- Disruptions to cell cycle or inability to carry out apoptosis can lead to cancer
Cancer Cells
- Cancer: unregulated/out of control cell division, results from genetic changes affecting genes whose proteins regulate the cell cycle
- Normal cells become cancer cells by the accumulation of mutations affecting proto-oncogenes and tumor-suppressor genes
- If gene mutates, protein product (often enzyme) changes which changes its function and causes improper regulation
- Abnormalities of cancer cells:
- Do not move through cell cycle in a regulated way; if stop dividing, only at random checkpoints
- Can divide forever with given nutrients
- Do not display anchorage dependence of density-dependence (divide past one layer)
- Evade signals that trigger apoptosis when something goes wrong
- Proto-oncogenes: normal version of genes that code for protein that stimulate cell growth (growth-stimulating)
- Oncogenes: dysfunctional, cancer-causing genes
- Transformation: When gene becomes oncogene
Causes for Oncogenes
- Gene Translocations: Chromosome broken and rejoined incorrectly; Errors may place gene close to control regions and then expression of wrong gene products can make cancer worse
- Gene Amplification: too many copies of gene → excess growth-stimulating proteins
- Epigenetic: abnormal chromatin condensation → proto-oncogene expressed at the wrong time or amount
- Point Mutations:
- In promoter, enhancer/control element → could increase expression → excess growth-stimulating proteins
- Within gene → could code for protein that is more/less to degradation
Tumors
- Cannot directly inherit cancer cuz need more than one oncogene but can be predisposed by being passed down a couple
- Major difference between the two tumors/cancers is a number of mutations
- Benign: ~5 mutations, generate mass, abnormal but NOT cancerous cuz do not spread→ stay at the original site due to specificity of structure
- Malignant: impairs the function of organ it’s in, cancerous ~7 mutations,
- Can metastasize: part breaks off, enters the bloodstream, divides and creates a tumour elsewhere in the body
- Release their own growth factors and cause blood vessels to grow towards it so it can nourish and spread
- Causes for changes in malignant tumours: excessive buildup, altered metabolism, cell surface changes, secrete sig. molecules
Treatments
- Radiation that harms localized tumours more than normal cells
- Chemotherapy: a toxin that kills all dividing cells by destroying spindle fibres that splits cell
GENES AND CANCER
- *Each cancer is caused by a different set of mutated genes, so there is no possible cure-all
Genetic Alterations and Cancer
- Tumor-suppressor genes: genes that can inhibit cell division and prevent cancer from developing (growth-inhibiting)
- Most mutated → stimulated cell division
- Protein products repair DNA, control adhesion, and regulate cell signalling pathways that inhibit cell cycle
- Defective version of a protein in an inhibitory pathway (p53) fails to act as a tumour-suppressor.
Interference with Normal Cell Signaling Pathways factor
With P53 Transcription Factor:
- Activated by signal transduction pathway when DNA is damaged from external factors and promotes transcription of cycle-inhibiting proteins
Without P53 Transcription Factor: 
- If gene mutates, damaged cells can proliferate and spread, becoming tumor
- Increased cell division
Ras gene:
- Gene that codes for G protein that relays growth factor message
When gene is mutated, causes ras protein to be overexpressed and cell cycle overstimulated 
