27th May 2001
By Victor Ivan
The judicial crisis regarding Chief Justice Sarath N. Silva is a question that could affect the politics of the country.
An independent judiciary is essential for a democratic political system. There was a time when the executive , the legislative and the judicial powers were concentrated on the same person or the same institution. However, in modern democracies, at a time when attention is paid to the sovereignty of the people, the separation of those three powers is considered essential.
In a democratic political system, the legislature makes laws and the executive, implements them. The judiciary is entrusted with the task of exercising vigilance over the activities of the legislature and the executive.
If the judiciary becomes a slave of the government, then the separation of powers between the executive and the judiciary, which is an essential condition in a democratic system, comes to an end, tolling the death knell of democracy in the country.
A fundamental obligation of the country is not to allow any legislation that deprives or limits people of their sovereignty, and also to protect the fundamental rights of the people.
To put it more specifically, it is the responsibility of the Supreme Court not to allow the enactment of laws that would extend the period of office of a legislature or permit it to establish its power in such a way as to curtail or distort the sovereignty of the people, not to allow a bill that would permit the executive to get funds for more than an year, not to allow any enactment of laws that would give special advantages to any ethnic or religious community or place any disabilities on them, and not to allow enactment of any laws that would harm the fundamental rights of the people.
At no time should the Supreme Court be a partner in a programme put forward by an executive that would go against those principles.
If the judiciary knowingly becomes a party to such a programme, that might be the lowest level to which a judiciary can fall.
If the Constitution of 1978 was the creation of an executive presidency, the best thing that happened from it was the creation of the provision for fundamental rights. Fundamental Rights existed in the 1972 Republican Constitution, but it was the 1978 Constitution that gave it teeth by making it justiciable. There were several judgments given by the Supreme Court which greatly displeased the executive even when the UNP had a five-sixth majority in Parliament.
Even during the period of Mr. Premadasa, who is considered to have been an extremely powerful ruler, there were a number of judgments which embarrassed the government. Although the courts have been acting in such a way as to broaden the framework of the fundamental rights, disregarding the adverse influence of the executive.
The Supreme Court should not regard the fundamental rights cases as creating unnecessary problem for the executive and which narrows the powers of the executive.
Otherwise without finding an early solution to the crisis, it will be impossible to achieve any reforms (including the building of democratic reforms and finding a peaceful solution to the ethnic problem).
If an institution like the Supreme Court functions as a slave of the executive rather than as an institution that takes independent decisions, it will not be possible to do anything that does not accord with the wishes of the executive.
Whatever wrongs it may do, it will not be challenged in a Court of Law. However, if it were otherwise the executive will lose that protection, and the institution will again come to a position of independence and there will be greater space for democracy in the country.
The writer is the editor of Ravaya
By Michael D. Lemonick And Alice Park
By February of last year, Victoria Reiter, 63, figured she had only a few months to live. A writer and translator living in Manhattan, she was suffering from chronic myeloid leukemia, an especially deadly form of blood cancer. The only treatment available was interferon, an immune-system booster that wasn't really working and that made her violently ill. Reiter had spent most of 1999 in bed, too sick to read, to walk, to do much of anything — although she had managed to put together lists dividing her possessions between her two daughters.
Then she went on an experimental drug called Gleevec, and within weeks everything changed. "All my energy started coming back," she says. "Suddenly I could read. I could take a walk." By August, tests showed her bone marrow was clear of leukemia cells; in December, she took up the Argentine tango. She still has the lists of what her daughters will get, but, she exults, "They're not going to get it yet!"
For Bob Ferber, a Los Angeles prosecutor specializing in animal-abuse cases, the Gleevec experience was very much the same. Less than two years ago, he was lying in a hospital room considering suicide to escape the pain radiating from his bones. "From crawling across the floor on my knees to go to the bathroom, I'm now back at work," says Ferber, 48. "I go to the gym. I'm volunteering for an animal-rescue group. I have a girlfriend. It's the dream of any cancer patient in the world to be able to take a pill that works like this. It's truly a miracle."
That's a tempting way to look at it, anyhow. Gleevec is effective enough that the U.S. Food and Drug Administration approved it in record time two weeks ago — even as researchers announced that it also works against a rare form of stomach cancer. The drug doesn't help everyone, and it can have side effects, including nausea, muscle cramps and skin rash. Moreover, nobody is claiming that it actually cures cancer. Patients may have to continue taking the drug, probably for the rest of their lives, and unless Gleevec is used in combination with some other drugs, it is likely their cancer will come back.
Despite all these caveats, Gleevec is still a breakthrough — not only for what it does but, more important, for the revolutionary strategy it represents. A full 30 years have passed since President Richard Nixon declared war on cancer and called for a national commitment comparable to the effort to land on the moon or split the atom. But over those three decades, researchers have come up with one potential miracle cure after another — only to suffer one disappointment after another. Aside from surgery, which almost invariably leaves behind some malignant cells, the standard treatment for most cancers continues to be radiation and chemotherapy — relatively crude disease-fighting weapons that have limited effectiveness and leave patients weak and nauseated.
