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    Liling Cassiopeia
    Cancer develops through a multi-step process as cells accumulate genetic mutations that disrupt normal cell growth controls. At least 5-6 critical mutations must occur for a cell to become cancerous, including mutations in proto-oncogenes that promote cell growth and tumor suppressor genes that inhibit growth. A primary tumor can metastasize by invading blood vessels, traveling through the bloodstream, and forming secondary tumors elsewhere. Key genes like p53, mutated in about 50% of cancers, normally induce DNA repair or apoptosis in damaged cells but defective versions allow damaged cells to continue dividing and increase cancer risk.

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    HFGHF

    Uploaded by

    Liling Cassiopeia
    230 views2 pages
    Cancer develops through a multi-step process as cells accumulate genetic mutations that disrupt normal cell growth controls. At least 5-6 critical mutations must occur for a cell to become cancerous, including mutations in proto-oncogenes that promote cell growth and tumor suppressor genes that inhibit growth. A primary tumor can metastasize by invading blood vessels, traveling through the bloodstream, and forming secondary tumors elsewhere. Key genes like p53, mutated in about 50% of cancers, normally induce DNA repair or apoptosis in damaged cells but defective versions allow damaged cells to continue dividing and increase cancer risk.

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    Cancer develops through a multi-step process as cells accumulate genetic mutations that disrupt normal cell growth controls. At least 5-6 critical mutations must occur for a cell to become cancerous, including mutations in proto-oncogenes that promote cell growth and tumor suppressor genes that inhibit growth. A primary tumor can metastasize by invading blood vessels, traveling through the bloodstream, and forming secondary tumors elsewhere. Key genes like p53, mutated in about 50% of cancers, normally induce DNA repair or apoptosis in damaged cells but defective versions allow damaged cells to continue dividing and increase cancer risk.

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    230 views2 pages

    HFGHF

    Uploaded by

    Liling Cassiopeia
    Cancer develops through a multi-step process as cells accumulate genetic mutations that disrupt normal cell growth controls. At least 5-6 critical mutations must occur for a cell to become cancerous, including mutations in proto-oncogenes that promote cell growth and tumor suppressor genes that inhibit growth. A primary tumor can metastasize by invading blood vessels, traveling through the bloodstream, and forming secondary tumors elsewhere. Key genes like p53, mutated in about 50% of cancers, normally induce DNA repair or apoptosis in damaged cells but defective versions allow damaged cells to continue dividing and increase cancer risk.

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    Cancer Summary

    (From Organisation and Control of Prokaryotic and Eukaryotic Genome)

    Tumorigenesis: Uncontrollable cell growth Malignant tumours: Invasive Metastatic - erodes normal surrounding tissue - can migrate to other parts of the body for clonal expansion

    Primary tumour metastasis secondary tumours Natural selection at work: fittest cancer cell survives Begins with genetic changes non-cancerous benign tumour malignant tumour Most cancers originate from a single aberrant cell e.g.: 1. 2. 3. 4. 5. 6. Cells grow as benign tumour in epithelium Break through basal lamina Invade capillary Adhere to vessel wall in liver Escape from blood vessel (extravasation) Proliferate

    Detailed Development: 1. Cell proliferation controlled at many checkpoints. All of these controls have to mutate to initiate cancer. 2. At least 5- 6 mutations in critical genes must take place before cell turns cancerous. 3. Combinations of such mutations much confer some growth advantage to the cell. E.g.: a. Become increasingly unresponsive to normal cell proliferation control b. Able to generate new blood vessels for nutrients 4. Multiplicity explains why cancer is relatively rare during an average human lifetime. 5. Cause of cancer are multifactorial: a. Environment b. Diet c. Lifestyles 6. Entire process from normal to cancerous cell can take 10-20 years. Critical Genes: Proto-oncogenes o Products promote cell growth o E.g.: Growth factor Growth factor receptor Growth signal transduction factors Page 1 of 2 summarised by aii

    Transcriptional factors

    o MUTATED form oncogenes Gain of function mutations Enhance cell function and thus tumorigenesis Via: Retroviral integration Missense mutation Gene amplification Chromosomal translocation

    Tumour Suppressor Genes o Products inhibit or slow down cell division Thus preventing cancerous growth

    o Loss of function mutations Leads to inactivity or decreased activity Thus promoting tumorigenesis

    o Mutations are usually recessive Both copies need to mutate or be deleted Since the other one that functions normally serves as backup

    o Classic example p53: Most commonly altered in human cancers About 50% of human cancers associated with defects in this gene Plays important when there is DNA damage: DNA cell repair Cell arrest Initiates apoptosis

    Defective p53 protein enables the propogation of cell cycle such that cell growth and division continues with the damage. The damaged DNA will replicate and risk of developing cancer cells is increased.

    Just remember: LOSS IN FUNCTION vs GAIN IN FUNCTION

    Page 2 of 2 summarised by aii

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