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Cancer I & II

QuestionAnswer
Define metastasis the development of secondary malignant growths at a distance from primary cancer site.
What are some basic causes of Genetic changes? Mutations, abnormalities e.g. translocations, introduction of genes by virus (which can express new proteins or alter the function of existing proteins).
How are cancers classified? based on tissue of origin.
Where are Retinoblastomas and Glioblastomas found? NS
Why is cancer associated with old age? Mostly: most cancers require several mutations to accumulate - takes years. Also: ageing reduces telomere length which increases the chance of fusions and chromosomal instability, AND: ageing reduces ability to deal with DNA damage/errors.
How might we be abel to reverse ageing and why? feed NAD+, moleculeS promotes DNA damage repair.
What are the hallmarks of cancer? Sustaining proliferative signalling, evading growth suppressors, activating invasion and metastasis, enabling replicative immortality, inducing angiogenesis, resisting cell death.
Steps of metastasis: (1) cells grow as benign tumour in epithelium (2) cells become invasive and enter capillary (3) adhere to blood vessel wall in liver (4) escape from blood vessel to form micrometastasis (5) colonise liver forming full metastasis.
what does the transition from normal cell to cancerous cell involve? multiple accumulated mutations.
define oncogene: a gene that when mutated or expressed at high levels, helps turn a normal cell into a cancer cell.
define proto-oncogene: the normal form of the gene - typically involved in processes that promote cell proliferation, growth or motility/invasiveness.
examples of proto-oncogenes: Ras, Myc, P13K, Twist
define tumour suppressor gene: gene that acts to prevent a normal cell from becoming a cancer cell.
How do TSGs work? limiting cell proliferation, promoting apoptosis, and senescence or preventing metastasis.
How does Burkitt's lymphoma come about? chromosome rearrangement - translocation - to a region of high transcriptional activity.
What is the clinical significance of Burkitt's lymphoma appears ass cancer of lymphatic system involving over-proliferation of B lymphocytes.
What is Myc? a transcription factor that can promote cell growth and proliferation by controlling expresison of target genes in response to many signalling pathways.
How does CML present? cancer in which marrow produced too many granulocytes (type of white blood cell). Leads to increased infection, anemia, easy bleeding.
What is CML caused by? reciprocal chromosomal translocation b/w 9 and 22.
what does the Bcr-Abl fusion protein do? it oligomerises through the BCR coiled-coil domain and undergoes auto-activation of ABL tyrosine kinase domain --> mis-regulation of cellular signaling pathway that it mediates.
How do most breast cancers get activated? Gene amplification in which a normal protein is overproduced (ErbB2).
How are most thyroid and bladder cancers activated? Deletion or point mutation in coding sequence - Mutant G12V H-Ras is a constitutively active protein.
What are 2 key TSGs? Retinoblastoma protein - Rb (regulates cell cycle) and p53 (regulates cell cycle, DNA repair, apoptosis).
From where do rb tumors develop? from neural progenitor cells in immature retina.
Why would people only develop tumours in one eye? nonhereditary retinoblastoma is extremely rare, require two successive hits to Rb gene and typically only produces a tumour in one eye.
Which is the most important TSGs in human cancers? p53
Why is p53 called the guardian of the genome? involved in almost every aspect of tumour suppression.
Where would you find homozygous loss of p53? in lots of carcinomas. Mutated form is also involved in leukaemias, lymphomas, sarcomas, neurogenic tumours.
What is Li-Fraumeni syndrome? cancer predisposition syndrome where the molecular basis is a loss-of-function germline mutation in p53 gene.
What can post-translational modifications do to p53? affect stability of p53, bind other proteins to p53, affect p53's function as a transcriptional factor.
How are levels of p53 kept low in cells? through action of ubiquitin ligase, Mdm2.
How does p53 actually control these cell processes? by turning on other genes.
What transcriptional factor is expressed in metastatic cell lines? How do we know? TWIST. Knockdown mouse experienced no metastasis.
What does TWIST promote? invasiveness and metastasis, drives EMT in Metastasis and predicts poorer survival of the cancer.
What role does Snail play in all this? twist upregulates snail, which represses E-cadherin, which is a cell-cell adhesion molecule in epithelial cells
What other genes does twist affect? cells stop expressing e-cadherin and beta-catenin, and start expressing mesenchymal genes like the intermediate filament protein, vimentin.
Where is e-cadherin strongly expressed? in breast epithelial cells. It's a strong TSG.
What is APC? a TSG. LOH causes polyps - tumour growth on colon wall - caused by overactivation of the Wnt pathway.
What is Ras? K-Ras is small GTPase, part of the MAP kinase pathway. Activation leads to increased expression of Myc.
Why can cancers be thought of as being in competition? A tumour is genetically heterogenous i.e. made up of cells with different mutations, and this genetic makeup evolves over time.
Why does genetic variation promote cancer? Variation provides raw material that allows cancer cells to evolve, survive and proliferate - cancers often acquire mutations that are involved in DNA damage response (increased mutation rate). Cancer cells become resistant to chemo = relapse.
What does Imatinib inhibit? BCR-ABL oncogenic kinase. Occupies the ATP-binding pocket of kinase domain.
What's the situation with melanomas and drugs? Melanoma caused by constitutively active form of RAF kinase, meaning MAP kinase pathway always ON. BRAF inhibitor drugs work, but resistance occurs = relapse and death.
Created by: lmdavis97
 

 



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