By: tellslikeitis
13 Sep 2004, 12:35 PM EDT
Msg. 166716 of 188686
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Elma presented the data for the AIDS cachexia trials in Israel that were presented at ASCO and restated and extolled those results. She also presented as outstanding, a study on 31 patients with mild to moderate rheumatoid arthritis that was conducted in Argentina. There was also an indication of the drug's efficacy and potential use in diabetes.

That being said, she indicated that the topic of the IND to be submitted in the beginning of next year would be in a variety of cancers. What nags at me is that if AIDS cachexia and arthritis are two indications for which clear efficacy and safety have been established in foreign trials, why is she now switching gears to something which is untested, and may or not prove as good, in cancer patients with heterogenous disease histories and treatment histories? Why not go for a sure thing to get the drug onto the market for something that is tried and true, rather than venture into uncharted territory and gamble on a trial on yet another new untested application of the drug? Clearly there is a huge global market for rheumatoid arthritis (and still a lack of safe, non-toxic drugs for its treatment) and an adequate market for an AIDS cachexia drug (which would be fast-tracked) to get AVR118 onto the market. Once on the market physicians would prescribe the drug for off-label use in other diseases and conditions.

Is the Hirschman syndrome of switching gears mid-stream (from AIDS to HPV to AIDS cachexia) plaguing us again with his successor Elma? Does AVR like to repeat costly mistakes?

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By: lovingitall0
13 Sep 2004, 09:39 AM EDT
Msg. 166682 of 188686
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More AVR118 exposure today: Advanced Viral Research Corp. (BB:ADVR) announced today [Sept. 8] that its CEO and President, Dr. Elma Hawkins, will be a presenter at The Wall Street Analyst Forum's Analyst Conference. The presentation will take place on Monday, September 13th, 2004 at The Roosevelt Hotel on Madison Avenue & 45th Street in New York City.

Dr. Hawkins will present on the progress the company is making with its flagship product, AVR118, to biotech and pharmaceutical analysts. The presentation will be simultaneously web cast at 10:20 a.m. ET at the following web address:

By: Ourobouros
15 Sep 2004, 12:08 PM EDT
Msg. 167111 of 188686
(This msg. is a reply to 167108 by mind31.)
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"recent prs no mention of DR H. whats he doing?"

diamond...selling his virtual shares he never bought in real life.

By: yanks04
15 Sep 2004, 12:59 PM EDT
Msg. 167116 of 188686
(This msg. is a reply to 167112 by mind31.)
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Friedlands are gone. If he does that Bregman should cough up his free shares. Only a third of Hirschman shares are free. Bregmans were free. Friedlands were free. Hawkins will have to look.

•  Trade like a pro with Qcharts



By: tellslikeitis
13 Sep 2004, 12:35 PM EDT
Msg. 166716 of 188686
Jump to msg. #  
Elma presented the data for the AIDS cachexia trials in Israel that were presented at ASCO and restated and extolled those results. She also presented as outstanding, a study on 31 patients with mild to moderate rheumatoid arthritis that was conducted in Argentina. There was also an indication of the drug's efficacy and potential use in diabetes.

That being said, she indicated that the topic of the IND to be submitted in the beginning of next year would be in a variety of cancers. What nags at me is that if AIDS cachexia and arthritis are two indications for which clear efficacy and safety have been established in foreign trials, why is she now switching gears to something which is untested, and may or not prove as good, in cancer patients with heterogenous disease histories and treatment histories? Why not go for a sure thing to get the drug onto the market for something that is tried and true, rather than venture into uncharted territory and gamble on a trial on yet another new untested application of the drug? Clearly there is a huge global market for rheumatoid arthritis (and still a lack of safe, non-toxic drugs for its treatment) and an adequate market for an AIDS cachexia drug (which would be fast-tracked) to get AVR118 onto the market. Once on the market physicians would prescribe the drug for off-label use in other diseases and conditions.

Is the Hirschman syndrome of switching gears mid-stream (from AIDS to HPV to AIDS cachexia) plaguing us again with his successor Elma? Does AVR like to repeat costly mistakes?

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View Replies »


By: buckaroobanzai10
13 Sep 2004, 12:57 PM EDT
Msg. 166717 of 188686
(This msg. is a reply to 166716 by tellslikeitis.)
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tells- Elma's going for cancer trials because her past work at Antigenics involved anti-cancer drugs. She probably has dealt with, and personally knows the Oncology Commiteee people at the FDA and preferes to work with familiar people than with unknown new people on an AIDS or Arthritis FDA Committee.

13 Sep 2004, 03:40 PM EDT
Msg. 166754 of 188686
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ELMS where i come from TALK IS CHEAP! BREGEMAN, DR H, ELI, DR D, we have heard all there BS for 18+ years. and .08 then and .14 now! ...PATHETIC
By: rickv
13 Sep 2004, 01:32 PM EDT
Msg. 166723 of 188686
(This msg. is a reply to 166700 by billblueyz.)
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there was a 34 page slide show it was very impressive with the data on it. i am hoping advr will have that slide show downloadable off of their website. it would be good for investors and would be investors. Elma knocked my socks off on how focused she was, professional and right to the point. She did an excellent presentation. May she succeed and we will be at 5 bucks in the future. IMO
By: ricourt0
13 Sep 2004, 12:06 PM EDT
Msg. 166705 of 188686
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Good presentation.....I admire your sincerity to this product!

no new news was presented that I could see.





By: chrome21st
14 Sep 2004, 09:01 AM EDT
Msg. 166857 of 188686
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By: lovingitall0
14 Sep 2004, 09:03 AM EDT
Msg. 166858 of 188686
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*****Re ADVR and AVR118: If anyone missed the presentation by our
CEO and President, Dr. Elma Hawkins, at The Wall Street Analyst Forum Conference on September 13, it will be available for 30 days thereafter.

Dr. Hawkins discussed the progress the company is making with its flagship product, AVR118, to biotech and pharmaceutical analysts.

You can tune into it at the following web address:



By: Ourobouros
15 Sep 2004, 12:08 PM EDT
Msg. 167111 of 188686
(This msg. is a reply to 167108 by mind31.)
Jump to msg. #  
"recent prs no mention of DR H. whats he doing?"

diamond...selling his virtual shares he never bought in real life.


By: yanks04
15 Sep 2004, 12:59 PM EDT
Msg. 167116 of 188686
(This msg. is a reply to 167112 by mind31.)
Jump to msg. #  
Friedlands are gone. If he does that Bregman should cough up his free shares. Only a third of Hirschman shares are free. Bregmans were free. Friedlands were free. Hawkins will have to look.

•  Trade like a pro with Qcharts
By: SUE32073
15 Sep 2004, 05:45 PM EDT
Msg. 167200 of 188686
(This msg. is a reply to 167196 by yanks04.)
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Yanks....she joined ADVR in February, which is 7 months. I do hear she has been able to obtain a Gold Card with Office Max, since her presentations (flip chart, slide projectors, etc., etc.) were costly.
By: lovingitall0
15 Sep 2004, 06:56 PM EDT
Msg. 167215 of 188686
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***Re ADVR and AVR118: If anyone missed the presentation by our CEO and President, Dr. Elma Hawkins, at The Wall Street Analyst Forum Conference on September 13, it will be available for 30 days thereafter.

Dr. Hawkins discussed the progress the company is making with its flagship product, AVR118, to biotech and pharmaceutical analysts.

