly degraded at the protein level in healthy adult cells.
In their study, the researchers created mice genetically engineered to maintain expression of the gene in an attempt to tease out its impact. They did so by inserting normal HIF-1 into skin cells or inserting copies of the HIF-1 gene lacking the portion of the gene that normally degrades HIF-1. This region is known as the oxygen-dependent degradation domain (ODD).
While researchers still must determine how HIF-1 prompts the development of healthy blood vessels in spite of over-expression of VEGF, the study reinforces the importance of the sub-unit. The finding also suggests the importance of focusing on the overall influence of the HIF-1 transcription factor, says Arbeit.
HIF-1, like the hormone estrogen, is a master regulatory transcription factor, meaning that it controls the expression of a vast number of genes representing various functions. HIF-1 is known to regulate 30 genes, but it may regulate as many as 100 genes, says Arbeit. The more scientists learn about the role of the genes in such molecular pathways the more opportunity they have for learning to manipulate them to treat disease.
A surgeon by training, Arbeit has seen the impact of both unwanted blood vessel growth, as in cancer, and oxygen-starved tissue, as in recalcitrant wounds.
"I don't ascribe to the hope for a magic bullet for treating disease," he says, "but targeting one molecule sitting at the head of an interlocking genetic network is a powerful therapeutic concept."
Other co-authors of the study were Gavin Thurston, PhD, formerly UCSF adjunct assistant professor of anatomy and now at Regeneron Pharmaceuticals, Inc; David G. Ginzinger, PhD, director of the UCSF Genome Analysis Core in the UCSF Comprehensive Cancer Center; Donald M. McDonald, MD, PhD, UCSF professor of anatomy and a member of the UCSF Cardiovascular Research Institute; L. Eric Huang, PhD, of the Laboratory of Human Carcinogenesis, National Cancer Institute; and Randall S. Johnson, PhD, associate professor of biology, UC San Diego.
The study was funded by the National Institutes of Health.
###
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"Silenced" gene suggests greater Risk and a possible diagnostic marker for African-Americans with prostate cancer
Among African-Americans with prostate cancer, a tumor-suppressing gene called GSTP1 is inactivated at a rate 3.5 times higher than among Caucasians, according to a study conducted at the San Francisco VA Medical Center (SFVAMC).
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say what?...http://cancerforums.net/viewtopic.php?p=4857

June 21, 05.....   Powered by    SAVE THIS / EMAIL THIS / Close   Nanotech delivers cancer treatment(CNN) -- Scientists using nanotechnology have devised a way of delivering cancer drugs that could make them up to 10 times more effective in combating the killer disease.By attaching a chemotherapeutic drug to manmade nanoparticles, the team of researchers at the University of Michigan were able to smuggle it inside cancerous cells, delaying the growth of tumors in mice by up to 30 days -- the equivalent of three years in a human.Professor of biologic nanotechnology James Baker, who led the research, said that the treatment might eventually turn cancer into a chronic but treatable condition.The study, which is published in the current edition of the Cancer Research journal, is one of the first successful therapeutic uses of nanotechnology on living animals."This is the first study to demonstrate a nanoparticle-targeted drug actually leaving the bloodstream, being concentrated in cancer cells, and having a biological effect on the animal's tumor," said Baker."We're very optimistic that nanotechnology can markedly improve cancer therapy."Baker said that the technique was based on a Trojan Horse principle.The vehicle delivering the drug is a manmade polymer molecule called a dendrimer that measures less than five nanometers in diameter, or five billionths of a meter, making it small enough to pass through cell membranes.The dendrimer's tree-like structure allows scientists to attach other molecules to its branches.Some of these are loaded with the cancer treatment drug methotrexate. But others carry folic acid, which cells -- and particularly cancer cells -- need to replicate.By baiting them with the folic acid, the cancer cells are tricked into also accepting the methotrexate, which then poisons them.The dendrimer is then flushed out of the bloodstream via the kidneys.The nanoparticle-based therapy was 10 times more effective at delaying tumor growth in mice and less toxic to other cells and tissue than conventional treatment.In chemotherapy, the drug is diffused across a cell membrane before getting inside cancerous cells. That requires a high concentration of drugs, which can damage healthy cells as well.If the toxicity problem can be overcome, the method may allow for the delivery of other, more powerful chemotherapy drugs and also enable more personalised cancer treatment, tailored for the specific requirements of individual patients."Targeting drugs directly to cancer cells reduces the amount that gets to normal cells, increases the drug's anti-cancer effect and reduces its toxicity. By improving the therapeutic index of cancer drugs, we hope to turn cancer into a chronic, manageable disease," said Baker.Further research is due to be undertaken to determine the maximum therapeutic dose, with the first human clinical trials scheduled to begin within two years.Emma Knight of the Cancer Research charity told the New Scientist magazine that the results of the study were "very interesting.""They show that nanotechnology has the potential to increase the effectiveness of modern-day cancer drugs by specifically targeting them to cancer cells," she said.   Find this article at: http://www.cnn.com/2005/HEALTH/06/21/cancer.nanotech/?section=cnn_latest    SAVE THIS / EMAIL THIS / Close   Check the box to include the list of links referenced in the article.   

