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Notes 10 30 09 (2)


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Notes 10 30 09 (2)

  1. 1. Notes 10-30-09 Loss of control of cell division -Proto-oncogenes: stimulate cell division by producing growth factors -oncogene: accelerator stuck, cannot be turned off. -proto-oncogene: normal gene found in cell who initiates division function -Tumor-suppressor genes: turn off cell division Discovery of oncogenes - Michael Bishop and Harold Varmus -1911 – virus that caused cancer in chickens -1978 – Michael Bishop and Harold Varmus discovered that this virus contained an altered version of a gene found in normal chicken cells (proto-oncogene) – incolved in cell division -cancer => genetic disorder due to accumulation of gene mutations -virus => package of genetic material surrounded by protein Types of Mutation -Produce a “hyperactive” protein—will not stop doing their job! -Multiple copies of the gene -Gene moved to a new locus and now under different controls Signal-transduction pathways -Ex. growth factor released when signal is received that a wound needs to be healed. Factor binds to signal protein, receptor protein changes shape, chain continues and produces signal. -Protein continues signal to divide when it is not appropriate to divide -ex. protein built in “on” position, signalling to divide -Different structural changes can cause these mutations Multiple genetic changes needed to produce a cancer cell -ex. first cell division gains 1 mutation -mutation copied, copies to both daughter cells -cell has two mutations, malformed genes copied again -repeat in copies causes sufficient genetic error enough to cause cancer cell Development of Colon Cancer 1) loss of tumour-suppressor gene APC (or other) small benign growth (polyp) forms 2) Activation of ras oncogene 3) Loss of tumour suppressor gene DCC Larger benign growth (adenoma) 4) loss of tumor-suppressor gene p53 5) additional mutations – malignant tumour (carcinoma)
  2. 2. Natural methods of protection -Limited life span -Senescence – cells can only divide so many times -Telomeres and telomerase Telomeres = caps on end of genes, destroyed slightly every time a cell divides [illustrated black]. Once telomeres are destroyed, cell usually dies. -In infancy telomerase adds bits to telomeres to continue replacing telomeres -in adulthood, telomerase does not exist . . . UNLESS you have cancer -Cancer cells produce telomerase continuously: immortality =telomere degenerates, telomerase replaces telomerase, and cells can reproduce an unlimited number of times. Hela cells => cells extracted from a cervical cancer patient, biopsied 60 years ago, still used in labs around the world today. Escape from programmed cell death -Death genes -“Apoptosis” – blebs -gene p53 – protein inhibits cell division but also prevents replication of damaged DNA – triggers cell death -MTS1 – regulates “survival gene C-myc”. C-myc turns off, cell dies -Make sure cell behaves properly, and if it is not, cell destructs itself. Apoptosis
  3. 3. Breakdown in cell adhesion -Cellular adhesion molecules (CAM) -Cancer cell secretes enzymes that break down this “glue” that holds neighbour cells together Causes of Cancer -Viruses -Human papilloma virus -Hepatitis B and C -Herpes viruses -Chemical carcinogens -Tobacco smoke -Oil, manufacturing waste -Radiation -Ultraviolet light -Radon gas Prevention of Cancer -Don’t smoke -Wear hats, long sleeves, sunscreen -Balanced, low fat diet -Lots of fruits and veggies -fiber dilutes contents of the digestive tract -binds carcinogens – spend less time in digestive tract -Antioxidants (?) – beta carotene, vitamins E and C