You can tune into it at the following web address:
By: lovingitall0
16 Sep 2004, 07:45 AM EDT
Msg. 167254 of 188686
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Linking Viruses & Cancer

Viruses and cancer are linked, but why?

Some say immune response to infection is the mechanism that turns infectious organisms into cancer

by Marie Rosenthal, Editor in Chief
February 2004, Infectious Disease News

NEW YORK – More than a dozen viruses have been linked with various cancers, although no one is entirely sure why this phenomenon occurs.

It is probably related to the immune responses to infection. Perhaps, immune modulators change the host gene in some people, which increases their risk for cancer development. In other words, “… the stuff that goes on in the environment of the infected cell – what we call the milieu – that deals not only with the release of immune modulators that causes the tissue to get red and swollen and hot – but causes some dysfunction,” explained James J. Goedert, MD, chief of the viral epidemiology branch, and senior investigator at the National Cancer Institute (NCI).

In some cases, he added, superinfection may release reactive oxygen species that damage DNA and alter the host gene expression.

Finding a link between infection and cancer has been difficult because finding a virus in a cancer does not prove causation, according to the American Society of Clinical Oncology (ASCO), which sponsored a seminar on the topic here. To make the relationship even harder to prove, not every infected individual will develop cancer, and uninfected people can develop the same cancer.

However, there are clear links between viruses and cancers, said Goedert. Overlapping epidemiology between viruses and cancers can be a clue to this link. Incidence of certain cancers is highest where specific infectious diseases are endemic. However, there is no way to know which person with a specific infection will develop cancer, said Goedert.

One way to understand the link better is to look at infections that are positively linked to cancers and try to determine why, he said.

HBV, HCV and liver cancer

Hepatocellular carcinoma accounts for more than 90% of primary liver cancers and is one of the most common malignancies in the world, accounting for about 500,000 cancers a year, according to Andrew X. Zhu, MD, PhD, assistant physician at Massachusetts General Hospital in Boston.

“This is a disease for which we have multiple treatment options, yet the prognosis remains dismal,” he said.

Although the incidence has been higher in developing countries than developed ones, this trend is changing, and hepatocellular carcinoma incidence and mortality in the United States has increased twofold between 1975 and 1998. “Although this increase is affecting all ethnic and most age groups, white men between 45 and 54 years of age have the fastest increase,” Zhu explained.

This increase, in part, is due to hepatitis B and C. There are 300 million people worldwide with chronic hepatitis B virus (HBV) infection, with 1.25 million chronically infected people in the United States. There are about 100 million people worldwide with hepatitis C (HCV), and 4 million people chronically infected with HCV in the United States.

“We do know from the epidemiological studies that there is a strong association between HBV–HCV infection and hepatocellular carcinoma development. We can develop different sophisticated testing to look for the HBV and HCV molecules in hepatocellular carcinoma. They are definitely present,” said Zhu.

The mechanism that turns HBV or HCV into hepatocellular cancer is a complicated interaction between specific viral gene products and the host immune system, as well as the underlying genomic stability. There is speculation that screening for the viruses may be beneficial in endemic areas to prevent cancer. This approach, however, has not been validated in a randomized control study.

Prevention appears to be a rational approach for these diseases because there are well-defined risk factors, Zhu said. In addition, there is an effective vaccine against HBV. However, the search for an HCV vaccine has been elusive.

“This virus is fairly smart. We have the different genotypes and quasi-species, so the virus has sophisticated ways of evading the immune system. Even if you develop one vaccine, probably it won’t be as effective as you think,” Goedert explained. “You may have to design a specific vaccine depending on the genotype in the particularly endemic area.”

Understanding the biology of how the cancer develops in the cells, and developing better prevention and treatment programs “will continue to represent very key strategies to prevent hepatocellular cancer,” said Zhu.

HPV and multiple cancers

Human papillomavirus (HPV) is the most common sexually transmitted disease in the United States, said Maura L. Gillison, MD, PhD, assistant professor of oncology at Johns Hopkins School of Medicine in Baltimore.

“There are more than 600,000 cases of cancer worldwide that can be attributed to HPV infection,” Gillison said. Most of the cancers are cervical, vulvar cancer, penile and a.n.a.l squamous cell carcinomas, but over the last three years there’s been “quite an explosion of data” to implicate HPV in head and neck cancers, she added.

Although cervical cancer incidence in the United States has declined because of effective screening, a.n.a.l and tonsillar cancer incidence has increased. “Cervical cancer is unique among the cancers that are associated with HPV in that HPV infection is necessary, although not sufficient for the development of cervical cancer. In all other cancers where there is an established association, it will likely be a subset of cancers at that anatomic site that are etiologically related to HPV,” she said.

The 130 types of HPV fall into cutaneous and mucosal types; the mucosal or genital HPVs are further divided into those that are strongly associated with cancer. The highest risk types are HPV16, 18, 31 and 33.

In cervical cancer, the cancer-causing types of HPV encode two oncoproteins, E6 and E7. HPV-E6 binds to another cellular protein that targets p53 for degradation. p53 is the tumor-suppressor gene that is most common in human malignancies. HPV-16 E7 binds to hypophosphorylated retinoblastoma protein and targets that protein for degradation. This releases transcription factors that are important in the progression of the cell cycle from G1 to S, explained Gillison.

“That means infection of a cell by a high-risk HPV type is functionally analogous to mutating two tumor suppressor genes that are important in the development of human malignancies,” she said. This causes a “loss of cell control, of DNA damage repair, progression through the cell cycle, genomic integrity, cellular differentiation and cell death. All of those contribute to how HPV causes cancers to progress,” she said.

A recent study in Cancer by Taiwanese researchers found that the presence of HPV-31 was an independent predictor of increased survival in patients with cervical cancer. As a result of their data, HPV genotyping of cervical carcinomas may have profound implications for future management of cervical cancer patients, they concluded.

Sexual behavior, including oral sex for head and neck cancers, is the single greatest risk factor for HPV exposure. “And if it wasn’t the person’s behavior, it’s the behavior of the sexual partner,” she said.

Immune state, genetic makeup and the type of HPV are important factors that determine whether infection will clear or become cancer. Smoking and long-term use of oral contraceptives may increase the likelihood that HPV infection will persist.

Most head and neck cancers that arise in the nonsmoker and nondrinker are associated with HPV. HPV-DNA is found in 20% of all head and neck cancers, and up to 70% of tonsillar cancers are HPV-associated. “We know that there is virtually an epidemic of tonsillar cancer in the United States that’s unexplained, and I think we’ve now explained it,” Gillison said.

There is work being done on HPV vaccines, however, they do not seem to be effective against all types of HPV, and will probably be type specific.

H. pylori and gastric cancers

Helicobacter pylori infection tends to be acquired in childhood and is lifelong unless antibiotic therapy eradicates the organism, said Charles S. Rabkin, MD, MSC, senior investigator, viral epidemiology at NCI.

It is almost universally present in the developing world where infection rates exceed 85% in most adults. In contrast, the risk of infection in the West is lower, so that infection rates of 10% to 20% are now being seen in adults.

No one completely understands how the infection is acquired, but there does appear to be person-to-person transmission, and the infection can cluster among family members.

H. pylori has developed good techniques for surviving in the acidic environment of the stomach, which kills most other organisms. These techniques, including the secretion of urease and lipopolysaccharide (LPS), help induce the diseases that are associated with helicobacter.

