Searchable abstracts of presentations at key conferences in endocrinology
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22nd Joint Meeting of the British Endocrine Societies

Symposia

Apoptosis/Survival Signalling

ea0005s12 | Apoptosis/Survival Signalling | BES2003

Building and demolishing cancers in vivo

Evan G

Cancers arise through accumulation of mutations that compromise control of cell proliferation, differentiation, adhesion, invasion, angiogenesis and apoptosis. To identify targets for effective therapy, it is important to determine which lesions are needed for maintenance of the tumor. We have constructed genetically manipulated transgenic and knock-in mice to directly explore the roles of activated Myc and inactivated p53 in the genesis, progression and maintenance of neoplas...

ea0005s13 | Apoptosis/Survival Signalling | BES2003

The role of mitochondria in cell death

Halestrap A

In addition to their role in cellular energy metabolism, mitochondria are now recognised as central players in cell death. Critical to this role is the mitochondrial permeability transition pore (MPTP) whose opening uncouples mitochondria, preventing them from providing for the energy needs of the cell leading to necrotic cell death. MPTP opening is important in the injury to the heart and brain that follows an ischaemic episode such as a heart attack or stroke and agents that...

ea0005s14 | Apoptosis/Survival Signalling | BES2003

Phosphoinositide 3-kinase dependent lipid signals in cellular survival responses

Downes C

Type I phosphoinositide 3-kinases (PI3Ks)are regulated by tyrosine kinases, Ras and G-protein coupled receptors and generate the lipid second messenger, phosphatidylinositol (3,4,5)-trisphosphate (PIP3). PIP3 regulates a bewildering variety of cellular responses primarily through binding and hence activating or targeting a range of proteins each of which posseses a specific PIP3 binding module, most commonly a pleckstrin homology (PH) domain. In terms of cell survival the key ...

ea0005s15 | Apoptosis/Survival Signalling | BES2003

Cell proliferation and death in endocrine glands: The corpus luteum paradigm

Fraser H

The corpus luteum (CL) is a dynamic but transient endocrine gland. Although proliferation of hormone-producing cells ceases after ovulation, proliferation of endothelial cells is intense and the CL becomes highly vascularised. However, unless the CL is rescued by pregnancy, all these cells will die. Investigation of cell death in the CL offers an opportunity to study the mechanisms underlying regulated death of parenchymal and endothelial cells. Apoptosis is extensive in the C...