cancer Flashcards
1
Q
cancer definition
A
uncontrollable division of abnormal cells in the body
2
Q
metastasis
A
the spread of cancer from an initial/primary site to a different/secondary site within the host’s body
3
Q
cancer grading vs staging
A
grading: a way to classify cancers depending on how abnormal the cells are in their structure and positioning
staging: a way to classify cancers depending on how far the tumour has spread
4
Q
benign tumours
A
- no metastasis
- retain function
- variable growth rate, often low
- normal cells
- ends in -oma
5
Q
malignant tumours
A
- metastasis
- lose function
- often slower growth rate
- abnormal cells
- usually ends in -carcinoma
6
Q
6 hallmarks of cancer
A
- resistance to anti-growth signals due to a mutation in TUMOR SUPPRESSOR genes
- induced ANGIOGENESIS (new blood vessels formed to provide the increasing number of cancer cells with oxygen)
- evasion of destruction by the body’s IMMUNE system defences which detect and remove foreign cells
- resistance to APOPTOSIS due to mutations in tumor suppressor genes
- activation of enzyme TELOMERASE which maintains the telomere section so that the cell senescence does not occur
- METASTASIS
7
Q
breast cancer risk factors
A
- age
- gender (women more at risk than men)
- obesity (adipose tissues are a major source of oestrogen production, high oestrogen levels are linked to breast cancer development)
- smoking
- family history (BRCA)
8
Q
BRCA 1/2 genes
A
- Tumor suppressor genes
- People who inherit harmful variants in one of these genes have increased risks of breast cancer, ovarian cancer, fallopian tube cancer
- BRCA1/2 genes are expressed in most cell types and tissues and are involved in a range of cellular regulatory pathways, including DNA‐damage response, cell‐cycle progression and regulation of gene transcription processes
9
Q
mRNA cancer vaccines
A
- biopsy taken and tumour sequenced to detect mutations
- personalised mRNA vaccines can be created according to the individual’s mutations
- mRNA codes for the abnormal protein produced by tumour cells which primes T cells to recognise these abnormal proteins
10
Q
CAR (chimeric antigen receptors) T cells
A
- reprogramming patients’ T cells against the malignancy
1. take patient’s blood and separate out the T cells
2. introduce gene that codes for CAR protein into the T cell
3. the CAR T cell can recognise tumour cells using the best portion of an antibody from a B cell whilst deploying the ability of T cell to eradicate the cancer cell
4. CAR T cells multiply in lab and patient is given a low dose of chemotherapy (conditioning) before large numbers are infused into patient’s blood to prevent immediate rejection
5. CAR T cells can detect tumour cells and multiply further to kill these cells - In 2019, NICE formally recommended the use of CAR T cell therapy for patients with some forms of leukaemia and lymphoma that have failed to response to conventional treatments
- However, this therapy extremely costly (up to £1 million)
11
Q
Anti-PDL1
A
- While PDL1 is expressed on healthy tissues, cancercells over-express this ligand -> when T cells interact with a cancer cell,they are overwhelmingly suppressed by the PD1-PDL1 interaction
- a monoclonal antibody therapy binds to PDL1, blocking the interaction with PD1 on T cells -> enhanced immune-mediated killing of the tumour
- this immunotherapy has moved into clinical trials, where it has been particularly effective in forms of malignant melanoma
- Side effects: PD1 is found on all T cells so all T cells will be overactive -> more chance of autoimmune diseases or inflammatory responses
12
Q
oncolytic viruses
A
- T-VEC contains a live herpes simplex virus with 2 genes removed so it can be destroyed by healthy cells but not be cancerous cells (as they have compromised infection defences)
- When the cancer cells burst after viral infiltration, the debris triggers the immune system to detect the malignant tumour and start destroying it
- The side effects of T-VEC are far milder than those of chemotherapy drugs, with patients only experiencing mild flu-like symptoms
- NICE has now approved the use of T-VEC on metastatic melanoma in adults when surgery and other immunotherapies are not suitable
13
Q
will we ever find a cure?
A
- At a biological level, it seems that cancer is an inevability because of the high likelihood of distortion of cell growth and regulation as age increases
- Clinically, because of treatments and our ability to prevent at an early stage it could be possible to find a cure in the sense that people aren’t dying of cancer and are less affected
- So, I think it is possible to find a way to live with cancer and it not having serious consequences to our health but due to the biological nature of it I don’t think it can be necessarily eradicated from existence
14
Q
two-hit hypothesis
A
- tumour suppressor genes may undergo a variety of mutations; however, most loss-of-function mutations that occur in tumour suppressor genes are recessive
- therefore in order for a particular cell to become cancerous, both of the cell’s tumour suppressor genes must be mutated
- e.g. people with one mutated BRCA gene do not have cancer because that requires 2 mutated alleles but they would be more likely to get cancer than someone with 2 normal copies as they only need 1 more mutation to have 2 mutated alleles
- proposed by geneticist Alfred Knudson in 1971
15
Q
immune checkpoints - restraining Tc cells
A
- CTLA4 is found on regulatory T cells and inhibits T cell activation and proliferation
- CTLA4 binds to CD80 and CD86 and removes them from dendritic cell surfaces->prevents naive Tc cell activation in the lymph node as it prevents signals being sent into the T cell via CD28
- PD1 (programmed cell death 1) on activated Tc cells binds to proteins called PD-L1 or PD-L2 that can be produced on cells in infected/damaged tissues
- Once bound to PD-L1 or PD-L2, PD1 sends inhibitory signals into activated Tc cells that stop them killing their target cells
- cancer cells can use these methods to avoid Tc cells