As it colonizes the mucosal layer, LPS and peptides secreted by H. pylori pass through the epithelial layer under the stomach lining. This attracts neutrophils and monocytes that release a number of factors, such as tumor necrosis factor, oxygen-free radicals, prostaglandins and interleukin-1 beta, damaging the gastric lining.

“So this is an indirect effect. It’s not direct contact with H. pylori, but rather it’s an effect of the secreted mediators that cause the gastric inflammation – the first step in the process of disease caused by helicobacter,” Rabkin said.

It’s a universal phenomenon that people with helicobacter infection develop gastritis, yet most are asymptomatic. Ulcer disease occurs in around one in 10 people who have H. pylori infection, and gastric lymphoma and gastric carcinoma happen in just 1% to 2% of people who are infected over many decades.

Although overall gastric cancer has been decreasing, adenocarcinoma of the esophagus is increasing. “The noncardia cancers are showing the declines, and that makes up the bulk of gastric cancer. This is what drives the rate of gastric cancer overall,” he said. “But very worryingly, the cardia cancers both in men and women and in whites and in blacks have been on the increase,” Rabkin said.

HTLV-1 and lymphoma

There are about 15 million to 20 million cases of human T-cell leukemia virus (HTLV-1) worldwide, said Francine M. Foss, MD, director of lymphoma and experimental therapeutics at Tufts-New England Medical Center. This was the first human retrovirus identified, and was isolated in 1980 from a patient with T-cell lymphoma. In 1982, researchers provided evidence that HTLV-1 could lead to the development of adult T-cell leukemia-lymphoma.

“In endemic areas, many people carry this virus, and it seems to be clustered in families and in women, suggesting that the transmission occurs more frequently from men to women and from women to children than it does from women to men,” Foss said.

An HTLV-1 carrier has a lifetime risk of developing acute leukemia of about 1% to 4%, so while the incidence of this virus is high in a population, the percentage that will get cancer is relatively low.

HTLV-1 is an RNA virus. Reverse transcriptase copies the genetic information into DNA once the virus has entered the host cell. This DNA copy (a provirus) is inserted into the chromosomal DNA of the host cell, where it becomes a part of the cell’s genetic makeup, Foss explained.

When this virus is in the cells and replicating, “there is an increased propensity for secondary genetic events and eventually you would select out a clone of cells that’s capable of independent or autonomous growth. It is thought that this may be how patients develop leukemia,” Foss said.

Insertion of the HTLV–1 provirus into the host-cell genome may disrupt normal cellular genes, which could contribute to cancerous changes in the cell. But this would not be sufficient to transform infected cells into cancer cells. The development of cancer in an infected cell requires changes in expression or damage to multiple other host cell genes, according to ASCO. However, the specific mechanisms by which HTLV-1 infected cells become cancerous are still being researched, according to Foss.


Even though Kaposi’s sarcoma (KS) had been associated with HIV infection, there were numerous clues that there was a second virus involved, said NCI’s Goedert, and eventually human herpes virus 8 (HHV8) was found to cause KS.

Classic KS occurs in older men of southern European and Middle Eastern origin. Endemic KS occurs in Africa. Children as well as adults can be affected. Iatrogenic KS occurs in organ transplants. Transplant recipients are 150 to 200 times more likely to develop KS than immunocompetent patients. AIDS-related KS is the most common form of this disease today.

Because KS is more common among the immunocompromised, researchers think that the immune system prevents progression to KS in normal people. About 5% of the people in the United States appear to be infected with HHV-8, yet the incidence of KS is estimated to be around 1.5 per million. Among elderly people in the Mediterranean who have HHV-8, but not HIV, classical KS develops in about one in 10,000 people annually. In parts of Africa, where 50% of the population has HHV-8 and 10% or more are coinfected with HIV, KS is the most common form of cancer.

“So the risk of getting the disease if you have AIDS and you have the virus in the blood, it’s extraordinarily high,” he said.

Before highly active antiretroviral therapy (HAART), about 35% of men with HHV-8 and HIV developed KS within 10 years. After HAART, there was “an abrupt reduction in KS risk among people with AIDS. It’s truly stunning and truly profound in terms of the impact that HAART has had,” Goedert said.

Researchers continue to look at possible links between infections and cancers. “I think it’s almost certain there will be some additional infections, particularly viruses, found that cause cancer in humans,” explained Goedert.

If links can be found with clear mechanisms of action, researchers may be able to find cures for cancers by preventing or treating the infection.

For more information:

Johnson BE, Goedert JJ, Zhu AX, et al. The virus-Cancer Link: Examining the Role of Viruses in the Development of Cancer. American Society of Clinical Oncology. Special Media Event: Meet the Experts. Dec. 10, 2003. New York City.

By: lovingitall0
16 Sep 2004, 08:28 AM EDT
Msg. 167259 of 188686
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First Glimpse Of DNA Binding To Viral Enzyme; May Serve As New Target For Antiviral Drugs

Source: Brookhaven National Laboratory
Date: 2004-09-14

UPTON, NY - Scientists at the U.S. Department of Energy’s Brookhaven National Laboratory and the Albert Einstein College of Medicine have produced the first molecular-scale images of DNA binding to an adenovirus enzyme — a step they believe is essential for the virus to cause infection. The images, which appear on the cover of the October 2004 issue of Molecular and Cellular Proteomics, show how binding to DNA may stimulate the enzyme and are already being used to design new antiviral drugs to block this interaction.

“We were quite surprised to see that DNA actually stimulated the activity of the enzyme,” said Brookhaven biologist Walter Mangel, a co-author on the paper. “If we can block this interaction, we should be able to prevent the virus from replicating, and thereby thwart infection.”

Adenoviruses cause respiratory, gastrointestinal, and eye infections, including highly contagious viral pink eye. Some adenovirus eye infections lead to blindness. Respiratory epidemics of adenovirus are often prevalent on army bases. And in patients with compromised immune systems, such as those infected with human immunodeficiency virus (HIV), an opportunistic adenovirus infection can be deadly.

During infection, adenovirus makes an enzyme called a protease, which cleaves or degrades viral “scaffolding” proteins to complete the maturation of newly synthesized virus particles. Mangel and others have been working to understand all the steps necessary for this enzyme’s function, looking for new ways to stop its action and, therefore, block an adenovirus infection (see: ).

The scientists didn’t expect the viral DNA to bind to the protease, but they figured they should look just to rule out such an interaction. “It was something we had to do, to make sure they did not interact,” Mangel said. The discovery that the viral DNA interacts with the protease was unprecedented and led them to characterize the interaction in detail. The scientists now believe that inside the virus particle the protease uses the DNA as a guide wire, sliding along the genetic material to remove the internal “scaffolding” proteins, all located near the DNA.

The team used a technique called synchrotron footprinting, which was pioneered by paper co-author Mark Chance and his colleagues at the Albert Einstein College of Medicine, to show where DNA binds on the adenovirus protease.

“Synchrotron footprinting is a technique recently developed at Einstein that allows structural information on the contacting surfaces of biological molecules to be precisely mapped. These contact points are regions providing critical communication in the cell,” Chance explained. “In this study the footprinting approach provided information on the DNA binding region of the adenovirus protease that has not been solved by other techniques and can be used in drug design.”

