Posted by rob on February 21, 2006 under Uncategorized | 
C.R. Sukumar
| Natco Pharma had challenged the grant of EMRs to Novartis. The grant of EMRs to Novartis had forced several Indian pharmaceutical companies such as Ranbaxy, Cipla, Sun, Hetero, Torrent and Emcure to withdraw their generics from the market. |
Hyderabad , Feb. 21
IN yet another blow to the Swiss pharmaceutical giant Novartis AG in the Indian pharmaceuticals market, the Indian Patents Office has terminated the exclusive marketing rights (EMRs) granted to the company on November 10, 2003 for Gleevac (Imatinib Mesylate), a life saving anti-cancer drug, with effect from January 25, 2006.
Interestingly, on January 25 this year, the Swiss company had lost a patent claim for the anti-cancer drug — Imatinib Mesylate — before the office of the Indian Controller of Patents & Designs, following serious objections through pre-grant opposition route raised by Natco Pharma Ltd, a Hyderabad-based pharma company.
The Controller of Patents had refused to proceed further with Novartis patent application for Gleevac, which is used in the treatment of chronic myeloid leukaemia.
Interestingly, the Indian Patents Office has now decided to cancel the EMRs granted to Novartis based on the same grounds raised by the Office of Controller of Patents & Designs.
Citing the order of Office of the Controller of Patents & Designs dated January 25 in a notification dated February 17, the Indian Patents Office said, “Therefore, as per Section 78 of the Patents (Amendment) Act 2005 read with Section 24B of the Patents Act 1970 as amended by the Patents (Amendment) Act 2002, the said Exclusive Marketing Right granted to Novartis AG is hereby terminated with effect from January 25, 2006.”
Natco Pharma, which launched a generic version of Gleevac under the brand `Veenat’, had challenged the grant of EMRs to Novartis.
The grant of EMRs to Novartis had forced several Indian pharmaceutical companies such as Ranbaxy, Cipla, Sun, Hetero, Torrent and Emcure to withdraw their generics from the market.
Though the price difference between Gleevec and its clones was around twelve-fold, the domestic pharmaceutical companies were restrained from manufacturing and marketing the cheaper clones due to a Court order.
This case is currently pending before the Supreme Court.
The Office of Controller of Patents on January 25 ruled that the patent applied for by Novartis AG did not qualify as an invention on the grounds that it was merely a modification of the key component in the drug, for which a patent had already been filed in 1993.
Therefore, according to the Controller of Patents, this key component can not be eligible for protection under new patent regime of India that was introduced in March 2005 to comply with the WTO agreement on trade related aspects of intellectual property rights (TRIPS) that recognises patents for chemical products filed there after 1995, the year the WTO came into existence.
The Hindu Business Line : Exclusive marketing rights for Novartis’ cancer drug cancelled
Posted by rob on under Uncategorized |
Research could shape new treatments
By NICHOLAS WADE
New York Times
Posted: Feb. 20, 2006
One day, perhaps in the distant future, stem cells may help repair diseased tissues. But there is a far more pressing reason to study them: Stem cells are the source of at least some, and perhaps all, cancers.
At the heart of every tumor, some researchers believe, lie a handful of aberrant stem cells that maintain the malignant tissue.
The idea, if right, could explain why tumors often regenerate even after being almost destroyed by anti-cancer drugs. It also points to a different strategy for developing anti-cancer drugs, suggesting they should be selected for lethality to cancer stem cells and not, as at present, for their ability to kill just any cells and shrink tumors.
“I think this is one of the most interesting developments in cancer research in the last five years,” said Robert Weinberg, a cancer geneticist at the Whitehead Institute in Cambridge, Mass. “I think more and more people are accepting it, and evidence is accumulating that cancer stem cells exist in a variety of tumors.”
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The idea that cancer cells possess the same properties as stem cells has been around for many years. Only recently have biologists developed techniques for identifying stem cells and their presence in tumors.
Cancer stem cells were first identified in certain types of leukemia in 1997 by John Dick and colleagues at the University of Toronto. They were harder to spot in solid tumors because biologists did not possess the means of recognizing the markers – characteristic proteins on the surface of a cell – that had been developed for a stem cell that makes red and white blood cells.
But in 2003, Michael Clarke, now of Stanford University, succeeded in finding cancer stem cells in breast tumors. Clarke showed that a vast majority of cells in a human breast tumor were incapable of further growth. Only a handful were able to seed new cancers, and these resembled stem cells in their ability to proliferate and generate mature cells.
In 2004, Peter Dirks of the University of Toronto identified similar stemlike cells in human brain tumors, and last year C. Parker Gibbs of the University of Florida reported seeing stemlike cells in bone cancer.
