Thyroid-sympathoadrenal Regulation Of Human Brown Fat
Funder
National Health and Medical Research Council
Funding Amount
$447,141.00
Summary
This project aims to determine how hormones influence the growth and activity of brown fat in humans. Majority of fat cells in the body are white fat cells, which store fat, and cause obesity when in excess. Brown fat cells function like generators. They burn fat and release energy as heat. Humans with lots of brown fat are lean. What controls brown fat activity is currently unknown in humans. This project investigates how hormones influence brown fat activity and may shed light on the therapeut ....This project aims to determine how hormones influence the growth and activity of brown fat in humans. Majority of fat cells in the body are white fat cells, which store fat, and cause obesity when in excess. Brown fat cells function like generators. They burn fat and release energy as heat. Humans with lots of brown fat are lean. What controls brown fat activity is currently unknown in humans. This project investigates how hormones influence brown fat activity and may shed light on the therapeutic potential of brown fat in obesity treatment.Read moreRead less
Exploring Models For Antibody Mediated Endocrine Disease
Funder
National Health and Medical Research Council
Funding Amount
$140,949.00
Summary
Common endocrine disorders like Graves’ disease, are mediated by auto-antibodies, causing uncontrolled hormonal expression and undesirable effects. However, due to the limited understanding of the antibody interactions, the treatment is still focused on controlling the hormone production/interactions instead of targeting the underlying autoimmune processes. This project aims to further characterise the role the antibody through animal studies and developing novel treatments based on the research ....Common endocrine disorders like Graves’ disease, are mediated by auto-antibodies, causing uncontrolled hormonal expression and undesirable effects. However, due to the limited understanding of the antibody interactions, the treatment is still focused on controlling the hormone production/interactions instead of targeting the underlying autoimmune processes. This project aims to further characterise the role the antibody through animal studies and developing novel treatments based on the research.Read moreRead less
Understanding The Role Of RAS Mutations In Thyroid Cancer.
Funder
National Health and Medical Research Council
Funding Amount
$463,854.00
Summary
My fellowship will examine the association of RAS mutations in thyroid cancer. RAS proteins are the most mutated in cancer and I will investigate how they work in thyroid cancer. RAS mutated thyroid cancer is more likely to cause death. This grant will be based in the pioneering lab of Prof Fagin at Memorial Sloan Kettering Cancer Center and the Garvan Institute of Medical Research. It is hoped by understanding these mutations, new treatments for thyroid cancer can be developed.
Impact Of Progesterone Receptor Subnuclear Localisation On Progesterone Action In Endocrine Target Cells
Funder
National Health and Medical Research Council
Funding Amount
$459,514.00
Summary
Breast cancer affects 10,000 Australian women annually and is a major cause of cancer death. The hormone progesterone, which is produced by the ovaries in women, is responsible for some aspects of the development of the normal breast in women and is also implicated in the development and response of breast and endometrial cancers. In normal cells progesterone acts via a specific protein (or receptor) in the nucleus, and we have shown that this protein accumulates into foci when it is active. We ....Breast cancer affects 10,000 Australian women annually and is a major cause of cancer death. The hormone progesterone, which is produced by the ovaries in women, is responsible for some aspects of the development of the normal breast in women and is also implicated in the development and response of breast and endometrial cancers. In normal cells progesterone acts via a specific protein (or receptor) in the nucleus, and we have shown that this protein accumulates into foci when it is active. We have noticed that in cancers, this accumulation is disrupted, and this is a bad sign for the cancer. As breast cancer develops, it causes many dramatic changes in the structure of cells of the breast, and particularly in the nucleus, which carries the genetic information that programs cancer cell behaviour. The nucleus normally is highly organised into compartments, which carry out different functions of the cell, such as duplication of the DNA, repair of DNA after damage, and switching on and off of particular genes important to the function of the cell. This organisation is altered dramatically in cancer cells, and it seems that this altered organisation is responsible for altered function. In this project we aim to work out what makes the receptor for progesterone form foci, how these foci are involved in the action of progesterone, and how the changed structure of the nucleus changes this process. This project will link the structure of the cell nucleus with the ability of progesterone to switch on or off particular genes, and this will provide the first signposts of how changes seen in cancer cell nuclei are reflected in changed hormonal signalling. Healthy women are regularly exposed to progestins in oral contraceptives and hormone replacement therapy. The known increased risk of breast cancer as a result of exposure to progestins creates an imperative to understand how progesterone may have aberrant effects. This project will address this important health issue.Read moreRead less
Alpha-2-Macroglobulin And The Transport And Uptake Of The Hormone, Hepcidin
Funder
National Health and Medical Research Council
Funding Amount
$533,541.00
Summary
Hepcidin is a peptide hormone that is a major regulator of iron metabolism. It has been suggested that hepcidin is free in the blood. However, we recently identified that hepcidin binds with alpha-2-macroglobulin (a2-M) in the plasma and this increases the efficacy of this peptide. The demonstration that a2-M plays a role in hepcidin biology will lead to a better understanding of hepcidin physiology, the development of methods for its measurement and improved treatment of iron related diseases.