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Biology 1002B Cycle 9 class 7
Biology for Science II (Biology 1002B)
The University of Western Ontario
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Normal Process: RTKs will bind to growth factors and send a signal transduction pathway, activating transcription factor to bind to the genome and activate expression to specific genes required for the growth of the cell - When cell and process is cancerous, cancer cells make it so that RTK sends signals down without binding to growth factors (typical cancer cells)
- Tumour suppressor genes: Genes that are normal in your cell
- Normally suppresses gene from becoming cancerous
- However, if gene gets mutated, it can no longer suppress other cells from becoming cancerous ⇒ cell becomes cancerous Without the tumour suppressor gene “suppressing” the genes, the cells grow uncontrollably
- Most common tumor suppressor gene = p53 (known as the guardian/father of the genome) and exists in the g1 and g2 checkpoint in the cell cycle
- P53 regulates the g1 checkpoint so that no mutated cells can duplicate P53 also plays big role in apoptosis ⇒ if it sees that there is a gene that could be oncogenic, it will induce apoptosis (will kill the oncogenic cell)
- P53 also plays role in cellular stress (DNA damage, activated oncogenes, hypoxia, ribonucleotide depletion, telomere erosion) and cellular responses (apoptosis, cell-cycle arrest, DNA repair, differentiation, senescence) P53 activates by translocating into the nucleus and binding to specific promoters and drives the transcription of various genes (p53 targets)
- The products of the genes (p53 targets) are responsible for the roles above in cellular responses Since p53 plays suge a huge role in preventing cells from becoming cancerous, 60% of all cancers result from the mutation of the p53 gene
In bottom right image ⇒ illustrates where mutations are in p - Most mutations are localized (occur) in the DNA binding domain ⇒ specifically used to bind to p - P53 also has a transcription-activated domain ⇒ what initially activates transcription of the gene
Cancer stem cells = red - Has many of the properties of a stem cell but it is cancerous (generates many oncogenetic cells but keeps self renewing) - One unique property is that the cancer stem cell is a slow dividing cell (stem cells in general divide slowly) while the other oncogenic cells surrounding the cancer cell divides rapidly Chemotherapy cannot get rid of cancer stem cells - Only removes rapidly dividing cells but cancer stem cells divides slowly - This is why cancer cells that can resist chemo exist
- Therefore, conventional (normal) cancer therapy (ex. chemo) often does not treat/remove cancer cells because it only removes the oncogenic cells surrounding the cancer stem cell ⇒ results in tumour relapse
- However, cancer stem cell specific targets the origin of cancerous cells (the cancer stem cell) and removing that will result in tumour regression
It has been discovered that Cancer Stem Cells exist in the brain, breast, colon, ovary, pancreas, prostate, melanoma, and multiple myeloma ⇒ more prone to resistance and relapse
Robert Weinberg took tumor mass from mouse and isolated the cancer stem cells from cancerous regular cells by observing markers of CD44+ and CD24- that each type of cell left - Isolated the cancer stem cell (200) and non-stem cell (20 000) and injected into two different mice - Results: the mice that got injected with the 200 cancer stem cell developed a tumor while the mice that got injected with 20 000 non-stem cancer cell did not develop a tumor
Conclusion: Cancer stem cells are the ones that cause tumour and cancer (not the non-stem cancer cells)
Biology 1002B Cycle 9 class 7
Course: Biology for Science II (Biology 1002B)
University: The University of Western Ontario