“It’s a very challenging population of cells to identify, but thus far in every cancer in which cells have been carefully screened they have been found,” said Gary Gilliland of Harvard University.
Process is unclear
Biologists are not yet sure how cancer stem cells are generated. It may be that the stem cells themselves suffer a mutation, or a change in their DNA instructions, that deranges the strict controls on their self-renewal. Or possibly their immediate progeny, known as progenitor cells, suffer some genetic damage after which, instead of developing into mature cells, they regain the power of self-renewal.
Self-renewal, the key property of stem cells, refers to their ability to divide unevenly. Other cells divide into two daughter cells, just as the parent cell does, but a stem cell can divide into a new stem cell and a progenitor cell. The progenitor cell loses the power of self-renewal but gains the ability to change or differentiate into the mature cell types of the tissue served by the stem cell.
After such a division, the number of stem cells in the tissue remains unchanged because one stem cell has been lost and one created. The stem cell population thus renews itself as it generates new cells.
The stem cells responsible for maintaining a tissue or an organ can presumably regulate their own numbers, perhaps by sensing through an exchange of chemicals when they have a quorum. Cancer stem cells differ in that they have lost control over their own population size.
The hypothesis explains several otherwise puzzling facts about cancer. Many of the body’s tissues that are most prone to cancer, like the blood, skin and lining of the gut, are composed of short-lived cells that suffer high wear and tear.
Yet cells are believed to become malignant only after a series of mutations has disabled their genetic control systems. How can a skin cell, which lives only a few weeks, survive long enough to accumulate the right sequence of mutations?
It is more plausible to suppose that mutations build up in the self-renewing population of stem cells that maintains the skin.
Pathologists have long recognized that tumors contain a variety of cells, including some that are characteristic of the tissue in which the cancer originates. But not all these cells are equally cancerous. If the cells from a tumor are injected back into a patient at a different site, as was done in a 1961 experiment that would now be considered unethical, more than a million cells must be used before a new tumor will form.
This supports the idea that only a tiny minority of the cells in a cancer have the ability to maintain it.
An amazingly successful anti-cancer drug is Gleevec, used to treat chronic myelogenous leukemia and three rarer cancers. Many patients who take Gleevec experience complete remission. But the drug does not cure the disease, which sometimes returns. It seems Gleevec is attacking not the cancer stem cells but the progenitor cells from which the cancerous white blood cells are generated.
Though many biologists believe that the cancer stem cell idea is interesting, not all think that it will lead to new therapies. In the view of Bert Vogelstein, a leading cancer researcher at Johns Hopkins University, everything depends on how much of a tumor consists of cancer stem cells.
Targeting tumors
If the proportion is large, as several experiments suggest, then current anti-cancer drugs must already be killing them, since they can kill up to 99% of the cells in a tumor. In which case, the idea is not so helpful.
“So the real attractiveness of the cancer stem cell hypothesis, in my view, is that if the 1 percent of cells that are left after successful chemotherapy are really cancer stem cells, then obviously that provides the rationale for different forms of therapy that target them,” Vogelstein said.
Gilliland, an advocate of the idea, acknowledged that 20% of cells in the solid tumors analyzed so far had stemlike properties. But with better markers, he said, it may turn out that a much smaller proportion are true cancer stem cells.
“If the growth of solid cancers were driven by cancer stem cells, it would have profound implications for cancer therapy,” Irving Weissman of Stanford has written. “Therapies that are more specifically directed against cancer stem cells might result in much more durable responses and even cures of metastatic tumors,” he and colleagues said.
Pharmaceutical companies are “waiting for more academic research before they take a clear view on how to proceed,” geneticist Weinberg said.
JS Online:Stem cells might be key to cancer
Posted by rob on under Uncategorized |
Research could shape new treatments
By NICHOLAS WADE
New York Times
Posted: Feb. 20, 2006
One day, perhaps in the distant future, stem cells may help repair diseased tissues. But there is a far more pressing reason to study them: Stem cells are the source of at least some, and perhaps all, cancers.
At the heart of every tumor, some researchers believe, lie a handful of aberrant stem cells that maintain the malignant tissue.
The idea, if right, could explain why tumors often regenerate even after being almost destroyed by anti-cancer drugs. It also points to a different strategy for developing anti-cancer drugs, suggesting they should be selected for lethality to cancer stem cells and not, as at present, for their ability to kill just any cells and shrink tumors.
“I think this is one of the most interesting developments in cancer research in the last five years,” said Robert Weinberg, a cancer geneticist at the Whitehead Institute in Cambridge, Mass. “I think more and more people are accepting it, and evidence is accumulating that cancer stem cells exist in a variety of tumors.”
