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Topics in Medical Biosciences > Cancer > Flashcards

Cancer Flashcards

1
Q

How many new cancer cases are there per annum?

A

300,000

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2
Q

What is the definition of a tumour?

A

The abnormal multiplication of cells

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3
Q

What is the difference between a Benign, Malignant and Metastatic tumour?

A

Benign - local multiplication of cells within a tissue
- no clinical impact
Malignant - tumour cells become “disorganised” and spread locally within a tissue
Metastatic - tumour cells escape from their host tissue and invade other organs

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4
Q

What is the Gleason grading of prostate tumours?

A

Looking at how disorganised the pathology is, and then grading how far along the cancer has gotten.

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5
Q

How do tumour cells regulate the behaviour of normal counterparts to create more of the tumour?

A

Through tumour angiogenesis

- tumour cells induce the growth and invasion of new blood vessels which infiltrate and oxygenate the tumour

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6
Q

What are the differences between normal and tumour cells?

A
  • requirement for growth factors
  • does not senesce
  • abnormal shape and requirement for attachment
  • invasive behaviour
  • genome instability
  • release agents which modify tumour environment
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7
Q

What are the 6 main things “hallmarks” that need to happen that turn a normal cell into a cancer cell?

A
  • evading apoptosis
  • self-sufficiency in growth signals
  • insensitivity to anti-growth signals
  • tissue invasion & metastasis
  • limitless replicate potential
  • sustained angiogenesis (formation of new blood vessels)
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8
Q

What Geographic variation is seen in cancer incidence and death rates?

A

Melanoma (skin cancer) country of highest risk is Australia but lowest is Japan.
- exposure to UVP in radiation cause for high incidence
For prostate cancer, the highest is the U.S but lowest is China.
- Prostate cancer is low in Osaka, but then the family is moved to Hawaii, rate increases.

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9
Q

How would you measure the efficacy of a cancer therapy?

A
  • elimination of tumour (no relapse)
  • prolongation of life span
  • relief of symptoms
  • reduction in cost of treatment
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10
Q

What are 3 approaches to cancer therapy?

A
  • Physical removal of the tumour
  • Drugs that kill the tumour
  • Drugs that modify the host response to the tumour
    through:
  • surgery
    -radiotherapy
    -chemotherapy
  • host modifiers
  • targeted therapeutics
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11
Q

What are some desirable features of an anti-cancer therapy?

A
  • effective
  • no impact on normal host cells
  • minimal toxicity
  • inability to develop resistance
  • easy to administer (no need for prolonged care with specialised doctors & nurses)
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12
Q

What are the benefits of surgery?

A
  • highly effective at reducing tumour mass
  • one time treatment
  • no possibility of resistance
    (breast cancer - lumpectomy)
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13
Q

What are the disadvantages of surgery?

A
  • tumour has to be surgically accessible
  • cannot treat metastatic disease
  • requires knowledge of the tumour
  • requires sophisticated facilities and expertise (Expensive)
  • potentially traumatic and dangerous
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14
Q

What are the benefits of radiotherapy?

A
  • effective at reducing tumour mass
  • is topologically precise
  • can treat tumours that cannot be surgically accessed
  • bulk reduction of the tumour
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15
Q

How does radiotherapy work?

A

Kills cells by irreversibly damaging DNA beyond repair

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16
Q

What are the disadvantages of radiotherapy?

A
  • significant host damage as it is not tumour specific, kills all cells
  • resistance can occur
  • limited effect on slowly dividing cells
  • requires expensive facilities
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17
Q

How does chemotherapy work?

A

use of compounds that kills cells that are rapidly dividing
- tumour responds by proliferating more of the cells that werent killed
- repeated treatment progressively kills the tumour growth fraction
(cisplatin)

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18
Q

What are the benefits of chemotherapy?

A
  • can be very effective in eliminating tumour mass
  • often used after surgery
  • is systemic in effect (drug connected to a drip so can go anywhere in the body needed)
  • cheap and easy to deliver
  • has palliative effect (patients have a better quality of life than before chemo)
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19
Q

What are the disadvantages of chemotherapy?

A
  • severe toxic effect on dividing host cells
  • does not eliminate slowly growing tumour cells
  • resistance to drug can occur
  • variable effectiveness between patients
20
Q

How do host cell modifiers work?

A

Target the host cell to:

  • stop supporting tumour growth (inhibit the growth of blood vessels)
  • kill the tumour (inducing the immune system to kill the tumour) (CART Therapy)
  • palliative effects (counteracting side effects such as pain, anemia)
21
Q

What are the disadvantages of host cell modifiers?

A
  • very expensive
  • delivery of effective dose to tissues is uncertain
  • host cell response can be toxic
  • variable responses in patients
  • counteracts effects of chemotherapy
22
Q

How do targeted therapeutics work?

