Cancer treatment

Why Preventing Cancer Is Not the Priority in Drug Development?

Most people would agree that it would be better to prevent cancer, if we could, than to treat it once it developed. Yet economic incentives encourage researchers to focus on treatment rather than prevention.

The way the patent system interacts with the Food and Drug Administration’s drug approval process skews what kinds of cancer clinical trials are run. There’s more money to be made investing in drugs that will extend cancer patients’ lives by a few months than in drugs that would prevent cancer in the first place.

That’s one of the findings from the work of Heidi Williams, an M.I.T. economics professor and recent MacArthur Foundation “genius” grant winner, who studied the problem along with Eric Budish, a University of Chicago economics professor, and Ben Roin, assistant professor of technological innovation, entrepreneurship and strategic management at M.I.T

“R & D on cancer prevention and treatment of early-stage cancer is very socially valuable,” the authors told me in an email, “yet our work shows that society provides private firms — perhaps inadvertently — with surprisingly few incentives to conduct this kind of research.”

To secure F.D.A. approval, after patenting a drug, drug companies race the clock to show that their product is safe and effective. The more quickly they can complete those studies, the longer they have until the patent runs out, which is the period of time during which profit margins are highest. Developing drugs to treat late-stage disease is usually much faster than developing drugs to treat early-stage disease or prevention, because late-stage disease is aggressive and progresses rapidly. This allows companies to see results in clinical trials more quickly, even if those results are only small improvements in survival.

Many more cancer trials focused on treatments for patients with late-stage cancers than for early-stage cancers, according to the study. Between 1973 and 2011, there were about 12,000 trials for relatively later-stage patients with a 90 percent chance of dying in five years. But there were only about 6,000 focused on earlier-stage patients with a 30 percent chance of dying. And there were over 17,000 trials of patients with the lowest chance of survival (those with recurrent cancers) but only 500 for cancer prevention, which confer the longest survival gains. The bias toward studies focused on patients with shorter survival duration is more prevalent among privately financed trials than for publicly financed ones.

Another approach is to extend the period of a drug’s market exclusivity to compensate for the commercialization lag. The Hatch-Waxman Act of 1984 already permits a partial extension — a half year for every year in clinical trial, up to a maximum of five additional years. Ms. Williams’s analysis suggests this is the right idea, but that there are still many potential drugs that receive only very short periods of market exclusivity. The Affordable Care Act includes a provision that grants 12 years of market exclusivity beginning from F.D.A. approval — a half year less than the typical 12.5 years remaining on a patent — but it applies only to biologic drugs.

Source: nytimes

Nearly 50% of cancers get diagnosed late: Study

A new study has found that nearly half of cancers are diagnosed only when the disease is at an advanced stage, meaning treatment is both more expensive and less likely to succeed.

Cancers, Cancer treatment, Cancer diagnosis, Cancer Research UK, disease

Cancer Research UK said that tens of thousands of patients could have their survival chances improved if doctors were able to catch cancer before it spreads around the body, adding that early detection would also save the NHS nearly 210 million pounds, the Independent reported.

Cancer Research UK’s chief executive Harpal Kumar said that their report “provides a compelling case for substantial investment in efforts to achieve earlier diagnosis” and not to invest in earlier diagnosis is to fail cancer patients.

He said that earlier diagnosis saves lives and it could save critical NHS funds. And in the face of an overstretched NHS and a projected growing number of cancers diagnosed in the years ahead, we need to do everything we can to ensure that all patients have access to the best treatment as early as possible.

Source: zee news

Scientists’ one step closer to magic bullet against cancer caused by asbestos

Researchers have come closer to finding a cure for Mesothelioma – a very aggressive cancer associated with asbestos exposure – usually diagnosed in an advanced stage.
In December, the research team of Antonio Giordano, an internationally renowned pathologist, Director and Founder of the Sbarro Health Research Organization in Philadelphia, PA and Professor of Pathology and Oncology at the University of Siena, Italy, published two separate studies aiming to address the urgent need to identify possible new methods for mesothelioma treatment.