possible fast track for oat cell in the near future?.... "These data are encouraging and indicate the potential of 2me2 and its new analogs for treating non-small cell lung cancer and small cell lung cancer in humans"

from PR this week... " Entremed said this preclinical trial found that panzem NCD blocked the in vitro growth of 19 different lung cancer cell lines".....blocking multiple signals?...#msg-6870155 ....Also "The company plans to begin Phase 2 studies this year"

It'd be a hoot if panzem blocks ALL sources....from master switch article.... "By pinpointing and blocking the source of ALL the signals".... "By blocking the master switch, we effectively blocked many of the proteins which promote angiogenesis"

I think they need to start a trial with sum Panzem NCD...... Source:University Of California, San DiegoDate:2003-03-18URL:http://www.sciencedaily.com/releases/2003/03/030318074607.htmUCSD Biologists Discover Key To Blocking InflammationBiologists at the University of California, San Diego have discovered that eliminating the ability of white blood cells to respond to low oxygen levels effectively blocks the development of inflammation in mice, an advance that could have widespread implications for the prevention of inflammation in humans. Their discovery, detailed in the March 7 issue of the journal Cell, could lead to the development of a new class of drugs for treating the debilitating and painful joint inflammation in the 43 million Americans who suffer from arthritis. It also may help doctors treat cancer more effectively, because tumor development is associated with a pronounced inflammatory response in the vast majority of cases. Scientists had previously documented the mechanisms by which white blood cells are directed to sites of injury by the low oxygen levels typically found at those locations. "When you have a cut, the local vascular structure surrounding the wound is disrupted and there's no longer a normal supply of oxygen being delivered," says Randall S. Johnson, an associate professor of biology, who headed the study. "White blood cells (leukocytes) constitute the first line of defense against invading microorganisms like bacteria or viruses and accumulate at sites of injury. Because these cells operate outside of the blood vessels, they need to be able to function in a low-oxygen environment." Leukocytes that enter these low oxygen, or hypoxic, environments also possess molecular and genetic "switches" that allow them to change their metabolism from an oxygen-dependent (aerobic) to an oxygen-independent (anaerobic) mode of generating energy. But until now, the importance of those switches to regulate inflammation was not well understood. By eliminating the ability of the white blood cells--specifically macrophages and neutrophils--to turn on their hypoxic response and generate energy anaerobically, the UCSD scientists were able to stop the usual development of inflammation in laboratory mice. "By altering the ability of these cells to operate normally in a low oxygen environment, we've essentially prevented inflammation in mice," notes Johnson. To demonstrate that this was the case, Johnson and Thorsten Cramer, a gastroenterologist from Berlin in Germany working as a research fellow in Johnson's UCSD laboratory, produced three different strains of mice, each of which had been genetically modified without a key factor in a biochemical pathway known to regulate the ability of the cells to adapt to low oxygen environments. Testing the responses of the three different strains, the scientists discovered that inactivation of a protein known as hypoxia inducible transcription factor-1, or HIF-1, strongly blocked the inflammatory response in mice. Johnson and Cramer were able to show that HIF-1 is essential for metabolism and energy generation of the white blood cells. In mice without a regulatory protein known as the von Hippel Lindau factor, or VHL, which degrades HIF-1 in normal cells, the UCSD scientists discovered that the inflammatory response was heightened, presumably due to the large excess of HIF-1 that accumulated in the white blood cells. "Chemists characterized the central importance of anaerobic energy generation for the function of white blood cells almost a century ago," says Cramer. "By using genetic technology we were not only able to confirm these experiments, we also identified a key molecular player involved in white blood cell energy synthesis. To me this is one of the most exciting details about our study." With the help of Yuji Yamanishi, Gary Firestein and Maripat Corr of the UCSD School of Medicine, the researchers also found that mice without HIF-1 could avoid the joint swelling and inflammation symptoms that typically occur when normal mice are subjected to an arthritis-inducing treatment. But the loss of HIF-1 does not come without a cost. Experiments conducted in collaboration with Victor Nizet of UCSD's School of Medicine showed that the loss of HIF-1 from white blood cells erodes their ability to kill bacteria. The scientists also found that the ability of the cells to leave the bloodstream and move through the body was significantly impaired without HIF-1. Other scientists who contributed to the study included Bjorn Clausen of the University of Amsterdam in the Netherlands, Irmgard Forster of the Technical University of Munich in Germany, Rafal Pawlinski and Nigel Mackman of the Scripps Research Institute, Volker Haase of the University of Pennsylvania School of Medicine, Rudolf Jaenisch of MIT, and Hans-Peter Gerber and Napoleone Ferrara of Genentech, Inc. Johnson says one advantage HIF-1 inhibition might have over methods for treating severe arthritic inflammation that involve reducing a patient's white blood cell count, is that blocking HIF-1 doesn't affect the number of circulating white blood cells. "This may prompt people to take a look at the large number of HIF-1 inhibitors being developed for anti-cancer treatment," he says. "These drugs may turn out to have an even bigger market in treating inflammation and arthritis." Johnson notes that the discovery may have its greatest value as an insight into the basic biology of cells, which all possess the ability to switch between aerobic and anaerobic metabolism, and cells that circulate through the body. "Cells that migrate throughout the body need to have the capacity to function in low oxygen environments," he adds. "If you remove that, you've limited the ability of the cell to function. But by blocking this pathway, you've also blocked unwanted inflammation." The study was financed by the National Institutes of Health and the Deutsche Forschungsgemeinschaft (German Research Foundation).This story has been adapted from a news release issued by University Of California, San Diego.

