Cancer Research Could Improve Survival Rates
Main Category: Cancer / OncologyArticle Date: 24 Nov 2009 - 2:00 PDT
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Scientists have begun a three-year study to analyse why cancer patients become resistant to treatments designed to fight the disease. A research team from Kingston University has been awarded £99,000 to investigate why some tumours are sensitive and respond to treatments and why other tumours do not. The study, funded by cancer charity BRIGHT (Better Research into Gastrointestinal Cancer Health and Treatment), will look at existing treatments for cancer of the colon and rectum, known as colorectal cancer.
Experts from Kingston's Faculty of Science will work with specialists at Royal Surrey County Hospital to examine tumour specimens from colorectal cancer patients. They aim to identify signs or markers which could indicate how patients respond to treatment with anti-cancer drugs. The scientists will also investigate whether cancer stem cells play an important role in the progression of colorectal cancer and could be responsible for the poor response or development of resistance to treatment with anti-cancer drugs.
Dr Helmout Modjtahedi, from Kingston University who is leading the research, said the study could help local health authorities to target drugs more effectively by identifying which patients would respond well to individual types of treatment. It would equally spare those who will receive no significant benefit from treatment with what are often expensive drugs. "We want to find out why some colorectal cancer patients respond well to particular drugs and why others don't," he said. "We also want to investigate why it is that after several cycles of chemotherapy, we tend to see resistance to the chemotherapy agents, which consequently have to be changed to overcome this drug resistance. Ultimately, we hope that the results of our investigation will improve survival among cancer patients. It should also help us and other scientists to develop new drugs to target those patients who do not respond well to medication currently available."
All the experimental works will be carried out at Kingston University's research laboratories and in the later stages scientists will examine tumour specimens from colorectal cancer patients, in collaboration with Dr Sharadah Essapen, Consultant Clinical Oncologist at the Royal Surrey County Hospital. Dr Essapen said the research could bring about improvements to patient care. "On behalf of the charity BRIGHT, we are very happy to support this important research which will help to improve our understanding of the response of colon cancer to current drug therapies," she said. "This may help to explain why some of our patients do better on chemotherapy than others, and hopefully lead to the development of new drugs that can target these cancers more effectively. Ultimately, our goal is to support research that may lead to improved patient outcomes."
Source: Kingston University
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Are Stem Cells The Root Of The Problem?
posted by Gregory D. Pawelski on 24 Nov 2009 at 8:34 amStem cells have that infinite ability to renew themselves and produce the many different cell types that make up a human. Cancer's hallmark is its ability to grow infinitely, multiplying into various cells that make up a tumor. Is cancer the result of a normal stem cell turned bad or an ordinary cell that somehow acquires a stem cell's immortality and versatility?
A recent finding that Temodar (temozolomide) increased the number of cancer cells with stem-like characteristics sounds eerily similar to the increase in the number of metabolic activity of mitochondria of the surviving cells from taxane (Taxol) therapy, even in cases where the majority of the cells are being killed by taxanes. It may indeed give clinical response (tumor shrinkage), however, these are mostly short-lived and relapses after a reponse to taxanes are often dramatic.
In stem cell research, anti-cancer treatments often effectively shrink the size of tumors, but some might have the opposite effect, actually expanding the small population of cancer stem cells that then are capable of metastasizing.
Maybe this new research would expose the faults of gene amplificaton/mutation studies. Genetic profiling assumes that all drugs within a class will produce precisely the same effect, even though from clinical experience, this is not the case. Nor can genetic profiling tell anything about drug combinations.
Are you sure that you’ve identified every single protein that might influence sensitivity or resistance to drugs? The "cell" is a system, an integrated, interacting network of genes, proteins and other cellular constituents that produce functions. You need to analyze the systems' response to drug treatments, not theoretical predispositions.
The fact that cancer stem cells may have unique biological properties more likely to fuel cancer, or unfavorable factors in the neighboring cells surrounding the tumor, such as mutated genes, proteins that encourage cell growth, it is important to look at the "forest" and not just the "trees."
There are many pathways to altered cellular (forest) function (hence all the different "trees" which correlate in different situations). Cell functional analysis measures what happens at the end (the effects on the forest), rather than the status of the individual trees.
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