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Cell Cycle Reg. & Cancer Chapter 1212.3 Pt. 2 AND 18.5 (pgs. 373-377) Objective: I can describe and explain how a disruption in the regulation of the cell.

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Presentation on theme: "Cell Cycle Reg. & Cancer Chapter 1212.3 Pt. 2 AND 18.5 (pgs. 373-377) Objective: I can describe and explain how a disruption in the regulation of the cell."— Presentation transcript:

1 Cell Cycle Reg. & Cancer Chapter 1212.3 Pt. 2 AND 18.5 (pgs. 373-377) Objective: I can describe and explain how a disruption in the regulation of the cell cycle and mitosis leads to cancer, as well as being able to offer a possible cure based on the signal transduction pathway

2 Cancer A growth disorder of cells: when cell regulation (checkpoints) not functioning, so cells grow and divide uncontrollably  Creates a mass of cells called tumor Benign tumors are contained (won’t spread)  can still grow large

3 Cancer (cont’d) Malignant tumors will spread – cancer cells will break off tumor and travel through blood stream to start tumor elsewhere  “Spreading cells” = metastases state = metastasis

4 Why is cancer bad? Tumor growth can put physical pressure on other important organs, etc. Cancer cells still need oxygen, glucose, blood, etc. to live  Will send out signals to make blood vessels feed “useless” cancer cells  Good cells die  You die

5 Causes of Cancer Chemicals (tobacco), radiation (UV rays) Damage/change DNA: mutation If specific damaged gene controls cell cycle (protein at checkpoint), may result in cancer  Proto-oncogenes: stimulate cell division If mutated to work too much, turn into oncogenes (divide excessively)  Tumor-suppressor genes: stop division If mutated to be non-functional, cell divides without control

6 Causes of Cancer (example) p53 = tumor-suppressor gene  if p53 mutated, p53 protein won’t function Won’t stop division if DNA bad  Allow cell to make more cells with same mutated DNA that will make more cells! = CANCER So, what type of gene?

7 Causes of Cancer (summary) Cancer can result from damaging any gene (and protein made from gene) that helps regulate cell division Think checkpoints, regulation molecules, and signals (more in ch. 19)

8 Curing Cancer Conventional treatments:  Surgery (remove tumor) – hard to remove ALL mestases (every little single cell)  Chemotherapy/Radiation – to kill cancer cells (but will also kill good cells) Newer treatments  Focus on fixing the gene or protein that was damaged/mutated that resulted in cancer Different cancers damage diff. genes

9 Normal cells are set to die After each division, telomeres get shorter (details in DNA)  helps cause aging  At some point, chromosome too short for cell to function  cell dies Telomerase = enzyme to repair telomere Telomerase An example of application (new scenario + cure)

10 Normal cells are set to die (cont’d) A gene will switch on after certain # of divisions to inhibit telomerase (via another protein), allowing cell to die If this gene mutated, telomerase runs wild, cells continue to live  CANCER  What type of gene is it? Tumor-supressor Cure for THIS type of cancer  Inject something that inhibits telomerase

11 Another Example Scenario Growth factor = protein that stimulates cell division (example: VEGF – make more blood vessels)  Good, when need to… grow body or replace cells (damage, etc.)  Bad if too much growth factor is made (too much VEGF = cancer) OR…  If receptor is mutated so that it signals cell division even without growth factor  Proto-oncogene…cure?


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