Cancer Recap Flashcards
1
Q
What is cancer
A
- Collection of diseases with shared features of uncontrolled cell division and invasion
- Can affect almost any organ/cell type
- Outcomes vary significantly - treatable to untreatable
- Different therapeutic approaches
2
Q
Normal cells to cancer cells
A
- Normal cell - undergoes multiple specific changes (known as mutations)
- Uncontrolled cell division
- Spread to surrounding and/or distant tissues
3
Q
Is a single mutation enough to cause cancer?
A
- A single mutation leading to a single acquired property such as increased proliferation is not enough to lead to cancer.
- A single cell has to be able to acquire (usually after multiple mutations) most or all of the hallmarks in order to progress to cancer.
4
Q
Where do mutations occur?
A
Occur in gene coding regions
○ Point mutation
○ Small insertions/ deletions
5
Q
Why do mutations occur?
A
- Alterations in transcription/splicing.
- Amplifications/deletions of chromosomal regions.
- Chromosomal translocations.
- Gains and losses of whole chromosomes.
- Changes in DNA modification e.g. DNA methylation.
6
Q
Risk factors for Cancer
A
- Lifestyle influences cancer progression
- UV and other radiation
- Viruses
- Chemicals: Smoking, Asbestos, Food
- Copying/repair errors: inherited susceptibility
7
Q
State the 6 hallmarks of cancer
A
- Gains growth factor independence
- Insensitivity to growth inhibitors
- Proliferate without limit
- Avoids apoptosis
- Promotes angiogenesis
- Invade and metastasis
8
Q
- Gains growth factor independence
A
- Don’t require growth factors to stimulate cell division
- e.g. they gain an oncogene.
- Cancer cells are able to grow and divide uncontrollably
9
Q
- Insensitivity to growth inhibitors
A
- Alterations in cell cycle regulation
- Cancer cells are able to bypass the normal mechanism that suppresses cell growth
10
Q
- Proliferate without limit
A
- Cancer cells can rebuild their telomeres using the enzyme telomerase.
- Possess unlimited proliferative potential.
11
Q
- Avoid apoptosis
A
Avoid programmed cell death
12
Q
- Promote angiogenesis
A
Angiogenesis = formation of new blood vessels
13
Q
- Invade and metastasize
A
- Cancer cells can invade nearby tissues
- Spread to other parts of the body
14
Q
Priorities in dealing with cancer: PET
A
- Prevention
- Early detection
- Total eradication
In most cases, these are unrealistic ideals
15
Q
Hierarchy of aims in cancer management (4)
A
- Cure:
eradicate tumour and metastasis - Remission/mitigation:
significant reduction in tumour load
increased survival - Symptomatic/pallation:
treat secondary complications
relief of symptoms - Terminal care:
improve QoL
optimise symptom control
16
Q
Modes of therapy - surgery
A
- For well-defined solid tumours
- In non-vital regions (e.g. mastectomy)
- Non-mutilating result
- Resection/reconstruction possible (e.g. gut)
17
Q
Modes of therapy - radiotherapy
A
- For diffuse but localised tumours (e.g. lymphoma)
- Vital organ/region (e.g. head and neck, CNS)
- Adjuvant therapy (e.g. post mastectomy)
- Palliation
18
Q
Modes of therapy - chemotherapy
A
- Adjuvant therapy following surgery or radiotherapy
- Neo-adjuvant therapy prior to surgery or radiotherapy
- Widely disseminated/metastasized
- Diffuse tumour e.g. leukaemia
- Palliation
- Some primary tumours (e.g. Hodgkin’s lymphoma)
19
Q
Rationale of chemotherapy
A
- Need to recognise features of tumour growth to understand the rationale of cytotoxic chemotherapy
- e.g. cell cycle time, growth fraction, number of cells - improtant for determining growth of tumour
- By the time tumours are clinically apparent, most are in the relatively slow phase of growth - chemo less likely to be effective
20
Q
When are tumours clinically apparent
A
~10^9 cells or more
21
Q
Chemotherapy combination
A
- Chemotherapeutic agents used in combo rather than single
- Should have minimal overlap in toxicity
- Treatment should be delivered on intermittent basis with shortest possible time between treatments
- Allow recovery of the most sensitive normal tissue
22
Q
Advantages of combo chemo
A
- More aggressive = Treatment remission
- multiple MoA = increased remission
- Note: also increased side effects
23
Q
Combined vs single agent therapy
A
New targeted treatment options
- e.g. tyrosine kinase inhibitors & mabs
- reignite competition over combination vs single agent
24
Q
Why are there SE to chemotherapy
A
- Cancer cells are rapidly dividing
- Chemotherapy drugs target rapidly dividing cells
- Most chemotherapy drugs are non-selective for cancer cells
- SE caused by impact of chemo on normal cells
25
SE
- Myelosuppression
- Gastrointestinal tract and bladder (ulcers)
- Fertility; teratogenic action
- Skin and hair (alopecia)
- N+V
26
Aims of minimising SE of chemo
Decrease
- Discomfort
- Morbidity and mortality
Increase
- Tolerable dose threshold and thus the dose that can be used
27
Ways to minimise SE
Close monitoring
- FBC
Prevention used wherever possible
- Allowing for bone marrow recovery between treatments
- Administering stem cell GFs with chemotherapy to selectively enhance marrow proliferation
28
Minimising SE of chemo that is nephrotoxic and bladder-toxic
* Forced diuresis is routinely given with these types of drugs
* This will reduce contact time and urine concentration
* Involved modest over hydration before therapy followed by a diuretic to maintain high urine output for at least 24 hours after therapy
29
What is mannitol
* Diuretic
* Often given after cancer chemotherapy that is nephrotoxic and bladder-toxic
