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eBMS2021 > TOPIC F: Cancer > Flashcards

TOPIC F: Cancer Flashcards

1
Q

What are the physical characteristics of a cancer cell compared to a normal cell

A 
Enlarged nucleus
Changes to cytoskeleton
Loss of specialised features
Little cytoplasm
Evidence of mitosis

No growth constraints (not limited by neighbouring cells or environment)
No physical attachment

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2
Q

What is a carcinoma

A

A cancer arising from epithelial cells of the skin and lining of organs

85% of all cancers

breast, lung, colon cancers

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3
Q

What is a sarcoma

A

Cancers arising from bone, muscle and blood vessels

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4
Q

What is a Lymphoma

A

Cancer arising from lymphoid cells and leukemias from white cells of the bone marrow

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5
Q

Do cancer cells require growth factors

A

No, can have greatly reduced requirement for growth factors

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6
Q

What is the relationship between cancer cells and telomeres

A

Cancer cells have chromosomal aberrations

  • change in no. of chromosomes
  • change in chromosome structure

Telomere shortening regulates how many round of cell division can occur. Cancer cells can ignore telomere shortening and keep dividing

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7
Q

What are the basic transitions of cancer progression

A

A single mutant cell

to a tumour

to metastasis (cancer spreads throughout body)

At least 4-6 mutations to reach the tumour state. process can decades for single mutant cell to proliferate into palpable tumour

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8
Q

What are the 2 types of tumours

A

Benign: look like original tissues. Localised (do not spread). Don’t cause problems unless in confined space (like brain)

Malignant: Do not look like original tissue. Physical changes, spread

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9
Q

Explain metastasis

A

When cancers invade other issues and spread throughout body.

Depends on type of cancer

Takes a lot of energy to proliferate and spread so angiogenesis occurs

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10
Q

Explain angiogenesis

A

The mechanism where tumours direct capillaries to travel into the tumour so it can have nutrients and oxygen for growth.

Angiogenesis can be targeted to stop cancer from growing

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11
Q

What are some of the implications of cancer genetic alteration

A

Increased cell growth

Resistance to apoptosis

Altered tissue invasiveness

Angiogenic proliferation

Ability to escape immune surveillance

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12
Q

What are 2 main causes of cancer

A

DNA damage

Viruses

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13
Q

Explain the types of DNA damage that can lead to cancer

A

Inherited (germ lime errors): every cell in body carries one copy of DNA with defect. 10% of cancers

Acquired (somatic errors): may lead to cancer in that tissue. only cancer cells carry mutation

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14
Q

How can acquired DNA damage leading to cancer be caused

A

Environmental exposure to:

radiation

viruses

bacteria

chemical carcinogenesis

age and diet

UV light

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15
Q

Cancer cells accumulate more and more errors over time. Why does this occur?

A

Ususally DNA repair enzymes can correct but

  • substantial mutations
  • loss of DNA repair enzymes
  • less time for repair mechanism (rapid cell cycle to divide)

can lead to further DNA damage

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16
Q

Explain how viruses can lead to cancer

A

Infectious agents like viruses are causal agents in some cancers.

15% of cancers like nasopharynx, cervical, liver and lymphomas

17
Q

Explain what an oncogene, tumour suppressor gene, mismatch repair gene, and proto-oncogene are.

A

Oncogene: promotes cancer

Tumour suppressor gene: act to prevent cancer

Mismatch repair gene: repair mutated DNA

Proto-oncogene: Normal genes that promote cell growth and division that could become an oncogene

18
Q

What mutations can occur on a proto-oncogene

A

Deletion or point mutation = hyperactivity

Gene amplification = normal protein overproduced

Chromosome rearrangement = changes in regulation

19
Q

Oncogenes are dominant meaning…

A

that one gain-of-function mutation can predispose a cell to cancer as it overrides the rest of cellular function