Along the way, though, scientists have amassed a wealth of information about how cancer works at the molecular level, from its first awakening in the aberrant dna of a single cell's nucleus to its rapacious, all-out assault on the body. Armed with that information, they have been developing a broad array of weapons to attack the disease every step along the way. Many of these therapies are just beginning to reach clinical trials and won't be available to save lives for years to come. If you have cancer today, these treatments are likely to come too late to help you. But, says Dr. Larry Norton, a medical director at Memorial Sloan-Kettering Cancer Center in New York City: "I think there is no question that the war on cancer is winnable."
That sentiment was pounded home last week at the annual meeting of the American Society of Clinical Oncology in San Francisco, where a record 26,000 cancer specialists from around the world briefed each other on the good news starting to pour out of their laboratories. Unlike chemo and radiation, which use carpet-bombing tactics that destroy cancer cells and healthy cells alike, these new medicines are like a troop of snipers, firing on cancer cells alone and targeting their weakest links.
Some of these therapies prevent a class of chemicals called growth factors from reaching a tumor, blocking signals that would otherwise instruct the cell to grow out of control. Others tip the delicate balance that every cell maintains between life and death, driving cancerous cells to self-destruct. Still others block enzymes that cancer cells use to chew openings in normal tissues and give themselves room to expand. And, most famously, the class of compounds known as angiogenesis inhibitors keep tumors from building new blood vessels to supply themselves with food and oxygen. "
Four years ago, for example, researchers at IDEC Pharmaceuticals in San Diego, Calif., hit just such a line-drive single with Rituxan, the first drug that successfully targeted proteins on cancer cells. Scientists had learned over the years that cancer cells are studded with an unusually large number of receptacles that compounds essential for survival, including growth factors, can plug into and fuel the cells' growth. Rituxan is a monoclonal antibody, a molecule specifically engineered to fit into the receptacles on non-Hodgkin's lymphoma cells and, in this case, single out the cancer cell for destruction by the immune system. Back in the early 1980s, monoclonal antibodies were hyped in the media as "magic bullets" that would wipe out cancer.
That proved far too strong a claim, but monoclonal antibodies have finally begun to live up to more modest expectations. Rituxan was the first, but just a year later, the same approach led to Herceptin, a drug that keeps growth factors from feeding certain kinds of breast-cancer cells. Such targeted treatments are effective only when the appropriate target exists. Herceptin, for example, latches onto a receptor known as her2, which is abnormally abundant in only about 30% of breast-cancer tumors. A biopsy can tell doctors whether a patient is likely to respond to Herceptin, but they'd hoped to find a molecule that would plug into a growth-factor receptor more prevalent in cancer cells.
Sure enough, they found one. Dr. John Mendelsohn, then at the University of California, San Diego, and now president of the M.D. Anderson Cancer Center in Houston, had been focusing since 1981 on a receptor called egfr, which is host to a protein called epidermal growth factor (EGF). It's a close cousin to her2, and Mendelsohn and his team know that it is present in a huge variety of tumors; two-thirds of all cancer types, in fact, are blanketed with EGF receptors. In 1984 Mendelsohn and his team showed in mice that blocking the EGF receptor with a growth-factor decoy prevented a cell from growing and dividing.
Making a drug out of that decoy would prove tricky, since the receptor, like her2, also shows up on noncancerous cells. Researchers are now learning, however, that normal cells are more adept than cancer cells at finding other growth factors on which to rely when EGFR is blocked. But when Mendelsohn applied for his first grant from the National Cancer Institute in 1983, he was rejected. "Nobody thought it would work," he says. The following year he turned to philanthropic sources for research dollars.
Those are only two drugs that keep EGF from doing its job. Gleevec, which reversed Reiter's and Ferber's leukemia so dramatically, is another; so is Tarceva, a drug from OSI Pharmaceuticals in Uniondale, N.Y., which is showing promise against some lung tumors as well as head and neck cancers. Neither of these compounds keeps EGF from docking with cells; instead, each worms its way inside the cells, where it intercepts growth messages percolating in from the surface. Astra Zeneca, headquartered in London, is testing a similar compound, Iressa, against some lung, stomach and prostate cancers.
And that's just the start. Gleevec, Tarceva and Iressa all break one of the most common signaling pathways by blocking an enzyme known as a tyrosine kinase. But the message that encourages a cancer cell to grow involves hundreds of biochemical signals that can travel by hundreds of different pathways. Each of those pathways represents a target, a link that could be interrupted with the properly designed drug.
Another reason cancers grow inexorably is that unlike normal cells, which die a natural death after a fixed number of divisions, cancer cells live forever. Scientists have been looking for compounds that will rewire tumor cells so they will know when it's time to go. The research is still in its early stages, but scientists in several labs have started looking at a group of enzymes called caspaces; inhibiting these enzymes disrupts the process of DNA repair that occurs each time a cell divides. - Time Magazine
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