Projects starting in October 2009 and ending in October 2012
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Dr Yong-Jie Lu
Barts and The Royal London School of Medicine and Dentistry, England
AICR grant: £192,685 (3 year grant)
Investigating testicular and prostate cancer at the genetic level
The way that cells grow, divide and die is normally tightly controlled by certain genes. Cancer is caused by damage to these genes which makes the cells to grow and divide in an uncontrolled manner, forming a tumour. Dr Yong-Jie Lu is using his AICR grant to study a gene called ZDHHC14 which he believes has a vital role in preventing tumours developing from healthy cells. He is investigating how ZDHHC14 controls cell growth and how it becomes damaged or deleted in prostate and testicular cancer.
Grants starting in April 2010 and ending in April 2013
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Dr Duncan Baird
Cardiff University, Wales
AICR grant: £176,473 (3 year grant)
How do bowel and prostate cancer progress?
The information our cells need to survive is encoded by our genes. The genes themselves are packaged into long, sausage-shaped structures called chromosomes. At the ends of the chromosomes are repeating sections called telomeres. When a cell divides to make new cells, the telomeres get shorter, eventually preventing the cells from dividing further. This is the basic cause of cellular aging and can be responsible for the death of old cells. However, cancer cells often have dysfunctional telomeres which can be unstable. This can lead to the loss of anti-cancer activities within the cells meaning they do not get old and die. In some cancers, one telomere can become glued or ‘fused’ to the end of another one. Dr Baird has developed a sophisticated technique to study the mechanism of telomere instability and fusion. He is using this technique to improve our understanding of how both bowel and prostate cancer progress.
Grants starting in October 2010 and ending in June 2013
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Dr Michelle M Hill
University of Queensland, Australia
AICR grant: £174,742 (3 year grant)
What is the link between obesity, cholesterol and prostate cancer?
Currently, there is a known link between prostate cancer, obesity and high cholesterol. How these conditions are linked remains unclear. A cell is covered by a cell membrane; this separates the inside of the cell from its external environment. Cholesterol is a component of this cell membrane that helps to organize the membrane into regions that are important for communication of the cell with the outside. One molecule that is controlled by cholesterol is called caveolin-1, and this molecule may play a role in aggressive prostate cancers. Dr Hill is using her AICR grant to investigate how caveolin-1 and high cholesterol are involved in prostate cancer. One theory is that the caveolin-1 molecule becomes altered in prostate cancer which causes changes in the way the cell membrane functions. These changes increase the ability of the prostate cancer cells to invade surrounding tissues and spread around the body, forming secondary tumours. Dr Hill and her team will test this theory using prostate cancer cells with or without caveolin-1 to mimic aggressive and non-aggressive prostate cancers, and study how these cells respond to changes in cholesterol in their environment. As the number of obese people increases and the population continues to eat a high cholesterol diet, a better understanding of how cholesterol and caveolin-1 contribute to prostate cancer is vital. Dr Hill’s team will use this system to find new molecules that could be used in diagnosis and to enable scientists to design and develop better treatments for prostate cancer in the future.
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Professor Lambertus Kiemeney
Radboud University Nijmegen Medical Center, the Netherlands
AICR grant: £196,954 (3 year grant)
Improving prostate cancer screening
Prostate cancer is the most frequently diagnosed cancer among men in the UK. It is estimated that 5-10% of cases are due to faulty genes passed on from our parents. Faults in two particular genes called BRCA1 and BRCA2, appear to cause a higher risk of prostate cancer and men with faulty BRCA2 genes also tend to develop the more aggressive forms of the disease which have lower survival rates. The prostate specific antigen (PSA) test helps detect prostate cancer but it is not perfect. Although the test has helped decrease the number of deaths from prostate cancer by around 20% it also leads to over-detection and over-treatment for many men who would have continued living a normal and full life, usually when they have mild forms of this cancer. However, men at a higher risk of developing prostate cancer, and particularly the more aggressive form, for example those with faulty BRCA1 or BRCA2 genes, may be more likely to benefit from PSA screening. Professor Kiemeney is conducting a study looking at the use of the PSA test for men with different faults in their BRCA genes along with a second screening test for prostate cancer which detects the molecule PCA3 in urine. Professor Kiemeney will then evaluate the use of the PCA3 marker in screening high-risk families with the hope that if it is successful, it could be added to the screening programme for men with a higher risk of developing the disease.
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Professor Colin S Cooper
Institute of Cancer Research, England
AICR grant: £148,443 (2 year grant)
Improving treatment for advanced prostate cancer patients
Prostate cancer cells normally only grow and divide in the presence of the male sex hormone androgen, which turns on a protein called the androgen receptor. The main drug treatments for prostate cancer work by blocking the production of androgens or the effect of androgens on the androgen receptor. However, although this treatment makes the cancer stop growing for a while the cells eventually become resistant to treatment. This means they become able to multiply despite the androgen-blocking treatments and the cancer comes back. One of the main reasons for this seems to be that the cells become extra sensitive to the remaining very low levels of androgens. Professor Cooper and his colleagues are investigating a process called androgen receptor ‘gene amplification’. Androgen receptor ‘gene amplification’ makes the cancer cells extra sensitive to androgens and has been reported in 20-30% of prostate cancers which continue to grow despite androgen blocking. Professor Cooper and his colleagues are now using an AICR grant to understand when the ‘gene amplification’ takes place. They will then assess whether it could be used as a marker to predict the outcome of the disease. They also hope to provide an initial assessment of whether prostate cancers which contain androgen receptor ‘gene amplification’ are more sensitive to treatment with the new drug abiraterone that can block the production of even very low levels of the androgens.
