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Genomic And Proteomic Dissection Of The Molecular Basis Of Kidney Development.
Funder
National Health and Medical Research Council
Funding Amount
$454,582.00
Summary
The number of nephrons present in the human adult kidney can vary by threefold. This is likely to be due to slight variations in the rate of nephron formation during development. Evidence is mounting that a reduced number of nephrons can predispose to renal failure later in life in response to stresses such as hypertension or substance abuse. 80,000 new cases of end stage renal failure occur each year in the US, with 25% of these related to hypertension and therefore possibly linked to a low nep ....The number of nephrons present in the human adult kidney can vary by threefold. This is likely to be due to slight variations in the rate of nephron formation during development. Evidence is mounting that a reduced number of nephrons can predispose to renal failure later in life in response to stresses such as hypertension or substance abuse. 80,000 new cases of end stage renal failure occur each year in the US, with 25% of these related to hypertension and therefore possibly linked to a low nephron number. While it is known that the kidney arises through a series of reciprocal inductive events between the metanephric mesenchyme and the ureteric bud, a better understanding of the molecular basis of these events is needed to understand what dictates nephron endowment. The Wilms tumour suppressor protein WT1 is not only mutated in some cases of the childhood kidney cancer, Wilms tumour, but is also critical for the normal development of the metanephros, as demonstrated by knockout experiments in mice. One of the earliest genes expressed in the metanephric mesenchyme, WT1 is thought to prevent this tissue from dying before differentiation, directing it to form the kidney and, postnatally, regulating normal podocyte function. Although known to be a nuclear regulatory protein, the genes directly regulated by WT1 have not been clearly or convincingly delineated. This study aims to directly screen for changes to gene expression and protein production levels induced by WT1. To do so, an array approach unique in its use of a specific array set derived from developing kidney will be used. In concert, additional specific clone sets derived from mouse kidney prior and post the commencement of nephron formation will be constructed and analysed. As WT1 is a nuclear protein involved in splicing, this study will involve a parallel investigation at a proteomic level of changes in spliceosomal proteins in response to changes in WT1.Read moreRead less
Functional Analysis Of Relapse Predictive Genes In Wilms Tumour
Funder
National Health and Medical Research Council
Funding Amount
$571,311.00
Summary
Wilms tumor is a paediatric kidney cancer, the most common abdominal tumour seen in children. About 20% of Wilms tumour patients have relapsing fatal tumours. We have found two genes that mark tumours which relapse: C-EBPB and CLK1. Characterization of C-EBPB and CLK1 will yield new information regarding the mechanisms underlying development and progression of Wilms tumours, leading to improved treatment for Wilms tumor patients. Both C-EBPB and CLK1 may also have roles in other human cancers.
Regulation Of SRC-Family And Focal Adhesion Kinase Function
Funder
National Health and Medical Research Council
Funding Amount
$381,338.00
Summary
Cells in our bodies stick to one another and to the cementing material called extracellular matrix surrounding them. An ezyme called focal adhesion kinase (FAK) is a major regulator of cell stickiness. It can catalyze the covalent attachment of a chemical group called phosphate to specific cellular protein. This proposal aims at studying how FAK is regulated by insulin stimulation and how FAK is regulated by a tumour suppressor called PTEN. Results of the study will shed light on how abberration ....Cells in our bodies stick to one another and to the cementing material called extracellular matrix surrounding them. An ezyme called focal adhesion kinase (FAK) is a major regulator of cell stickiness. It can catalyze the covalent attachment of a chemical group called phosphate to specific cellular protein. This proposal aims at studying how FAK is regulated by insulin stimulation and how FAK is regulated by a tumour suppressor called PTEN. Results of the study will shed light on how abberrations in the regulation and PTEN contribute to the development of development defects, heart attack, and the spreading of cancer cells.Read moreRead less
Breast cancer is the most frequent malignancy among women, with an estimated 1 million new cases per year worldwide. A family of enzymes known as protein tyrosine kinases (PTKs) are fundamental in the initiation and progression of tumour growth and they are frequently hyperactivated in breast cancer. This proposal will examine whether inactivation of the enzyme known as TCPTP contributes to PTK hyperactivation and tumorigenicity in breast cancer.
