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Epimutations As Germ-line Defects In Hereditary Cancer Syndromes
Funder
National Health and Medical Research Council
Funding Amount
$385,925.00
Summary
Traditionally familial cancers were thought to be caused and inherited by spelling mistakes within the genetic code of cancer prevention genes. Our group has found that a 'chemical coat' around the MLH1 gene, causing it to be switched off, can also be inherited in some cases of bowel cancer, without any mistakes within the gene's code. We will determine if this 'coat' causes other types of cancer and if this runs in families. We also hope to find out how the coat is formed and may be reversed.
Germline Mutations Identified In Melanoma-prone Kindreds Can Impair The Function Of The P14ARF Tumour Suppressor
Funder
National Health and Medical Research Council
Funding Amount
$257,036.00
Summary
Approximately 10% of people in Australia are at high risk of developing melanoma because they carry a faulty gene. Many of these melanoma-prone individuals carry a single mutation that can disrupt two genes, p16INK4a and p14ARF. These genes are both involved in regulating the growth of cells via different pathways. The role of p16INK4a in cancer development is well established and the many functions of this gene are under intense investigation. In contrast, the role of p14ARF in melanoma progres ....Approximately 10% of people in Australia are at high risk of developing melanoma because they carry a faulty gene. Many of these melanoma-prone individuals carry a single mutation that can disrupt two genes, p16INK4a and p14ARF. These genes are both involved in regulating the growth of cells via different pathways. The role of p16INK4a in cancer development is well established and the many functions of this gene are under intense investigation. In contrast, the role of p14ARF in melanoma progression has not been studied. We will be analysing in detail how faulty p14ARF promotes uncontrolled cell growth and cancer development. Our research, will dissect the functions of p14ARF and determine whether p14ARF and p16INK4a co-operate in maintaining normal cell growth. This work is essential to our understanding of melanoma development and will provide clinically useful information regarding the biology of human cancer.Read moreRead less
P14ARF Induces P53-independent Growth Arrest By Modulating The Activities Of The E4F And E2F Transcription Factors
Funder
National Health and Medical Research Council
Funding Amount
$235,500.00
Summary
Cutaneous malignant melanoma is an important public health problem, affecting 1 in 30 Australians at some time in their lives, and the incidence of this disaese is increasing rapidly. Approximately 10% of people in Australia are at high risk of developing melanoma because they carry a faulty gene. Many of these melanoma-prone individuals carry a single mutation that can disrupt two genes, p16INK4a and p14ARF, that are involved in regulating the growth of cells via different pathways. The role of ....Cutaneous malignant melanoma is an important public health problem, affecting 1 in 30 Australians at some time in their lives, and the incidence of this disaese is increasing rapidly. Approximately 10% of people in Australia are at high risk of developing melanoma because they carry a faulty gene. Many of these melanoma-prone individuals carry a single mutation that can disrupt two genes, p16INK4a and p14ARF, that are involved in regulating the growth of cells via different pathways. The role of p16INK4a in maintaining cell cycle control is well understood and the many functions of this gene are under intense investigation. In contrast, the functions of p14ARF in normal cell regulation are not well understood. We will be analysing in detail how p14ARF protects the cell from uncontrolled growth and inhibits cancer development. Our research will dissect the functions of p14ARF and determine the protein partners that co-operate with p14ARF in maintaining normal cell growth. This work is essential to our understanding of normal cell proliferation and melanoma development and will provide clinically useful information regarding the biology of human cancer.Read moreRead less
Using The A33 Antigen Gene Locus To Generate Novel Mouse Models Of Colon Cancer
Funder
National Health and Medical Research Council
Funding Amount
$376,320.00
Summary
Colorectal (or bowel) cancer is a major health problem in Australia. It is the most common cancer reported to Australian cancer registries and was responsible for 14% of cancer deaths in 1990, the latest year for which national figures are available. Only lung cancer, which caused 20% of cancer deaths was a more common cause of cancer death. Approximately 1 in 21 Australians will develop colorectal cancer during his-her lifetime. The risk of colorectal cancer increases with age, with risk rising ....Colorectal (or bowel) cancer is a major health problem in Australia. It is the most common cancer reported to Australian cancer registries and was responsible for 14% of cancer deaths in 1990, the latest year for which national figures are available. Only lung cancer, which caused 20% of cancer deaths was a more common cause of cancer death. Approximately 1 in 21 Australians will develop colorectal cancer during his-her lifetime. The risk of colorectal cancer increases with age, with risk rising progressively and sharply from age 50 onwards. Like all cancers, colorectal cancer results from the progressive acquisition of mutations in genes that normally ensure a balance between cell growth and cell death. Mutations which predispose individuals to colorectal cancer accumulate in the epithelial cells that provide the lining to the bowel. The progression of colorectal cancer proceeds through a number of distinct anatomical stages which can be easily recognised by pathologists. Mutations in a number of genes (known as APC, beta-catenin, Kirsten-ras, p53, SMAD2, SMAD4) are commonly found in colorectal tumours. Moreover, some of the mutations are highly associated with distinct stages of colon tumour development. As yet, however, we have no real insights into how these mutations cooperate with each other to produce full-blown (malignant) colorectal cancer. In our proposal, we are aiming to establish colorectal cancer in mice. Our approach will be to progressively introduce mutant genes into intestinal epithelial cells (singly and in combination) and study how they cooperate with each other to produce benign, and ultimately, malignant tumours in the intestines of mice. This will help us to understand which mutant genes are required for each stage in tumour development and may provide more rational approaches to bowel cancer screening and treatment.Read moreRead less