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Blood Test Clue for Small Cell Lung Cancer Treatment


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Cancer Research UK-funded scientists have identified a new molecular marker in blood which could indicate how patients with a type of lung cancer will respond to treatment, according to research published in Clinical Cancer Research.

Researchers at the Physiological Laboratory, University of Liverpool and cancer specialists at Clatterbridge Centre for Oncology found that a molecule called SCG3 mRNA** in the bloodstream has a high association with a type of lung cancer called neuroendocrine small cell lung cancer (SCLC).

The marker could be developed for use in blood tests to see how well patients might respond to treatment for this type of lung cancer. The discovery may in future help doctors make more informed decisions about therapy or recommend that patients take part in trials to try new treatments that might be more effective for them.

There are presently no clear biological markers in blood suitable for identifying how well SCLC patients will respond to treatment, so all patients presenting with SCLC - one of the two main types of lung cancer- are usually treated with the same standard form of chemotherapy.

Patients with neuroendocrine SCLC are not usually able to have surgery because of multiple tumours which make operations difficult. Many patients initially respond to chemotherapy and radiotherapy, but their tumours are likely to reoccur, which is why it is so important to ensure that patients receive the optimum treatment for this disease.

Dr Judy Coulson, Cancer Research UK-funded lead author based at the University of Liverpool's, School of Biomedical Sciences, said: "There are currently no blood-based markers routinely used to monitor patients with this type of lung cancer.

"We found that SCG3 mRNA is an incredibly sensitive marker of these tumours and it could be used to detect circulating tumour cells in patients with this disease."

Lung cancer is the greatest UK cancer killer – some 33,500 individuals die from the disease in the UK each year accounting for 22 per cent of UK cancer deaths. Progress in improving survival for lung cancer has been very slow especially in comparison to some of the other common cancers such as breast or bowel cancer where survival rates have increased steadily over the past three decades.

Cancer Research UK has launched a five year strategy to reduce cancer death. This will see £300 million spent each year in core areas of science and will include increased investment in those cancers where survival remains poor, including lung, pancreas and oesophageal cancer.

Lesley Walker, Cancer Research UK’s director of cancer information, said: "This discovery is an important step to understanding how to treat lung cancer patients more efficiently. Lung cancer can be very difficult to treat in the later stages, either because it has spread of because there are too many tumours. Chemotherapy is therefore a vital part of lung cancer treatment.

"Anything that improves our knowledge of how to best treat lung cancer is crucial work.”

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(BigPond, UK, Source: Clinical Cancer Research: Cancer Research UK: January 26, 2009)


The information contained in these articles may or may not be in agreement with my own opinions. They are not being posted with the intention of being medical advice of any kind.

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In normal tissue, new blood vessels are formed during tissue growth and repair. In cancerous tissue, tumors cannot grow or spread (metastasize) without the development of new blood vessels. Blood vessels supply tissues with oxygen and nutrients necessary for survival and growth.

Endothelial cells, the cells that form the walls of blood vessels, are the source of new blood vessels and have a remarkable ability to divide and migrate. The creation of new blood vessels occurs by a series of sequential steps. An endothelial cell forming the wall of an existing small blood vessel (capillary) becomes activated, secretes enzymes that degrade the extracellular matrix (the surrounding tissue), invades the matrix, and begins dividing. Eventually, strings of new endothelial cells organize into hollow tubes, creating new networks of blood vessels that make tissue growth and repair possible.

Most of the time endothelial cells lie dormant. But when needed, short bursts of blood vessel growth occur in localized parts of tissues. New capillary growth is tightly controlled by a finely tuned balance between factors that activate endothelial cell growth and those that inhibit it.

About 15 proteins are known to activate endothelial cell growth and movement. At a critical point in the growth of a tumor, the tumor sends out signals to the nearby endothelial cells to activate new blood vessel growth. Two endothelial growth factors, VEGF and basic fibroblast growth factor (bFGF), are expressed by many tumors and seem to be important in sustaining tumor growth.

Angiogenesis is also related to metastasis. It is generally true that tumors with higher densities of blood vessels are more likely to metastasize and are correlated with poorer clinical outcomes. Also, the shedding of cells from the primary tumor begins only after the tumor has a full network of blood vessels. In addition, both angiogenesis and metastasis require matrix metalloproteinases, enzymes that break down the surrounding tissue (the extracellular matrix), during blood vessel and tumor invasion.

Research has shown that controlling production of new blood vessels can restrict tumor growth, often prolonging the life of the cancer patient. Perhaps the most widely-used anti-angiogenic agent to emerge to date has been the drug Avastin.

It is increasingly being realized that circulating microvascular cells may be important markers for a wide variety of cancers. An article in the Journal of Internal Medicine reported a novel system that was developed for testing anti-microvascular drug effects in fresh biopsy specimens of human tissue, cavitary fluids and blood.

Three-dimensional microclusters of tumor cells were isolated from fresh tumor biopsy specimens and cultured for 96 hours (polypropylene, round-bottomed, 96-well microplates) in the presence and absence of test drugs. A private laboratory has worked with the use of DMSO and/or alcohol as an anti-angiogenic enhancer and potentiator and has measured it with fresh "live" specimens in cell culture assays.

What alcohol does is to reduce the secretion of VEGF by the tumor cells. The assay shows the abrogating effect of alcohol upon VEGF. It both reduces VEGF and makes a drug like Avastin work better, possibly overcoming tumor resistance to Avastin. Alcohol may have a membrane effect, basically puts the cell to sleep so that it doesn't think it requires a blood supply. In the presence of a drug like Avastin, you have a lethel 1-2 combination which knocks out the new vessels which are dependent on VEGF for survival.

Confirmatory activities are ongoing. The system is being offered currently to selected clients on a research basis and as an adjunct to a standard assay or a tyrosine kinase assay.

Source: J Intern Med 2008; 264: 275-287

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