At the National Synchrotron Light Source — a facility that produces extremely bright beams of x-ray, infrared, and ultraviolet light at Brookhaven Lab — Einstein’s Sayan Gupta, the study’s lead author, bombarded different solutions of the adenovirus protease and DNA with x-rays and characterized the changes that occurred on the surface of the protein. With this technique, the team was able to deduce the location of the DNA binding site based upon the changes in accessible surface area.

“There is extensive contact between the enzyme and the DNA,” Gupta said. “The DNA wraps around more than half the enzyme molecule. It appears like a strap, holding two parts of the protease together.”

Since the DNA binding site is quite long, there are numerous locations along it that could be used as targets for drugs to block the interaction and act as antiviral agents, Mangel said. The scientists have already begun looking for such drugs and hope to have the National Institutes of Health test some of them for anti-viral activity within a year.

This work was funded by the Office of Biological and Environmental Research within the U.S. Department of Energy’s Office of Science, the Biotechnology Resource Centers Program of the National Institute of Biomedical Imaging and Bioengineering of the National Institutes of Health, and by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health.

This story has been adapted from a news release issued by Brookhaven National Laboratory.

By: SUE32073
16 Sep 2004, 09:52 AM EDT
Msg. 167262 of 188686
(This msg. is a reply to 167251 by shemp1248.)
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Shemp says, "AVR118 not only enhances the immune systems attack on invaders, but also it's ability to protect the immune system as other agents used to fight disease carry the side effect of immuno-destroyer. This is also done with a minimal amount of toxicity when given to humans in all forms."

Hmmmmm.....I was under the impression AVR118 was "totally" NON-TOXIC. Doesn't "TOXIC" mean harmful, destructive or deadly. How can a drug be "sort of non-toxic"! Who, in your opinion, has been given AVR118 and has had a "minimum amount of toxicity"???? What "form of humans" have taken AVR118 and have survived despite the usage of the drug??? I am very, very curious.

Thanks for any comment, which may clear up and make for a better understanding of your "most" profound statement.

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By: nvphyl
16 Sep 2004, 11:01 AM EDT
Msg. 167269 of 188686
(This msg. is a reply to 167251 by shemp1248.)
Jump to msg. #  
shemp pretty upbeat opinion.

This part worries me.

"...I know that there has been a multitude of formulas in this area that have worked, But I beleive AVR118 is the frontrunner...."

You know (fact) one thing that could be bad for ADVR.

You believe (opinion) that ADVR is the front-runner.

That begs the question if other formulas have worked why do you believe ADVR is the front-runner. One might think a suitor or three might be knocking if that were the case. Just curious why a healthcare professional like yourself believes ADVR is in front. I think many of us thought that at one time but are worried that may not be the case now especially after reading your post.

tia nvp

(Voluntary Disclosure: Position- Long)

By: dirtysneakers0
16 Sep 2004, 04:45 PM EDT
Msg. 167309 of 188686
Jump to msg. #  
Give Elma a chance. She inherited the Israel trials which has/will produce important data. She has laid out a plan and is following it (pre-IND meeting). Granted we all would like faster results. With her experience we have to hope she knows what she is doing. Unfortunately in some respects it may seem like we are starting over. But as stated in her meeting with Wall Street analyists all the previous data can hopefully be used to some extent. I am hoping after the IND we will go right to Phase II. Good luck to us.

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By: lovingitall0
18 Sep 2004, 09:04 AM EDT
Msg. 167451 of 188686
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Experts Warn of Rising AIDS Stats from East Europe

Sep 17, 2004
By Darius James Ross

VILNIUS (Reuters) - A lack of information and public funding is helping fuel the spread of HIV/AIDS in several recent European Union entrants and threatens to become pandemic across the bloc, a panel of experts said on Friday.

They said the opening of borders on Europe's eastern flank could allow for an influx of infections into western Europe from areas such as the Baltics, where cash-strapped governments find it difficult to fund prevention and costly treatment programs.

In addition, they added, a lack of information on prevention and transmission of HIV, the virus that leads to AIDS, coupled with public prejudice against those who have tested positive, may worsen the situation.

"The reality is that we have disturbing figures in Western Europe and even more serious figures in Eastern Europe," European Commissioner Pavel Telicka told Reuters on the sidelines of an AIDS conference in the Lithuanian capital.

In Estonia, which joined the bloc in May, around one in every 100 people is infected.

AIDS and HIV-related deaths have been on the decline in western Europe due to the availability of treatment, mainly expensive antiviral drugs.

But experts at the conference pointed out that infection rates are still rising because of waning government commitments to prevention efforts and complacency linked to the availability of treatment. The number of people living with HIV in western Europe rose from 540,000 in 2001 to 580,000 by the end of 2003.

"In Europe, you have many countries with rich economies in which citizens have been lulled into a sense of complacency," said Jack Chow, WHO Assistant Director-General for HIV/AIDS, tuberculosis and malaria.

"We have seen a doubling of the epidemic in Western Europe in the last 10 years."

Ominously, Telicka said that in Russia and Ukraine, which share a border with the EU after enlargement, there has been a 50-fold increase in infections to about one adult per 100.

Statistics presented at the conference showed approximately 2 million people are living with HIV/AIDS in eastern Europe and Central Asia.

"If we take just Russia, Ukraine and Estonia, we have a prevalence of HIV-infection of 1.0-1.5 percent, which is as bad as it was in India in the 1980s," said Lars Kallings, special envoy to United Nations Secretary-General Kofi Annan for HIV/AIDS in Eastern Europe.

"This is a very dangerous situation."

The United Nations estimates some 40 million people around the world are infected with HIV and more than 25 million people have died from AIDS. Sub-Saharan Africa is the worst affected region, with about 26 million people infected.




By: lovingitall0
18 Sep 2004, 09:05 AM EDT
Msg. 167452 of 188686
Jump to msg. #  
Earlier Treatment for HIV Infection May Reduce Mortality

By Will Boggs, MD

NEW YORK (Reuters Health) Sept 14 - Survival of HIV-infected patients approaches that of HIV-negative patients only when therapy begins at CD4 cell counts greater than 350 cells/microliter, above the recommended level for starting antiretroviral therapy, according to a report in the September 15th issue of The Journal of Infectious Diseases.

"This does not indicate that the treatment guidelines should be changed at this time, but does raise for discussion the issue of considering treatment at earlier stages of HIV infection," Dr. David Vlahov from Johns Hopkins University Bloomberg School of Public Health, Baltimore, told Reuters Health.

Dr. Vlahov and colleagues evaluated survival after initiation of highly active antiretroviral therapy (HAART) in a large group of injection drug users who have been followed prospectively for up to 14 years and compared their survival to that of HIV-negative injection drug users.

The analysis included 1503 study participants followed from January 1, 1997 to January 1, 2001, a period during which HAART was available.

The mortality rate in the HIV-negative group was significantly lower than all HIV-positive groups except those who began receiving HAART at CD4 cell counts above 350 cells/microliter, the authors report.

Among patients with CD4 counts above 350 cells/microliter, HAART-treated patients had 56% the mortality rate of those who did not receive HAART.

Compared with HIV-negative participants, the researchers note, the risk for all-cause mortality was significantly higher among HIV-positive participants with baseline CD4 cell counts between 200 and 350 cells/microliter and below 200 cells/microliter, regardless of whether they received HAART.