The idea that cancer cells possess the same properties as stem cells has been around for many years. Only recently have biologists developed techniques for identifying stem cells and their presence in tumors.
Cancer stem cells were first identified in certain types of leukemia in 1997 by John Dick and colleagues at the University of Toronto. They were harder to spot in solid tumors because biologists did not possess the means of recognizing the markers – characteristic proteins on the surface of a cell – that had been developed for a stem cell that makes red and white blood cells.
But in 2003, Michael Clarke, now of Stanford University, succeeded in finding cancer stem cells in breast tumors. Clarke showed that a vast majority of cells in a human breast tumor were incapable of further growth. Only a handful were able to seed new cancers, and these resembled stem cells in their ability to proliferate and generate mature cells.
In 2004, Peter Dirks of the University of Toronto identified similar stemlike cells in human brain tumors, and last year C. Parker Gibbs of the University of Florida reported seeing stemlike cells in bone cancer.
“It’s a very challenging population of cells to identify, but thus far in every cancer in which cells have been carefully screened they have been found,” said Gary Gilliland of Harvard University.
Process is unclear
Biologists are not yet sure how cancer stem cells are generated. It may be that the stem cells themselves suffer a mutation, or a change in their DNA instructions, that deranges the strict controls on their self-renewal. Or possibly their immediate progeny, known as progenitor cells, suffer some genetic damage after which, instead of developing into mature cells, they regain the power of self-renewal.
Self-renewal, the key property of stem cells, refers to their ability to divide unevenly. Other cells divide into two daughter cells, just as the parent cell does, but a stem cell can divide into a new stem cell and a progenitor cell. The progenitor cell loses the power of self-renewal but gains the ability to change or differentiate into the mature cell types of the tissue served by the stem cell.
After such a division, the number of stem cells in the tissue remains unchanged because one stem cell has been lost and one created. The stem cell population thus renews itself as it generates new cells.
The stem cells responsible for maintaining a tissue or an organ can presumably regulate their own numbers, perhaps by sensing through an exchange of chemicals when they have a quorum. Cancer stem cells differ in that they have lost control over their own population size.
The hypothesis explains several otherwise puzzling facts about cancer. Many of the body’s tissues that are most prone to cancer, like the blood, skin and lining of the gut, are composed of short-lived cells that suffer high wear and tear.
Yet cells are believed to become malignant only after a series of mutations has disabled their genetic control systems. How can a skin cell, which lives only a few weeks, survive long enough to accumulate the right sequence of mutations?
It is more plausible to suppose that mutations build up in the self-renewing population of stem cells that maintains the skin.
Pathologists have long recognized that tumors contain a variety of cells, including some that are characteristic of the tissue in which the cancer originates. But not all these cells are equally cancerous. If the cells from a tumor are injected back into a patient at a different site, as was done in a 1961 experiment that would now be considered unethical, more than a million cells must be used before a new tumor will form.
This supports the idea that only a tiny minority of the cells in a cancer have the ability to maintain it.
An amazingly successful anti-cancer drug is Gleevec, used to treat chronic myelogenous leukemia and three rarer cancers. Many patients who take Gleevec experience complete remission. But the drug does not cure the disease, which sometimes returns. It seems Gleevec is attacking not the cancer stem cells but the progenitor cells from which the cancerous white blood cells are generated.
Though many biologists believe that the cancer stem cell idea is interesting, not all think that it will lead to new therapies. In the view of Bert Vogelstein, a leading cancer researcher at Johns Hopkins University, everything depends on how much of a tumor consists of cancer stem cells.
Targeting tumors
If the proportion is large, as several experiments suggest, then current anti-cancer drugs must already be killing them, since they can kill up to 99% of the cells in a tumor. In which case, the idea is not so helpful.
“So the real attractiveness of the cancer stem cell hypothesis, in my view, is that if the 1 percent of cells that are left after successful chemotherapy are really cancer stem cells, then obviously that provides the rationale for different forms of therapy that target them,” Vogelstein said.
Gilliland, an advocate of the idea, acknowledged that 20% of cells in the solid tumors analyzed so far had stemlike properties. But with better markers, he said, it may turn out that a much smaller proportion are true cancer stem cells.
“If the growth of solid cancers were driven by cancer stem cells, it would have profound implications for cancer therapy,” Irving Weissman of Stanford has written. “Therapies that are more specifically directed against cancer stem cells might result in much more durable responses and even cures of metastatic tumors,” he and colleagues said.
Pharmaceutical companies are “waiting for more academic research before they take a clear view on how to proceed,” geneticist Weinberg said.
JS Online:Stem cells might be key to cancer