There was a complete response in a early trial with a panzem ( old formulation trial) taxotere combo..Now a panzem NCD /taxotere trial is planned...great news.

Duke..Duke...Duke!...remember this awhile back?...master switch..http://www.charitywire.com/charity280/05584.html

That's fantastic news.....That's more evidence from Duke supporting a panzem/ chemo combo...note last paragraph...Media contacts: Vince Dollard, 404-778-4580, vincent_dollard@emoryhealthcare.org April 22, 2003  WCI Researchers Outline Mechanics of Anti-Tumor Activity in Clinical Trial Drug Atlanta -- Inhibiting the growth and the angiogenic properties of cancer is an important modality for cancer treatment and research. Angiogenesis, the development of new blood vessels from pre-existing vasculature, supports the development of many diseases including cancer, rheumatoid arthritis and others. In the case of cancer, angiogenesis is essential for the growth, progression and metastasis of a tumor and thus, agents that inhibit angiogenesis are attractive therapeutic options. In an article published today in the April issue of Cancer Cell (Vol. 3, No.. 4, pg. 363), Winship Cancer Institute (WCI) researchers report that 2-methoxyestradiol (2ME2) inhibits tumor growth and angiogenesis by suppressing hypoxia-inducible factor-1 (HIF). HIF is a factor that is over-expressed in more than 70% of human cancers and their metastases, including breast, prostate, brain, lung, and head and neck cancers. Besides cancer, HIF is also associated with diseases of the bone and diseases that are mediated by inflammation such as rheumatoid arthritis. The paper, "2ME2 Inhibits Tumor Growth and Angiogenesis by Disrupting Microtubules and Dysregulating HIF," was authored by WCI and Emory University scientists Nicola J. Mabjeesh, MD, PhD, Daniel Escuin, and Paraskevi Giannakakou, PhD. The paper was co-authored with scientists Theresa LaVallee, PhD, Victor Pribluda, PhD, and Glenn Swartz from EntreMed, a biopharmaceutical leader in angiogenesis research and product development.. 2ME2 is a well-tolerated, orally active small molecule with anti-angiogenic and anti-tumor activity currently in Phase I/II clinical trials under the name Panzem. The trials are being conducted by EntreMed. "This report contributes to the body of knowledge that will help us better understand the basic mechanism by which 2ME2 inhibits cancer cell growth and tumor angiogenesis," says Dr. Giannakakou. Drs. Mabjeesh and Giannakakou report that 2ME2 inhibits tumor growth and angiogenesis by targeting microtubules, or a cell's skeleton, and suppressing HIF activity. "The study is the first to demonstrate that an agent, 2ME2, inhibits the assembly of microtubules in the tumors of treated animals," says Dr. Giannakakou. "Microtubule disruption results in the down regulation of HIF-1a and, while this effect is not unique to 2ME2, it is the most potent HIF inhibitor of all the microtubule-targeting chemotherapeutic agents tested that are used to treat cancer." The paper outlines the mechanism by which 2ME2 downregulates HIF; a finding that had not been previously discovered. Utilizing a pharmacological approach and xenograft models, which are mouse models of human cancer, investigators showed that 2ME2 depolymerizes microtubules and blocks HIF-1a nuclear accumulation and HIF-transcriptional activity, or the transfer of genetic code information from one kind of nucleic acid to another. "This research is important because