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31 Cards in this Set
- Front
- Back
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Why do mutations in DNA arise? |
1) inherited predisposition eg.BRCA1 2) Chemical agents eg. Tobacco 3)Radiation eg. Radon gas 4) Infections eg. HPV 5)Inflammation eg. Colon cancer 6) Chance eg. cell division or oxidative stress |
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Which cell types are cancers made up of? |
Cancer Stem Cell Cancer Cell Immune inflamatory cells invasive cancer cell pericyte Endothelial cell Cancer associated fibroblast |
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What is an oncogene? |
Cancer inducing gene, that can transform cells |
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What is a tumour supressor |
A gene whose inactivation leads to an increased likelihood of a cancer developing Constrains cell proliferation (gatekeeper) Maintains genomic integrity - making sure DNA is not changed(care taker) |
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Outline the process of transformation of a piece of DNA to a cancer gene |
1) Normal epithelium - loss of APC tumour supressor gene 2) Hyperplastic Epithelium - DNA hypomethylation 3) stages of adenomas - activation of K ras, loss of 18q TSG - loss of p53 4) carcinoma 5)invasion and metastasis |
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What does APC stand for? What does TSG stand for? |
Adenomatous plyposis coli tumour suppressor involved in WNT signalling and cell division TSG - tumour suppressor gene |
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How does normal epithelium change into hyperplastic epithelium? |
Loss of adenomatous polyposis coli tumour suppressor (tumour suppressor) changes normal epithelium more proliferated epithelium |
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How does hyperplastic epithelium change into early adenomas? (Benign cancer in gland) |
DNA hypomethylation |
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How is an early adenoma changed into a intermediate adenoma and then a late adenoma? |
Activation of k ras and loss of 18q TSG |
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How is a late adenoma changed into a carcinoma? |
Loss of p53 (tumour suppressor) |
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What can cause variations in speed of onset of cancer? |
Different oncogenes and tumour surpressors being activated |
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Which 2 cell types lead to breast cancer |
Basal cells and Luminal Cells |
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What are the 8 characteristics a cell needs to be considered malignant cancerous |
1) Avoiding immune destruction 2) Preventing shortening of teleomeres 3) Allowing cancer to spread by metastasis 4) Resisting cell death (Hayflick limit) 5) Creating a new blood supply from old blood vessels 6) Lifting regulation on cell energy distribution 7) Continuing signals for proliferation cascade 8) Allowing a cell to continually divide. |
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Challenges faced by curing cancer? |
Killing cells is easy hard to target cancer cells |
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What are the features of new cancer drugs |
Targeting specific proteins that are only present in cancer cells
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DNA binding drugs |
eg. Alkylating agents and Platinums Cause direct DNA damage block DNA replication |
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Antimetabolites |
eg Purine/Pyramidine analogs Anti folates Interfere with synthesis of nucleotides Can be incorporated into DNA Block DNA replication |
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Topoisomeraseinhibitors |
eg, Topotecan, Etoposide Block action of enzymes involved in DNA Winding/Unwinding of DNA Causes DNA strands to break |
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Tubulin acting drugs |
eg. Vinca alkaloids Inhibit microtubule formation Block chromatid separation to daughter cells
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Tubulin acting drugs TAXANES |
Promote microtubule formation BLock separation of chromatids to daughter cells |
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What are the 4 classes of cytotoxins? |
Tubulin acting drugs, Antimetabolites Topisomeraseinhibitors DNA binding drugs |
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Which cancers are curable by chemotherapy |
Testicular, Ovarian, Ovarian germ cell, High grade NHL, Hodgkin lymphoma, |
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What are the prognostic factors of breast cancer |
Tumour size Number of positive axillary nodes Lymphatic and vascular invasion Histologic tumour type and grade Hormone receptors : Oestrogen and progesterone receptors ERBB2 HER2 overexpression |
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What are the steps for local control of breast cancer |
Surgery radiotherapy aesthetics and reconstruction
90% of women live for more than 5 years |
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If breast cancer metastisies |
It is no longer curable but symptoms may be managed
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What are molecular targets?
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Specific molecules involved in tumour growth which these drugs try to target |
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What can be achieved by activating EGFR receptors |
Migration, cell survival, adhesion, angiogenesis (makng a new blood supply from an old one) |
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What receptor is overexpressed in cancers? |
EGFR |
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What factors can arrest cancer growth |
Blockage of ECFR or ERBB2 (HER2) receptors |
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What is the change that takes place in the ECFR receptor in a normal and mutated gene |
Normal - ligand is required to fire action potential Mutated - Ligand not required |
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Ras in the cell is found in 2 states (off/on) how does it cycle between these 2 states |
Ras GDP is off Ras GTP is on addition of a phosphate molecule switches gene on, loss switches it off.
When Ras GTP is activated this means it can cause a conformational change which means it can interact with other proteins
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