In the first study, published in the scientific journal Cell Cycle, Giordano’s researchers tested on mesothelioma cells the effect of two drugs designed to reactivate the p53 protein, one of the most important ‘tumor suppressors’, which is turned off in most human cancers.

Lead author Francesca Pentimalli of the National Cancer Institute of Naples “In mesothelioma, although p53 is rarely mutated, it is inactivated by alterations in its pathway. Both of the drugs used in the study target p53, but with different mechanisms of action. One in particular, called RITA, proved to be very toxic. Specifically, RITA caused mesothelioma cells, and not ‘healthy’ cells, to undergo apoptosis – a type of programmed cell death that occurs through the activation of a specific ‘cascade’ of events.

The second study, published online in Cancer Biology and Therapy and led by Paola Indovina of the University of Siena and the Sbarro Institute for Cancer Research and Molecular Medicine, Temple University in Philadelphia, was designed along the same lines as the first study.

In the second study, the authors tested, for the first time in mesothelioma, a new drug called MK-1775 in combination with cisplatin. MK-1775 is a selective inhibitor of WEE1, a protein that is crucial in activating a ‘checkpoint’ for the repair of damaged DNA before the cell starts its division process.

Source: Yahoo news

Grape seed Extract Kills 76% of Leukemia Cancer Cells in 24 Hours

A new study by Indian origin researcher has revealed that the synthesis of the most active component of grape seed extract, B2G2, encourages the cell death known as apoptosis in prostate cancer cells while leaving healthy cells unharmed.

“We’ve shown similar anti-cancer activity in the past with grape seed extract (GSE), but now we know B2G2 is its most biologically active ingredient which can be synthesized in quantities that will allow us to study the detailed death mechanism in cancer cells,” Alpna Tyagi, PhD, of the University of Colorado Skaggs School of Pharmacy and Pharmaceutical Sciences, said.

Previous studies have shown the GSE effectiveness against cancer cells and have also shown its mechanism of action. However, Tyagi said that until recently, they didn’t know which constituent of GSE created this effect. This naturally occurring compound, GSE, is a complex mixture of polyphenols and also so far it has been unclear about the biologically active constituents of GSE against cancer cells.

Eventually the group pinpointed B2G2 as the most active compound, but, “it’s expensive and it takes a long time to isolate B2G2 from grape seed extract,” Tyagi says.

The current study reported the success of this effort, including the ability to synthesize gram-quantity of B2G2 reasonably quickly and inexpensively.

The study also showed anti-cancer activity of synthesized B2G2 similar in mechanism and degree to overall GSE effectiveness.

The study was published in the journal Nutrition and Cancer.

Source: Zee news

 

New method could help in early detection of colon cancer

Bettina Scholtka, said that tumour cells are released into stool from the surface of precancers and early-stage colon cancers

Scientists have found a new method to detect genetic variations that initiate colon cancer could be readily used for non-invasive colon cancer screening.

Bettina Scholtka, Ph.D., assistant professor in the Department of Nutritional Toxicology at the University of Potsdam in Nuthetal, Germany, said that tumour cells are released into stool from the surface of precancers and early-stage colon cancers, but detecting a cancer-initiating genetic mutation among a large quantity of normal DNA from a patient’s stool is like looking for a needle in a haystack.

Scholtka said that by combining for the first time locked nucleic acid-based, wild-type blocking polymerase chain reaction and high-resolution melting, we were able to achieve the desired sensitivity.

Scholtka and colleagues used 80 human colon tissue samples representing cancers and precancers to detect genetic variations using a combination of two techniques: The first technique — locked nucleic acid (LNA)-based, wild-type blocking (WTB) polymerase chain reaction — suppressed normal DNA present in large quantities in the sample; and the second technique — high-resolution melting (HRM) — enhanced the detection of genetic variations.

The researchers were able to detect APC variations in 41 of the 80 samples. They were also able to detect previously unknown variations in APC. In contrast, the routinely used technique called direct sequencing could detect variations only in 28 samples.

They then analyzed 22 stool samples from patients whose colon tissues had APC variations, and nine stool samples from patients whose colon tissues did not have APC variations, as controls. They were able to detect APC variations in 21 out of 22 samples.

The study has been published in Cancer Prevention Research.