we see for the first time a mechanistic link between targeting of the microtubule cytoskeleton and inhibition of angiogenesis," says Dr. Giannakakou. "This work will provide a new framework to study and develop novel compounds for the treatment of cancer." In addition to Drs. Mabjeesh, and Giannakakou and PhD-candidate Daniel Escuin, WCI investigators Margaret T. Willard, PhD, Hua Zhong, PhD, and Jonathan Simons, MD contributed to the paper. About Panzem[2-methoxyestradiol (2ME2)] is a naturally occurring metabolite of endogenous estrogens. Its versatile properties allow a wide range of potential formulations for drug delivery to treat numerous indications. In Phase I and Phase II oncology trials, orally administered Panzem" has demonstrated anticancer activity in patients with breast cancer, prostate cancer and multiple myeloma, a blood cancer. Clinical investigators reported patients have shown tumor response, stable disease and/or clinical benefit, including one patient who received Panzem in combination with Taxotere having a complete tumor response. Panzem was well tolerated by all patients. Results in preclinical models with ocular implants of Panzem have demonstrated that it may inhibit neovascularization of age-related macular degeneration (ARMD). Allergan and EntreMed are developing the localized use of Panzem for the treatment of ARMD and other diseases of the eye. Return to April IndexFor more general information on The Robert W. Woodruff Health Sciences Center call Health Sciences Communication's Office at 404-727-5686,or send e-mail to hsnews@emory.edu Copyright © Emory University, 2001. All Rights Reserved.

The timing is interesting...Cool graphics, looks like a bottle of NCD surrounded by clear vials of something else. That butterfly on a sunflower is outta sight. I like the new site.....http://www.entremed.com

tip.....ENMD

war is hell.....http://thenausea.com/usa-iraq.html

a riddle....Rookie bank robber enters a bank and makes a beeline to "info" desk across from teller windows. The receptionist informs the robber that she doesn't deal with cash....Ooooops!...Robber panics and hauls out the front door, to be caught later....(true story)....there's a ENMD analogy in there somewhere.....to da moon!......soon

rubik's cube....http://focus.hms.harvard.edu/2004/March19_2004/oncology.html

I have a June 2005 ENMD cycle buy....no target...eom

Maybe ENMD's planning funding for a manufacturing plant, cranking out Panzem 24/7....Probably not though, if Panzem is a big hit, ENMD is too small to handle the rush of business.

ot...7.2 quake off California coast...Drudge

The buzz around here, so says my barber, is an influx of folks from CA and AZ buying McMansions with pocket change....http://www.amarillo-homes.com/html/6403_Tarrington.cfm

LA riots tonight?...eom

looks like bubble vision jinxed GOOG, she topped the day they put a GOOG bug on the screen.

Merriman thinks bonds might top soon....what the heck?....http://www.mmacycles.com/artweek.htm

The current action is similar to the late March, early April period. then the Dow went flat for 3 weeks, then boom a wild up/down day right before the nosedive.

I smell a Dow gravestone doji at the close....Buy puts!

I had a hunch gold would be up....note rising red line, the commercials...bullish....http://www.marketpit.com/Gold.htm

marketpit update, SnP commercials (red line) took a dive last two week, bearish.....bottom of page....http://www.marketpit.com/S&P500.htm