AIDS-related mortality increased moderately as CD4 cell counts declined, the investigators report, and rates were similar within CD4 cell count strata, except when CD4 cell counts fell below 200 cells/microliter.

In contrast, non-AIDS-related mortality was generally higher among patients not receiving HAART than in participants receiving HAART.

In the lower CD4 cell count strata, HIV loads of 55,000 copies/mL or higher were associated with a significantly higher risk of death, compared with HIV-negative participants, the report indicates.

"While the benefits of therapy have been clear for those with late-stage HIV infection, the issue of treatment of those with earlier stages is complicated and challenging especially with the need to maintain strict adherence to regimens," Dr. Vlahov said. "Data from this study contribute information suggesting that benefits of earlier treatment should be considered in reviews of treatment guidelines."

"Probably the most important message is that highly active antiretroviral therapy works well in injection drug users, a major risk group for HIV related outcomes," Dr. Vlahov concluded. "

"It is reasonable to initiate therapy for most asymptomatic individuals with CD4 cell counts below 350 cells/microliter," writes Dr. Mauro Schechter from Universidade Federal do Rio de Janeiro in Brazil in a related editorial.

"At present," concludes Dr. Schechter, "I would not recommend antiretroviral therapy for patients with CD4 cell counts above 350 cells/microliter. Nonetheless, I believe that it is reasonable to consider initiating treatment for selected individuals with rapidly declining CD4 cell counts and very high virus loads."

J Infect Dis 2004;190:1046-1054,1043-1045.



By: lovingitall0
18 Sep 2004, 09:11 AM EDT
Msg. 167453 of 188686
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HHV-8 May Be Passed From Mother-to-Child Via Saliva

By Anne Harding

NEW YORK (Reuters Health) Sept 16 - The largest study to date of mother-child pairs provides strong evidence that human herpesvirus 8 (HHV-8) can be transmitted from mother to child.

"In Africa HHV-8 passes from mother to child via saliva, so practices that involve an infant coming into contact with their mother's saliva should be avoided," the study's lead author, Dr. Martin Dedicoat of the Cancer Research UK Epidemiology Unit in Oxford, told Reuters Health.

In-utero transmission of the virus, or infection of the infant at birth, is rare, but cannot be ruled out, Dr. Dedicoat and his team note in the September 15th issue of The Journal of Infectious Diseases.

Most diseases caused by HHV-8, including Kaposi sarcoma, primary effusion lymphoma and Castleman's disease, only strike immunocompromised individuals, Dr. Dedicoat told Reuters Health, but the virus can occasionally cause Kaposi sarcoma or primary pulmonary hypertension in apparently healthy individuals.

The researchers tested the blood of 2546 mother-child pairs recruited from clinics in rural South Africa for antibodies to lytic and latent HHV-8 antigens.

Forty percent of mothers tested had antibodies to HHV-8 lytic antigens and 14% were positive for latent antigens. The corresponding figures for the children were 12% and 7%. Lytic antibodies were more common among HIV-positive mothers and children.

As mothers' HHV-8 antibody titers increased, the prevalence of HHV-8 antibodies in their children increased as well, the researchers found.

The researchers tested saliva from 973 mothers, and found HHV-8 DNA in 15% of the samples tested. Saliva was tested only once, so the figure is likely an underestimate of the percentage of mothers with HHV-8 in saliva, the researchers note.

Among children, 13% of those whose mothers did not have the virus in their saliva were HHV-8 seropositive, compared with 29% of the children whose mothers had a HHV-8 load of more than 50,000 copies/mL. Among women with the highest lytic antibody titers, 34% had HHV-8 DNA in their saliva, compared with 9% of those who were seronegative. The presence of latent antibodies was not associated with saliva carriage of HHV-8 DNA.

The researchers also tested breast milk samples from 43 mothers, finding 12 carried HHV-8 DNA, but at levels several orders of magnitude lower than in the saliva.

The researchers note that traditional medical practices common in Africa, such as the use of saliva to ease itchy insect bites, could promote the spread of the virus from mother to child.

J Infect Dis 2004;190:1068-1075.

By: shaggydogs
18 Sep 2004, 12:48 PM EDT
Msg. 167457 of 188686
Jump to msg. #  
An online newspaper reporting the issues of Securities Fraud
[All this would be unnecessary if short selling was outlawed!]

SEC Denies responsibility for Trade Settlement Enforcement - September 17, 2004

By Dave Patch

It has been a long and arduous task trying to get the SEC to take responsibility for securities fraud associated with “Naked Shorting”. From one form of denial to another the SEC has relinquished all responsibility to enforce the settlement of our securities. SEC’s media relations spokesman John Heine claims settlement failures are not securities law violations but in fact contract law violations. According to Mr. Heine “the SEC is not in the enforcement of contract law”. Actually the SEC is rarely in the enforcement of anything.

Trade Settlement failures is a violation of Securities Law if you assume that the SEC is responsible for enforcing the Securities Act of 1934.

In the General Rules and Regulations Promulgated by the Securities act of 1934 comes Rule 15c6-1. Rule 15c6-1 addresses the Settlement Cycle for all trades executed. This rule states that no Broker-Dealer may enter into a contract for the sale of a security whereby the payment for that security and the delivery of that security is greater than 3 business days. The only exemption to this comes when a written agreement between both parties has been entered into.

Today the SEC and NASD have agreed that trade settlement failures are not only harmful to the markets, but also admit that in some cases the settlement failures will exceed the entire public floats of companies. For this to be the case, Broker-Dealers are not meeting the guidelines of Rule 15c6-1. Broker-Dealers are entering into contracts for trades that exceed 3 business days and yet the SEC refuses to enforce the rules. Ameritrade recently told one client that if they wanted physical delivery of shares it would take 4 – 6 months and they would be restricted from selling during that timeframe. Mr. Heine claims it is not the SEC’s job to address these violations. If not the SEC’s whose is it?

I went deeper into my research and began to look up Client agreements between an investor and their broker-dealer. I found that much of the issue we speak of as investors hinges on the word settlement. The SEC claims that settlement simply refers to a share showing up electronically into your account. It is not, however, what investors think of as the meaning of settlement nor is it what we have written into our client agreements. To most settlement is the actual transfer of ownership of a security and all rights that go with it.

Let’s review how settlement is defined:

Section 17A of the Securities Act of 1934: Establish a system …”prompt and accurate clearance and settlement of securities transactions, including the transfer of record ownership”

SEC Regarding Trade plus 3 Settlement: “Investors must settle their security transactions in three business days…. When you sell a security, you must deliver to your brokerage firm your securities certificate no later than three business days after the sale.”

NASD Glossary: Settlement: “The conclusion of a securities transaction; a broker/dealer buying securities pays for them; a selling broker delivers the securities to the buyer's broker.”

ETRADE Agreement: Settlement Date. The day on which a transaction is to be completed. On this day, buyers are to pay for their purchases and sellers are to deliver their securities. Generally, for equity transactions, settlement date is three (3) days after a trade executes, for options trades settlement date is the day after the trade executes, and settlement for mutual funds can vary depending on the particular fund family.

But what about the “Book-Entry” settlement? The SEC has denied the abusive nature of the issue by claiming shareholders are not harmed due to “Book-Entry” settlement whereby our Broker will put shares into our account prior to them actually receiving transfer of ownership from the seller. Unfortunately, there is no publication I could find that justifies this position.

