March 26, 2013.docx

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University of Toronto St. George
Laboratory Medicine and Pathobiology

Cancer Genetics – molecular bases – March 26 Determination of cell – needs to prolifeate and divide Signal transduction – crucial to all cells – a number of ways to stimulate cells to grow Signal transduction – relay message through cell – received on surface of cell – send signal to nucleus – theme for many pathways RAS binds nucleotides – bound in inactive form to dinucleotide; when activated, bind GDP – when trigger RAS, it mediates whole signalling cascade not requiring anything from outside of cell – when trigger RAS, signal on route to get to nucleus – RAF1 If xternal factor present, signal relayed If not growth factors available or receipient ligands – no message relayed Key things to remember for pathways and how to deal with external cues – some conflicting, some driving forward – lots of components and steps – many proteins in canonical pathway that are members of same gene family – different members can respond – can have intricate response to various external stimuli – one cell can have different receptors and respond to different stimuli Can lead to cancer in different organs – depend on where expressed Players that can act in others – one such is MYC (important!) If can get to nucleus and drive the program that says to proliferate without having received external signal ABL gene – not receptor – tyrosine kinase Examples of genes that when mutated, act as onocogenes so promote development and progression of cancer*********** Oncogenes – in process of cell division – generally tigtly controlled process but this can be disregulated – lead to inappropriate growth or cell division – in normal circumstances – lead to cells growing inappropriately when in normal situations, they would not – growth regulating signals that can be coming from external cues – could be signal transduction process – act on cells from outside and stimulate cell into cell cycle – ultimately, there is coordination of events – cell division not cell proliferation – cell division is cell dividing itself, not the same as cell receiving signal to grow – recognize cell cycle with a number of check points Three cycle chekcpoitns G1 phase – at this point where the cell is still receving signal from outside – but pass this point, cell will make decision to divide regardless of external cues Later checkpoitns important for cell checking all DNA is properly divided; environment enough space for diviing cell Transition from G1 to S phase of the cell cycle Interreleated pathways – look at what drives cell signalling – variety of genes involved and some key players are cyclins Cell cycle genes have had multiple renditions of naming G1 to S phase – major inihbiitso to cell cycle p15, p16, etc Another aspect of cell cycle – G1 S checkpoint primary CLNE PCNA – activating to allow E2F to get to nucleus to tell cell to divide – All components that work together – also a variety of inhibitors – important to contributing and putting brakes on – inhibitors responses to diferent things including recognition that there is problem ith DNA – DNA damage and there isn’t time there has not yet been time for DNA to repair – the idea of monitoring and checking DNA damage is ongoing – these inhibitors can come and work on the checkpoints to tell the cell cycle to halt – the cyclins are also fairly tightly regulated Apoptosis – If disregulate this process – or take it away and block apoptosis – P53 is major tumour suppressor gene – will repress the BCL2 gene and if the BCL2 gene concentration is decreased – lead to apoptosis – cause increase in transcription of BAX gene, which if increased – lead to apoptosis – BAX contributes to stimulating apoptosis and BCL2 will inhibit it – if increase amount of BCL 2 will increasingly inhibit process – BCL2 is common onco-gene in some types of cancer – causes bypass of apoptosis – one and a few examp
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