Regulation Of The Tumour Suppressors APC And BRCA1 By Nuclear Export
Funder
National Health and Medical Research Council
Funding Amount
$530,874.00
Summary
Cancer cells lack the ability to control their own growth, and thus continously divide in their local environment, leading to tumour formation. Tumour suppressor proteins, like APC and BRCA1, normally function as regulators to help cells respond to outside signals and to stop growing when necessary. The inactivation and altered cellular localisation of tumour suppressor proteins can contribute to cancer development. We have found that the APC and BRCA1 proteins, whose inactivation leads to devel ....Cancer cells lack the ability to control their own growth, and thus continously divide in their local environment, leading to tumour formation. Tumour suppressor proteins, like APC and BRCA1, normally function as regulators to help cells respond to outside signals and to stop growing when necessary. The inactivation and altered cellular localisation of tumour suppressor proteins can contribute to cancer development. We have found that the APC and BRCA1 proteins, whose inactivation leads to development of colon cancer and breast cancer, respectively, contain signals that dictate their movement within the cell. Our novel preliminary findings reveal that APC and BRCA1 are able to move in and out of the cell nucleus. We aim to define how this occurs, and examine how the regulation of their cellular location affects the normal function of these cancer-suppressing proteins. Finally, abnormalities in the nuclear passage of APC or BRCA1 might explain their altered cellular location in cancer cells.Read moreRead less
Regulation Of The Tumour Suppressor PTEN By Phosphorylation And Oligomerization
Funder
National Health and Medical Research Council
Funding Amount
$241,650.00
Summary
The tumour suppressor PTEN is an enzyme involved in controlling cell growth, cell death, and cell migration. PTEN was identified as a tumour suppressor because many tumour cells were found to carry mutations in the PTEN gene that cause the loss of PTEN protein or the loss of PTEN enzyme activity. Hereditary mutations of the PTEN gene are the causes of a rare genetic disease called Cowden's disease. Cowden's disease patients are predisposed to developing skin, thyroid, and breast cancers. In labo ....The tumour suppressor PTEN is an enzyme involved in controlling cell growth, cell death, and cell migration. PTEN was identified as a tumour suppressor because many tumour cells were found to carry mutations in the PTEN gene that cause the loss of PTEN protein or the loss of PTEN enzyme activity. Hereditary mutations of the PTEN gene are the causes of a rare genetic disease called Cowden's disease. Cowden's disease patients are predisposed to developing skin, thyroid, and breast cancers. In laboratory conditions, increasing the abundance of PTEN in tumour cells such as brain and prostate tumour cells can suppress their growth, hence its role as a tumour suppressor. In addition to its role as a tumour suppressor, PTEN controls cancer cell spreading. Although much is known about the involvement of PTEN in cancer formation and the spreading of cancer cells, how PTEN suppresses tumour cell growth and spreading is not fully understood. The enzyme activity of PTEN enhances the removal of a chemical group called phosphate group from proteins and the fat-soluble compounds called phospholipids in the cell membrane. The ability of PTEN to suppress cell growth and spreading is due to its enzyme activity. However, exactly how the enzyme activity of PTEN is regulated is not well understood. In order for PTEN to efficiently enhance the removal of phosphate group from specific cellular proteins and phospholipids, PTEN needs to be located in close vicinity to these proteins and phospholipids. However, exactly how PTEN moves to the locations where these proteins and phospholipids are present remains elusive. This proposal aims at studying the regulation of PTEN enzyme activity and movement inside the cells. Results of the proposed studies will shed new light on how PTEN gene mutations contribute to cancer formation and the spreading of cancer cells and may facilitate the search for the cure of cancers.Read moreRead less