The SEC defines “Book-Entry” Settlement here: "Street Name" Registration — The security is registered in the name of your brokerage firm on the issuer's books, and your brokerage firm holds the security for you in "book-entry" form. "Book-entry" simply means that you do not receive a certificate. Instead, your broker keeps a record in its books that you own that particular security.”

You can’t own something until you take delivery.

How harmful is unsettled trades?

The SEC publication to Investors: “Unsettled trades pose risks to our financial markets, especially when market prices plunge and trading volumes soar. The longer the period from trade execution to settlement, the greater the risk that securities firms and investors hit by sizable losses would be unable to pay for their transactions”. To these words Mr. Heine states: “No Question the language is correct”.

So with the harm that unsettled trades can have to our financial markets, why is it the SEC refuses to step in and address the issue? Who is responsible for enforcing rule 15c6-1? If trades are not being settled, and brokers are entering into these contracts knowing that these trades will not settle in 3 days, who is responsible for enforcing actions against the brokers for entering the contracts or breaking the contracts without written approval of the clients? The Industry has the information; all the client has is a false account statement that claims trades settle when they haven’t. The Industry is now fighting hard to insure that the pending lawsuits do not go into discovery where they would have to open their books for investors to finally see the realities of what is happening.

To seek these and other answers I once again asked Mr. Heine for answers and once again I got the SEC duck. No Comment!

I had asked the SEC in a written request for specifics on what circumstances the SEC would see as justification for trades failing the 3 day settlement period. In the request I asked what the SEC felt were reasonable causes for settlement failures and what would be a natural timeline for those trades to then settle. Mr. Heine initially stated that the question was unanswerable and later suggested I speak with investor relations. Mr. Heine was smart, he was not about to give up on the secrets only the SEC is allowed to know and understand. Even the NASD proposed a maximum limit of 10 days to settle trades but the SEC denied that proposal for unknown reasons. The NASD proposal now lies dormant in the halls of the SEC’s Division of Market Regulation.

The bottom line is simple. The SEC is negligent in performing duties that support the best interests of all investors.

Trade settlement failures are a violation of securities laws and are a breach of securities agreements between the SEC and the broker-dealers, the broker-dealers to each other, and the broker-dealer to the client. There is no written agreement for an alternate settlement date between parties. The Brokers act in a “good-ole-boy” network where they forgive each other’s sins at the safety of our investments and the financial markets. The SEC in turn looks the other way in violation of enforcement of the Securities Act of 1934.

The SEC’s doubletalk and confusion on this issue is clear. The SEC does not want to enforce trade settlements. Years ago the SEC initiated actions to move from T+5 to T+3 and now they have a concept release to go to T+0. These are wasted and costly efforts if the SEC won’t stand up with a backbone and enforce the rules. It is time the SEC accounts for their actions.

It is now time Congress steps out and takes hold of this situation.

For more on this issue please visit the Host site at .

Copyright 2004

By: lovingitall0
19 Sep 2004, 10:10 AM EDT
Msg. 167638 of 188686
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'Cure' a 4-Letter Word for Cancer Doctors

Few cancer doctors are willing to declare patients cured despite high rates of remission

AP - Sept. 19, 2004 — At a time when more people are cured of cancer than ever before, fewer doctors seem willing to say so. They call the cancer undetectable, or in remission. They tell patients they can quit seeing cancer specialists. They quote statistics and say chances are slim that the disease will come back.

They say these things because the simple truth is, they can't tell when or if someone has been cured. Even the most widely used benchmark being alive five years after diagnosis has no real basis in science, experts admit.
There wasn't any doubt six years ago that Doug Jensen had cancer.

The Oregon engineer's blood was clogged with the immature cells that are sure signs of leukemia. Treatment with a new wonder drug, Gleevec, made them disappear.

Since then, doctors repeatedly have searched his blood, even individual molecules, for bits of DNA and other substances that would reveal he still had the disease. None has been found.

Is he cured?

"They don't use that word," said Jensen, who would dearly love to hear it.

There's a label for people like Jensen who are in cancer limbo "survivor."

Some wear it with pride, having fought the enemy and lived to tell about it. Others think it drafts them into a club to which they don't want to belong Veterans of Forever Wars.

Nearly 10 million Americans have battled cancer, including 1.4 million who had it more than 20 years ago and are called "long-term survivors" by those afraid to call them cured.

Their ranks include Lance Armstrong, who heads a survivorship foundation and boasts of beating testicular cancer that had spread to his lungs and brain. Can he ever be declared cured, or must he always carry "survivor" with his Tour de France titles?

"The medical community has backed off the term 'cured,'" said Julia Rowland, a psychologist who directs the federal Office of Cancer Survivorship, which was started in 1996, the year Armstrong began treatment.

The reasons involve more than just semantics, she and others say. Cure is a term with emotional and medical meanings about which there is little agreement.

To many people, it means that the cancer is gone and is not going to come back.

But some cancers certain lymphomas and leukemias in particular never go away completely yet are controlled so that they're no longer life-threatening. Some call that a remission, but others consider it a cure.

Other cancers look like they've gone away no signs of them can be found by exquisitely sensitive and sophisticated tests but recur many years later, suggesting that they weren't really cured after all. Breast cancer is notorious for this.

"What today does 'cure' really mean?" asked Dr. Len Lichtenfeld, deputy chief medical officer of the American Cancer Society. "Does that mean there's no cancer cells in your body from this cancer any more, or does that mean that at this particular time, there's only 2, 3, 4 5 percent chances it's going to come back?"

He's not the only one trying to define the concept.

"It's something we've had discussions about internally," said Diane Balma, public policy director for the Susan G. Komen Breast Cancer Foundation, which calls its fund-raiser Race for the Cure, not Race for the Remission.

She is distrustful of absolutes. Diagnosed with breast cancer at age 30 but with no sign of it nearly a decade later, "I will never consider myself cured," she said. "Cure means there's no possibility of recurrence, and that's why I don't like the word. We all know there's a possibility of recurrence."

Ellen Stovall, who had Hodgkin's disease and now heads an advocacy group, the National Coalition for Cancer Survivorship, tries to ignore the issue.

"Cure is a term that I don't need to have in order to fell well and healthy," she said. "It's a word without meaning in some respects. It may be useful for testifying before Congress or getting a job," but it doesn't predict future health.

When doctors do declare someone cured, how can they tell?

In the past, it was when they could cut out a tumor and surrounding tissue until no more abnormal cells could be seen. Many doctors today are willing to call testicular, prostate and certain other kinds of cancer cured if the tumors are small and confined to a gland or organ that can be removed.

But Dr. David Carbone, a lung cancer expert at the Vanderbilt-Ingram Cancer Center in Nashville, Tenn., would be reluctant to say that about the type of cancer he treats.

"All the time, I see patients who had surgery done and the surgeon says they got it all, they're cured. Statistically, they may have a good chance of being cured. But it's all a probability. Has that surgeon done them a favor by saying that?"

The opposite situation also is true: Doctors sometimes declare a cancer cured even after it had spread beyond the place it originated. This used to be considered an inevitably terminal condition, but it's often conquered now with chemotherapy, radiation and other treatments.

Still, it's much harder to predict someone's ultimate survival after cancer has spread. Doctors look at factors like how aggressive a tumor is and where and how quickly it traveled, but not all patients get such tests. Most of the time, only time will tell.

"Some of these people have long-term survival, and some of them are going to be cured of their disease. We don't know what to tell them," Lichtenfeld said.