A
  • identify specific molecular features of the tumour (e.g mutation)
  • inhibit the biochemical activity of the target molecule
  • exploits the hallmarks of cancer paradigm
  • personalised therapy based on tumour genotype
23
Q

Give examples of some targeted therapeutics.

A

Herceptin
- antibody that binds to the HER2 receptor in abnormal breast cancer cells
Gefitinib (Iressa)
- compounds that inhibits signalling via EGF receptors in non small cell lung cancers

24
Q

What are the disadvantages of targeted therapeutics ?

A
  • very expensive to develop and deliver
  • excellent responses in subset of patients but overall impacts are modest
  • acquisition of drug resistance
  • different tumour types differ in response to the same drug
25
Q

How can occupation influence cancer incidence?

A

Working at government occupation - more at risk of breast cancer than gen population
Tailor - incidence is lower than gen population

26
Q

What is the relationship between BMI and cancer incidence?

A

The higher the BMI, the higher the risk of kidney cancer and leukaemia but the lower the incidence for squamous cell carcinoma.

27
Q

How can cancer incidence be linked to exposing carcinogens?

A

If people are exposed to the carcinogen or chemical compound, more likely to develop a tumour

  • Mr Yamigawa painted area of rabbits with coal tar
  • rabbits developed tumours in the ears - inducting tumours through exposing compound
28
Q

What is the Ames test used for?

A

To test for mutagenic agents in everyday life

29
Q

Name some carcinogens

A

Tobacco, Asbestos, UV rays, Radon Gas

30
Q

How can a viral infection induce cancer?

A

Virus acts like an infectious agent. It has to interact in a certain way with the host cell including setting up conditions to replicate.
- immune system must be compromised, pre-requisites already existing

31
Q

What viruses can lead to cancer in humans

A

Epstein Barr Virus (EBV)
- EBV causes Glandular Fever
- predisposes you to Burkitt’s Lymphoma
- predominantly exits in sub-saharan africa
Human Papilloma Virus (HPV)
- extremely common, 6.2 milli new infections annually
- persistent HPV infections account for 100% of cervical cancers
- pre-requisite for cervical and head and neck cancer

32
Q

Name cancers that are inherited.

A
  • retinoblastoma
  • Li Fraumeni Syndrome
  • Cowden Syndrome
33
Q

What is Retinoblastoma?

A
  • tumour of the retina
  • rare
  • early onset
  • frequently multiple tumours
34
Q

What is Li Fraumeni Syndrome?

A
  • soft tissue tumours
  • very rare
  • early onset
  • frequently multiple tumours
35
Q

What is Cowden syndrome?

A
  • inherited hamartomas
  • affects breast, thyroid and endometrium
  • abnormal pigmentation and mental health
  • rare
36
Q

What is the two-hit hypothesis with inheriting mutant alleles?

A

Inherited one copy of the mutant gene and have 1 wild type copy of the gene
- Only need a single mutational event on the other wild type gene for the whole phenotype to appear as will be homozygous
For people with 2 wild -type copies (no inherited mutant copy) need 2 mutational events to occur for the phenotype to appear
- Leads to onset to be later in life rather than early as 2 mutations need to occur

37
Q

What is penetrance?

A

The proportion of individuals carrying a particular variant of a gene (allele or genotype) that also expresses an associated trait
- will depend on the exposure people are getting

38
Q

What is risk?

A

The probability that an individual will develop a tumour

39
Q

What populations is predisposed to breast cancer?

A

Jewish populations

- mutations in BRCA1 and BRCA2 genes

40
Q

How can we classify tumours?

A

By looking at the frequency of the copy numbers

- HER2 protein is expressed at much higher levels due to amplification of the gene copy number

41
Q

How could a translocation produce cancer?

A

Seen in blood cancers

  • bits of genetic info become merged together
  • The Philadelphia translocation produces a fusion protein BCR ABL which is an activated kinase that tells cells to proliferate
42
Q

What is the difference between driver and passenger mutations?

A

Driver mutations contribute to the growth and dissemination of the tumour. Passenger mutations are a result of the genome mutations but do not contribute to the growth of the tumour.

43
Q

What is the ratio of woman who get breast cancer?

A

1 in 8

44
Q

What is the triple assessment used to diagnose breast cancer?

A
  • assessed clinically
  • radiologically tested
  • needle biopsy to look at the pathology
45
Q

What is the prognostic factor?

A

any measurement available at the time of surgery that correlates with disease-free or overall survival in the absence of therapy. Able to correlate with the natural history of the disease.

46
Q

What is the predictive marker?

A

the measurement associated with response to a given therapy

Topics in Medical Biosciences (12 decks)

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