Cancer Flashcards
(17 cards)
Compare normal cells and cancer cells
Growth factors
N: require external growth factors to divide
C: divide without growth factors
Contact inhibition:
N: cell division cease upon contact with other cells
C: continue to grow afterr contact wth other cells
No.of cell division
N: cell age and die via apoptosis
C: telomerase activated hence have unlimited no. of cell division without triggering apoptosis
Cell damage
N: cease to divide
C: continue to divide and accumulate damages
What is tumour suppressor gene and its function
Gene codes for proteins that send appropriate signals to prevents cell division and lead to cell death
Function:
- halt cell cycle
- carry our DNA repair
- trigger apoptosis
Decscribe the mutation of TSG that leads to cancer
Loss of function mutation
TSG no longer able to inhibit cell growth
Is loss of fucntion mutation of TSG recessive or dominant
Recessive
Describe the p53 anti cancer mechanism
- Activates DNA repair proteins
- holds cell cycle at G1 checkpoint allowing DNA repair proteins to have time to fi damage before continuing the cell cycle
- induce apoptosis
What is an proto-oncogene and its function
Proto-oncogenes code for proteins that send signals to nucleus to stimulate cell division
What is an oncogene
Oncogene is derived from the gain in functio mutation of a proto-oncogene leading to overstimulation of cell division
Is the gain fucntion mutation of proto-oncogene dominant or recessive
Dominant
How does gain in function mutation come about
Chromosomal rearrangement: bracing and rejoining of DNA
- change in protein coding region : hyper active fusion protein
- change in control region: overproduction of normal protein
Gene amplification: error in DNA relplication prodcung extra copies of genes
- overproduction of normal protein
Insertional mutagenesis: insertion of retrovirus, integrate into DNA at region nearproto-oncogene, hence gene is under control of rhetorical promoter sequence which is unresponsive to signals
- overproduction of normal protein
Point mutation
- in coding region: hyperactive protein
- in control region: overproduction of normal protein
Describe the effect of mutated RAS gene
Codes for G-protein involved in cell signalling
Mutated gene, lead to translation into new sequenc of amino acids causing change in 3D configuration of RAS protein.
RAS protein loses ability to hydrolyse GTP to GDP causing protein to by hyperactive and continue delivering signals fo celll growth leading to to uncontrolled cell division
Describe how dysregulation of checkpoints in cell division may lead to cancer
- Cells allowed to proceed in cell cycle eve when conditions in G1, G2 and M checkpoints are not met
- Allows accumulation of mutation resulting in ucnontrolled celll division, forming tumours and may lead to cancer
Outline the steps in cancer development
- Mutated cells have slight growth advantge ver normal cells
- DNA damages are passed on to all daughter cells from mutated cell
- Daughter cells may suffer another mutation in another cell regulatory gene
- Line of clones have higher rate of mitosis, increasing chance of further DNA damages
- When so many mutation have accumulated, growth of cell become completely unregulated resulteing in uncontrolled proliferation of cells
Outline the development of malignant tumour
1.Initial tumour lack ability to spread to other tissues
2. Further mutations causing metastasis where tumor invades normal tissues, migrant to other parts of the body, penetrate blood vessels and proliferate at another site
3. Further mutations induce angiogenesis where new blood vessels form to supply nutrients and oxygen to growing tumour
What are the internal factors which increases chances of cancerous growth
Loss of immunity
- cytotoxic T cells rid cells infected by virus and cells hat transformed by cancer but not yet able to evade immune system
Genetic factor
- born with one defective copy of tumour suppressor gene inherited by parents
Explain why individuals who inherit mutations trend to develop breatsc cancer at younger age
- Development of cancer require accumulation of mutations in at least a proto-oncogene and several tumour suppressor gene
- When individuals already have inherited gene mutation , less time is required for cell to become cancerous
- Cell with mutations are uanleto carry out DNA repair hence continue to divide and accumulate mutations increasing rate of cancer development
What is require for cancer development
Gain in function of at least 1 proto-oncogene and
Loss in fucntion of several TSG
External factors which may increase changes of cancerous growth
Chemical carcinogens
- damage or alter DNA
UV ad ionising radiation
- causes DNA bass top be more reactive
