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. 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. 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