20
Q

What cell functions are tumour suppressor genes involved in

A

Control cell cycle check points

Induce transcription of regulatory inhibitory genes

Overall, negatively control cell growth

21
Q

What mutation can occur for a tumour suppressor gene

A

Loss of function mutation

Can be inherited or acquired

Both copies of gene must be lost for cancer to develop (two hit hypothesis)

22
Q

Explain the two hit hypothesis

A

Loss of one copy of a tumour suppressor gene causes a slight cell progression advantage

Loss of both copies causes complete inactivation, significant growth advantage and predisposition to cancer

23
Q

What is retinoblastoma

A

Rare childhood tumour of the retina (neural precursor cells of retina)

Caused by non-function retinoblastoma (Rb) tumour suppressor gene

2 forms: hereditary and sporadic

Both copies of gene must be lost

24
Q

Explain the 2 types of retinoblastoma

A

Hereditary: young age, tumours in both eyes, mutant Rb allele on chromosome 13 in every cell of body

Non-hereditary/sporadic: 1 tumour in 1 eye, later age, mutant only in tumour cells

25
Q

What are the usual cell functions of p53

A

master regulator of cell death

cell cycle arrest

senescence

cell differentiation

apoptosis

DNA repair

26
Q

How does p53 cause cell death

A

Inducing selective gene expression to inhibit cell growth or induce apoptosis

stabilising p53 protein leads to increase in p53 levels

27
Q

What are the results of p53 mutation

A

Chromosomes become fragmented, incorrectly rejoined

Successive cell divisions produce largely mutated genome

28
Q

Explain MMR genes roles in cancer and mutation

A

8 MMR genes including MSH, MLH, PMS

Often lost or defective in cancers

2 hit hypothesis

29
Q

What does hereditary cancer motivate

A

routine screening for cancers

genetic counselling

30
Q

What are some of the features of inherited cancer

A

Several close relatives with common or related cancers

2 family members have the same rare cancer

Early age onset

Bilateral cancers in paired organs

Tumours in 2 different organs

31
Q

What is penetrance

A

The percentage of individuals with specific genetic defect who will get the disease

Varies depending on gene

32
Q

What are some features of inheritance of BRCA 1 and 2 breast cancers

A

Mutliple early onset cases in family

Breast and ovarian cancer history

Breast and ovarian cancer in same woman

Bilateral breast cancer

Ashkenazi jewish heritage

Male breast cancer

33
Q

Explain tyrosine kinase receptor as an oncogene

A

Mutation or over-expression can cause cellular transformation (cancer) as they are involved in activating multiple oncogenes

34
Q

Outline chronic myeloid leukemia (CML)

A

Leukemic cells have 9:22 translocation causing abnormal tyrosine kinase receptors

Arises from single abnormal hematopoietic stem cell

Proliferation of immature white blood cells

CML cells proliferate unchecked leading to

  • bone marrow replacement
  • increased liver size
  • white blood cell increase
35
Q

What is the Philadelphia chromosome

A

Shortened chromosome 22

End of chromosome 9 (containing abnormal tyrosine kinase) dused with B cell receptor (BCR) on chromosome 22

Fusion of bcr-abl produces a fusion protein which increases tyrosine kinase compared to normal and causes leukemia

36
Q

How can CML be diagnosed

A

demonstration of chromosomal translocation by standard cytogenetics, FISH or PCR

37
Q

What are the 3 main types of cancer treatment

A

Chemotherapy: kills rapdily dividing cells but also normal cells

Surgery: Cut cancer out, not always possible

Targeted therapies: find molecular cause and design therapies

38
Q

For cancers with TKR signalling like CML what are some treatment strategies

A

ATP - competitive inhibitors: stop TKR binding to ATP, blocking activity

Other anti-TK drugs: Antibodies against receptor or ligands, blocking activation

Antibodies against RTK or lignads: Block ligand binding, receptor internalisation

Anti-angiogenics: TK inhibitors as a target for anti-angiogenesis

eBMS2021 (8 decks)

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