Lecture 4

Lecture 4 - Lecture #4 Thursday 4/10/09 Last lecture was on...

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Lecture #4 – Thursday 4/10/09 - 1 - Last lecture was on oncogenes: the concept, Varmus and Bishop’s discovery of oncogenes in context of retroviral infections, viral relation and different aspects of its discovery (uses, relevance, etc.) There are ~100 retrovirus and DNA viruses known to promote tumor growth in animals. Their oncogenes have been identified/isolated. Fall into a number of different categories. - Relation to actual human tumor formation: o Not all oncogenes have been found mutated in every type of cancer. o Oncogenes by definition have the ability to induce malignant transformation when mutated , but that doesn’t mean they always do. o All sorts of oncogenes people isolated from these tumor viruses that have counterparts in genes found in the normal genome that when mutated can promote malignant transformation. But we don’t see those when we look in human tumors and finding what their genetic alterations are. Q. If they’re not mutated, aren’t they called proto-oncogenes? A. Proto-oncogenes are non-mutated version of the gene in the host genome. Oncogenes are the mutated forms in a viral agent or other external factors or mutated in genome leading to malignant transformation. Some combinations of oncogenes that predispose malignancy in some tissues are not always seen in other tissues. No one blueprint for oncogenic or malignant transformation for every tissue - There isn’t a standard set of oncogenes that exist for all tissues. - Combinations are tissue specific and even sometimes circumstance/conditionally specific. - Ex. Different genes mutated in breast cancers versus colon and brain and lung, etc. There are classes of oncogenes seen however if you group the ~100 or more oncogenes together. Outside of the cell in. (Note: there is no relevance in the order of these classes.) BE CAREFUL not to equate mutations in these genes alone to malignancy by themselves. Change in one oncogene isn’t generally enough. Need multiple genetic changes. Cancer is a disease that results from a combination of multiple mutations. - Extracellular oncogenes – pretty small group of oncogenes, only a few have been found to be overexpressed and then ultimately lead to malignant transformation. o Growth Factors (ex. TGF α ) - Membrane associated oncogenes – one of the largest classes (we’ve already talked about them in the last lecture) o Growth Factor Receptors (GFR) – ex. EGFR is found mutated in a large number of breast cancers - Organelle associated oncogenes o Ex. Mitochondria related Bcl genes (involved in apoptosis). The mitochondria is associated with the apoptotic process so mutations in these related genes are of primary relevance.
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Lecture #4 – Thursday 4/10/09 - 2 - o Defects in apoptotic process can lead to malignant transformation. Bcl can end up being oncogenes if they prevent or interfere with apoptosis. -
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Lecture 4 - Lecture #4 Thursday 4/10/09 Last lecture was on...

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