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
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2
Q

Normal cells to cancer cells

A
  1. Normal cell - undergoes multiple specific changes (known as mutations)
  2. Uncontrolled cell division
  3. Spread to surrounding and/or distant tissues
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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.
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4
Q

Where do mutations occur?

A

Occur in gene coding regions
○ Point mutation
○ Small insertions/ deletions

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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.
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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
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7
Q

State the 6 hallmarks of cancer

A
  1. Gains growth factor independence
  2. Insensitivity to growth inhibitors
  3. Proliferate without limit
  4. Avoids apoptosis
  5. Promotes angiogenesis
  6. Invade and metastasis
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8
Q
  1. 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
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9
Q
  1. Insensitivity to growth inhibitors
A

Alterations in cell cycle regulation:
- Loss of tumour suppressor genes (i.e. pRb)
- Upregulation of positive cell cycle regulators (i.e. CDC25 or cyclins)
- Cancer cells are able to bypass the normal mechanism that suppresses cell growth

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10
Q
  1. Proliferate without limit
A
  • Cancer cells can rebuild their telomeres using the enzyme telomerase.
  • Possess unlimited proliferative potential.
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11
Q
  1. Avoid apoptosis
A

Avoid programmed cell death

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12
Q
  1. Promote angiogenesis
A

Angiogenesis = formation of new blood vessels

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13
Q
  1. Invade and metastasize
A
  • Cancer cells can invade nearby tissues
  • Spread to other parts of the body
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14
Q

Priorities in dealing with cancer: PET

A
  • Prevention
  • Early detection
  • Total eradication

In most cases, these are unrealistic ideals

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15
Q

Hierarchy of aims in cancer management (4)

A
  1. Cure:
    eradicate tumour and metastasis
  2. Remission/mitigation:
    significant reduction in tumour load
    increased survival
  3. Symptomatic/pallation:
    treat secondary complications
    relief of symptoms
  4. Terminal care:
    improve QoL
    optimise symptom control
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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
Q

SE

A
  • Myelosuppression
  • Gastrointestinal tract and bladder (ulcers)
  • Fertility; teratogenic action
  • Skin and hair (alopecia)
  • N+V
26
Q

Aims of minimising SE of chemo

A

Decrease
- Discomfort
- Morbidity and mortality

Increase
- Tolerable dose threshold and thus the dose that can be used

27
Q

Ways to minimise SE

A

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
Q

Minimising SE of chemo that is nephrotoxic and bladder-toxic

A
  • 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
Q

What is mannitol

A
  • Diuretic
  • Often given after cancer chemotherapy that is nephrotoxic and bladder-toxic