Cancer Flashcards
Why must exactly half of the progeny of a stem cell must stay as a stem cell?
LESS
- Regenerative capacity of the tissue is compromised
MORE
- Cancer?
What is hypertrophy?
Increase in cell size
What is hyperplasia?
Increase in cell NUMBER
When does hyperplasia occur?
- In tissues that can divide
- In tissues with abundant stem cells
What is metaplasia?
- Change in cell differentiation
- Replacement of one MATURE cell type with another MATURE cell type
- Altered differentiation of stem cell
What is dysplasia?
- Changed in cell differentiation
- Replacement of one MATURE cell type with a LESS MATURE cell type
- Disordered
What are the reversible abnormal cellular growth and why?
- Hypertrophy
- Hyperplasia
- Metaplasia
- Dysplasia
Reversible because they are a result of a STIMULUS
What is an irreversible abnormal cellular growth and why?
Neoplasia (resulting from metaplasia –> dysplasia –> neoplasia)
Is a result of an autonomous factor (mutations)
What is cancer?
1) Uncontrolled cell proliferation (eg. mitosis)
2) Aberrant differentitation
- Usually balances with proliferation
3) Uncontrolled cell interaction (invasion and metastasis)
- Not in situ
- Can invade other tissues
4) Cancer cell host interactions
What are 4 cancer cell host interactions?
1) Angiogenesis
- Tumour cells need blood supply
- Hormone dependency
- Hormone production
- Immune response
Tumours are ‘foreign’
What are benign tumours?
- Confined
- Well defined structures
What are the stages in malignant tumour formation?
1) Dysplasia
2) Anaplasia (severe dysplasia)
3) Invasion
4) Metastasis
How do spread (metastasis)?
- Break through the basement membrane
- Into the blood vessels
- Travel to a distant site in the blood vessel
- Fuse with the vessel wall, through the vessel wall
- Colonise distant sites
What are the 4 carcinogenic factors that cause cancer?
1) Chemical
- Smoking
2) Parasites
3) Radiation
- UV
- Ionising radiation
4) Viruses
- insert into the genome
What are the genetic causes of cancer?
- Loss of function in tumor suppressor genes (recessive)
- Gain of function of oncogenes (dominant)
- Need MULTIPLE mutations to initiate neoplasia
Examples of tumor suppressor genes?
Rb
p53
Examples of oncogenes?
myc
ras
abl
What does the stochastic model suggest about cancer?
- Cells have unlimited proliferative capacity
- ALL the cells of a tumour are tumour-initiating so therefore ALL cells can be targets for anti-cancer treatments
- Mutating cells transform growth
- Heterogeneity of cellular composition is limited
What are the problems with the stochastic model?
1) Tumours when treated can recur
2) Tumours are heterogeneous in cellular composition
What do tumours contain?
- Lots of differentiated cells
- High degrees of heterogeneity
In a tumour, where does heterogeneity extend to?
- Differentiation rates
- Proliferation rates
- Migratory and invasive capacity
- Size
- Therapeutic response
What do functional assays show about cancer cells?
- Only a small subset of cancer cells are capable of extensive proliferation
- Only some populations of cells in a tumor can reform tumours in secondary transplantation assays
- Implying there is a hierarchy in a tumours tissue architecture
(only SOME cells are tumour initiating)
What are the implications of tumour heterogeneity?
1) Not every cell in a tumour is the same
- Hard to treat
2) Only some cells n give rise to cells with higher proliferative targets
3) Only SOME cells appear capable of re-initiating the tumours
When treating tumours, what cells do we want to target mostly?
The ‘dormant’ cells which are not highly proliferative but give rise to the highly proliferative cells