Which is why many doctors turn to statistics, and five-year survival is their favorite. By that measure, cancer surely is being cured: Nearly two out of three patients make it to that point today; only half did 25 years ago.

However, there is nothing magical about that benchmark. Survival is a continuum, and five years is no more meaningful a dividing point than two, three, six or nine years.

"I honestly don't know where that came from. It goes back a long time," said Rowland at the federal cancer agency. She and others think it grew from a need to have some way of measuring survival and tracking cancer trends in the overall population.

More relevant statistics take into account the type of cancer someone has. With some, like bladder cancer and many of the blood and bone marrow malignancies, if someone is alive after a year or two, their long-term outlook is pretty good. But much to the chagrin of breast cancer advocacy groups and people with the deadly skin cancer melanoma, five-year survival doesn't bring great assurance that those diseases won't come back years later.

Dr. David Johnson, deputy director of Vanderbilt-Ingram Cancer Center and president of the American Society of Clinical Oncology, thinks the five-year benchmark became balm for doctors and patients who found the unpredictability of their situations intolerable.

"Physicians were reluctant to say 'you might recur,' so they'd use these terms like 'OK, in five years, you'll be cured,'" he said.

Johnson and his colleague, Carbone, both have survived lymphoma and are past the five-year mark. But statistics only tell what happens to the masses, not to individual patients.

"They can't be half-cured, like they can't be half-pregnant. So a lot of time discussing percentages often isn't productive," Johnson said.

"You're either cured or you're not," Carbone agreed.

Complicating matters is the risk of second cancers. Some of the very treatments used to cure cancer, like chemotherapy and radiation, actually can trigger new cancers down the road. People with an inherited genetic flaw that predisposed them to cancer still have that underlying problem after being treated successfully.

"The fact that you've had cancer once means that you can get it again," Johnson said.

But some of the trickiest situations today involve people like Jensen. Average survival for his form of cancer, chronic myelogenous leukemia, was only five years until 2001, when Gleevec, one of a new generation of drugs that more precisely target cancer, came on the market.

More than 95 percent of CML patients do stunningly well on Gleevec, "but this may be more akin to controlling diabetes with insulin than curing diabetes," said Dr. Brian Druker, the Oregon Health & Science University cancer specialist who pioneered the drug's development.

"When we look at our patients with extremely sensitive techniques, we can still see leukemia cells," he said. "Our concern is that if we stop Gleevec, then their leukemia will come back. Are they cured? Probably not. Are they well controlled? Absolutely, yes."

Jensen is one of the few CML patients who show absolutely no sign of cancer. He has taken Gleevec since 1999, when he enrolled in an experiment that still provides him the drug for free. It doesn't make him sick because it attacks the root causes of his cancer without killing healthy cells.

He feels like he could take it forever, and wants to. But he and his doctors are considering taking him off.

"I honestly don't know what the right thing to do is," but stopping the drug is the only way to find out if he and others like him are cured, Druker said.

"That's a little scary, I have to admit. Everything's going along so well," Jensen said. But he talked it over with his wife and decided that if Druker and his other doctors ask him to, he'd probably go off the drug.

"They say it's undetectable," he said of his cancer. "I'd like to have them say I'm cured."



By: lovingitall0
19 Sep 2004, 10:33 AM EDT
Msg. 167639 of 188686
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Explaining how flu virus defends itself

Jerusalem Post, Sept. 19, 2004
Judy Siegel-Itzkovich

Fighting viruses is often a frustrating business: No sooner have you found a way to destroy them, than they've found a way to neutralize the anti-viral treatment. How, exactly, do viruses accomplish this?

In the cover story of a recent issue of the journal Proteins, Hebrew University researcher Prof. Isaiah Arkin reveals how influenza-causing viruses adapt to nullify the effectiveness of the anti-viral drug symmetrel (generic name). The discovery may have significant consequences in helping drug researchers develop more effective means of blocking influenza and other viruses in the future.

Flu, Arkin emphasizes, is a major killer, even though many people tend to shrug it off as an unpleasant seasonal nuisance. In the US, for example, it is the leading cause of death from infectious disease, claiming about 40,000 lives annually, mostly among the elderly.

Arkin, of the department of biological chemistry at HU's Silberman Institute of Life Sciences, has demonstrated how flu viruses counteract symmetrel. Assisting him were graduate students Peleg Astrahan and Itamar Kass, as well as Dr. Matt Cooper from Cambridge University in Britain. Administered soon after the onset of flu symptoms, symmetrel is intended to destroy the virus by binding to and blocking a proton-conducting channel which the virus needs in order to continue multiplying.

Instead of conceding defeat, however, the virus takes its own counter-actions - either by narrowing its channel to the extent that the blocking element in the drug is unable to bind and create a seal, or by widening its channel so that the blocker can get in but can't totally seal the channel. Arkin notes that the latter action is the more surprising and unexpected one.

While the virus's response to the drug has been previously noted, this is the first time the activity that lies behind this phenomenon has been demonstrated, said Arkin. This is because researchers had previously concentrated on examining the binding action of the blocker to the viruses, but not the process taking place in the viruses' channel. Thus, there was only a limited picture of what was actually happening.

This new information on the mutating abilities of the influenza virus will have to be taken into consideration in further anti-viral research, he concluded.

By: ricourt0
19 Sep 2004, 11:25 AM EDT
Msg. 167640 of 188686
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ADVR better hurry!

Possible West Nile Virus Drug
9/8/2004 5:00 PM

Scientists in Oregon say they may have found a drug that neutralizes the effects of the West Nile Virus in humans. AVI 4020 was first used on penguins at a midwest zoo; the drug kept the penguins alive. Now, doctors at AVI-Biopharma, a biopharmaceutical company, are trying to make the AVI 4020 drug safe for humans. The drug works by binding to the West Nile Virus, rendering it inactive.

Scientists say if they can make the drug safe for humans, it could also be used to treat polio or Parkinson's disease.


By: lovingitall0
19 Sep 2004, 12:29 PM EDT
Msg. 167644 of 188686
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Biotech returning to favor

Companies strive to woo VC investors

William Patalon III, Baltimore Sun
Friday, August 13, 2004

After a nearly four-year slowdown, money is beginning to flow again into the biotechnology sector. But it's more a trickle than a torrent.

During the first six months of this year, initial public offerings raised more than twice what they did in all of 2003. Biotech companies that are already public are going back into the market with secondary offerings, and promising young startups are winning venture capitalists' attention.

At the same time, wary investors are being highly selective and driving harder deals, industry executives and experts say. The upshot: Capital-hungry biotechs -- which typically rack up years of losses as they struggle to bring a product to market, are pursuing every strategy they can to secure funds.

"It is a difficult time, and companies are being forced to be very creative," said Tom Salemi, editor of the Venture Capital Analyst/Healthcare trade journal in Wellesley, Mass.

Winning financing for biotechnology ventures has always been arduous. It takes years and millions of dollars, estimates range as high as $800 million to $1 billion, to develop a new drug. And the risk is high.

Even if a drug is successful in winning Food and Drug Administration approval and getting to market, it typically has already used up years of its patent life, giving it a much shorter window to earn back the huge investment and generate a profit for its developer.

And there's always a chance that the drug will be trumped by another offering. Still, companies are finding opportunities, and IPOs, an indicator of venture-capital financing for the sector, have surged this year.

After vaulting from $374 million in 1999 to $3.5 billion in 2000, IPOs of venture-backed biopharmaceutical firms slumped to $187.5 million in 2001 and $205 million in 2002, according to Alternative Investor, publisher of the Venture Capital Analyst trade journal. After rising to $437.8 million in 2003, IPO activity soared to $1.15 billion in the first two quarters of this year, according to the most recent figures available.

The surge is important not only because it means more money for companies, but also because the IPOs represent the exit strategy for the venture-capital investors who cash out, said James Barrett, general partner with the Baltimore office of New Enterprise Associates, a VC firm.

That cashing out, in turn, frees up money that can be used to invest in another biotech startup.

It's no coincidence, then, that the active IPO market at the start of this year also translated into a bustle of venture-financing activity. This year's first quarter was the most active for venture funding in at least six years. Biopharmaceutical firms received a total of 57 investments with an aggregate value of $1.47 billion, about $25.75 million per deal.

But this time, investors, aware of the long gestation for biopharmaceuticals, "are being very precise" in valuing bioscience firms, Barrett said.

They're favoring established firms and companies with proven technologies or existing products.



By: lovingitall0
20 Sep 2004, 09:29 AM EDT
Msg. 167800 of 188686
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Cancer Drug Shows Promise Against Lupus

A drug now used to treat a type of cancer appears to be very effective at treating lupus, with just one injection easing symptoms in several patients for a year or more. The results of the clinical trial involving 17 patients are in the August issue of Arthritis and Rheumatism.

The finding has its roots in a hypothesis put forth by the team of physicians at the University of Rochester Medical Center who did the study. They suspected that because lupus involves the same immune cells as lymphoma, a drug successful at treating lymphoma might also help lupus patients. So doctors tested the medication rituximab, approved in 1997 to treat lymphoma, in patients with the chronic inflammatory disease where the immune system mistakenly attacks a person's own tissues.

The results bear out the hypothesis. Eleven of the 17 patients had a significant drop in immune cells known as B cells, and the health of those patients improved significantly, an improvement that was evident for the 12 months that the study lasted. Several were able to reduce or go off their traditional lupus medications.

"In most patients, their lupus improved significantly," says rheumatologist R. John Looney, M.D., who led the study. "Since lupus differs a great deal from person to person, the ways that patients improved varied. Some had less joint pain; some had fewer skin rashes. But everyone who had fewer B cells had significantly improved health.

"These patients were treated for a very brief period of time, and some of them are still doing just great, several years later."

The benefit wasn't as marked for everyone, including patients who did not receive the full dose of the medicine in the "dose-escalation" study, as well as African-American patients. Scientists are investigating the differences.

Unlike many autoimmune diseases that target a specific system or organ, lupus can affect a person's joints, skin, blood, kidneys, and even organs like the lungs and brain. Fatigue, arthritic joints, and infections are among the most common symptoms. Many patients live a normal life while taking medicine and working with a doctor to keep tabs on the disease, perhaps feeling some joint pain or having a rash occasionally, while others are debilitated by the illness and have severe infections or organ failure. Women are about 10 times as likely as men to be diagnosed with lupus. Doctors estimate that anywhere from about half a million to 1.5 million people in the United States have the disease.

"Some patients don't need much treatment, while others need all you can offer and more," says rheumatologist Ignacio Sanz, M.D., an author of the paper and a lupus expert.

Besides the drug's success in treating the disease, scientists noted the lack of significant side effects with rituximab. Some patients had a reaction to the infusion of the medicine, but in the study, it occurred far less often than it does with cancer patients taking the drug.

Current lupus treatments, in contrast, are laden with severe side effects. The anti-inflammatory drugs used to dampen the immune system leave patients vulnerable to infection, while steroids at high levels can cause an array of problems, everything from thinning bones, weight gain, weak muscles, and heart disease to glaucoma and depression.

The difference in side effects is a result of the precision, or lack thereof, of the medicines. Current lupus treatments affect nearly all the cells of the body, including healthy and vital cells. In contrast, rituximab targets only B cells and is aimed at lowering their numbers. That's why the drug is available to lymphoma patients: Most have too many B cells, which make antibodies that flag down and kill microbes and other invaders in the body.

Lupus is also a problem with B cells: They're found in the wrong proportion in the body's blood and tissue, and they're often misguided, making too many antibodies that mistakenly attack the body itself. The infighting clogs up the body with cellular debris, causing a variety of symptoms; then when the immune system detects the problem, it tries to ease up, leaving the patient open to infection.

"Lupus patients tend to have fewer B cells than normal, but their B cells are hyperactive and function in a very abnormal way," says Sanz. "The immune system is hyperactive but disorganized; it's over-reacting to some things but not enough to other things."

It was Looney's idea to target B cells to treat lupus. A great deal lot of traditional research had pointed to other immune cells known as T cells as the major culprit. But Looney and his team uncovered a more complicated process than had been imagined, where cooperation between B and T cells is at the core of the disease. The success with rituximab opens up a whole new vista – targeting B cells, reducing their numbers, and ridding the body of errant B cells – for treating the disease.

The Rochester team is now helping to design a much larger study of patients that may begin within the next year or so at multiple sites around the country, including Rochester.

"Our basic knowledge of lupus has been increasing exponentially during the past few years, but there have been few new treatments," says Sanz, who heads the University's NIH-funded Autoimmunity Center of Excellence, where lupus is one of three diseases studied by two dozen researchers. "Prognosis has improved because of better support therapies like blood pressure control, anti-cholesterol drugs, dialysis and antibiotics, but this is the first really new and targeted therapy to come along in a long time."


Looney, Sanz, and rheumatologist Jennifer Anolik, M.D., Ph.D., run the University's lupus clinic at Strong Memorial Hospital, where about 800 patients who have symptoms of lupus are seen regularly. The clinic is one of 26 centers in the nation that make up the Lupus Clinical Trials Consortium, where patients have access to the latest experimental treatments.

Source: University Of Rochester Medical Center
Date: 2004-09-16



By: yanks04
20 Sep 2004, 09:13 PM EDT
Msg. 167895 of 188686
(This msg. is a reply to 167888 by fenderbender60.)
Jump to msg. #  
How much pull did the old founders have on the Argentina HPV game?
By: lovingitall0
20 Sep 2004, 09:23 PM EDT
Msg. 167896 of 188686
(This msg. is a reply to 167895 by yanks04.)
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"How much pull did the old founders have on the Argentina HPV game?"

Hmmmm, please if I may....

It could have been huge with AIDS alone. HPV indication would have been a great joint venture with a capable partner. ADVR needed to own it all. They still do, until proven otherwise.

When they stop reinventing the wheel they will be on their way to riches and much success. Share the wealth that they do not have.


Now, how's that?

Just some thoughts!

Nitey nite, now...


By: mind31
21 Sep 2004, 03:53 AM EDT
Msg. 167909 of 188686
Jump to msg. #  
So maybe the Elma fans are right. Maybe she did need all this time to go over the "data" and maybe she determined that the most honest thing to pursue would be cachexia because maybe she determined that the rest of the "data" is a pile of hog wash. And maybe Nowinski saw the same problems and that is why we dropped HPV. And maybe that is why we are turning away from AIDS at this point also. I think Martin Delaney said years ago that the drug made him eat and nothing more. Maybe that should have been a clue.