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Cancer Week > Year 1 What is Cancer? > Flashcards

Year 1 What is Cancer? Flashcards

1
Q

Define cancer?

A
  • An abnormal growth of cells
  • multiply in an uncontrolled way
  • in some cases metastasize
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2
Q

Define tumour or neoplasm?

A
  • abnormal mass of tissue growing in an uncontrolled or uncoordinated matter
  • can be benign or malignant
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3
Q

What are neoplastic cells?

A
  • lost control of normal processes such as growth

- irreversible process, cannot go back to being normal cells

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4
Q

Define a mutation

A

Abnormal change in a gene

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5
Q

Define oncology

A

Study of tumours or neoplasia

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6
Q

Define benign tumours

A

Grow locally and do not invade nearby tissue

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7
Q

Define malignant tumours

A

May invade nearby tissues and metastasise

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8
Q

Define metastasis

A

Spread of cancer cells from primary tumour to surrounding tissues and distant organs
- can develop a secondary tumour

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9
Q

Define carcinogenesis

A

multi-step process transforming normal cell to a cancer cell

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10
Q

Define transformation

A

Conversion of one cell phenotype to another

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11
Q

Define carcinogen

A

An agent which changes a cell population and can cause cancer

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12
Q

Define carcinoma

A

Cancer which arises from the epithelium of the skin or internal organs

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13
Q

Define differentiation

A

Process by which cell develops/matures allowing it to perform a specific function

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14
Q

What is cancer?

A
  • unregulated growth of malignant tumours
  • can invade surrounding tissues and metastasise
  • caused by a number of mutations (multi-hit process)
  • can be solid or haematological malignancies
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15
Q

What is the significance of cell signals?

A
  • cancer cells do not require external signals to tell them to grow as mutations over-ride this signalling
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16
Q

What cells are needed for tumour development?

A
  • immune inflammatory cells
  • endothelial cells for vasculature for oxygen
  • pericytes
  • cancer associated fibroblast
  • stem cell
  • cancer cell
  • invasive cancer cell
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17
Q

What are the 6 hallmarks of cancer?

A
  • self sufficiency in growth signals
  • insensitivity to anti-growth signals
  • evade apoptosis
  • limitless reproductive potential
  • sustained angiogenesis
  • tissue invasion and metastasis
18
Q

How do cancer cells have self sufficiency in growth signals?

A
  • normal cells require mitogenic growth signals to move into active proliferative state
  • oncogenes in cancer mimic normal growth and tumour cells generate own growth signals (autocrine signalling)
19
Q

How are cancer cells insensitive to anti-growth signals?

A
  • normal cells have anti-proliferative signals maintaining cellular quiescence
  • growth inhibitory signals received by transmembrane cell surface receptors coupled to intracellular signalling
  • antigrowth signals block proliferation by forcing out cells from cell cycle in G0 or induce cells to enter post mitotic state for terminal differentiation
20
Q

How do cancer cells evade apoptosis?

A
  • determined by rate of proliferation and cell attrition
21
Q

How do cancer cells have a limitless replicative potential?

A
  • maintain the telomeres so do not shorten preventing apoptosis
22
Q

What are the enabling characteristics of cancer cells?

A
  • modify metabolism to support growth
  • evade destruction by immune system (exploited by immunotherapy)
  • genomic instability promote more genetic alterations
  • inflammation by immune cells are tumour promoting
23
Q

What is a proto-oncogene?

A
  • responsible for cell growth, division, motility
  • undergo mutations in cancer cells creating uncontrolled growth
  • once mutated = becomes an oncogene
  • gain of function
24
Q

What are tumour suppressor genes?

A
  • allow cell to stop at checkpoint in cell cycle and allow DNA repair
  • if mutation cell mutation is not stopped and replication is continued
  • loss of function as DNA repair cannot occur
25
Q

What are the 5 categories of proto-oncogenes?

A
  • growth factors
  • growth factor receptors
  • signal transduction proteins
  • transcription factors
  • pro or anti apoptotic proteins
26
Q

What is an example of GF overexpression?

A
  • VEGF = BPH
  • PDGF = glioblastoma
  • TGFa elevated levels = oesophageal cancer
  • HER2/ErB2 = breast cancer
27
Q

What happens if the HER2/ErB2 GF is overexpressed?

A
  • uncontrolled growth
  • mutated cells survive
  • tumour cells invade
  • tumour cells migrate

(receptor activated when GF absent, unregulated autocrine loops)

28
Q

What is an example of a signal transduction proteins?

A
  • K-ras
  • normally binds to GTP causing phosphate to phosphorylate K-ras and activate it, protein gets dephosphorylated and deactivated in a normal cell (under control of phosphorylation)
  • phosphorylated k-ras activates ERK pathway
  • when K-ras mutated, GTP very slowly very slowly hydrolysed to GDP so K-ras phosphorylated for longer and activating MAP kinase pathway for longer (major growth pathway)
29
Q

What is an example of a TF?

A
  • c-MYC regulates normal functions (cell cycle, DNA replication, cell adhesion, differentiation, growth, metabolism)
  • promotes transcription of cyclin genes which promote cell cycle progression
  • elevated expression in cancer cells
  • c-MYC translocations = Burkitt lymphoma
  • c-MYC overexpression = breast cancer, colon, lung
30
Q

What is the difference between c-MYC translocations and overexpression?

A
  • overexpression alone cannot induce tumorigenesis

- need additional translocations and evade tumour suppressing checkpoints to induce tumorigenesis

31
Q

What are the significance of apoptotic and anti-apoptotic proteins?

A
  • cancer cells undergo up regulation of anti-apoptotic proteins
  • survive even when challenged by DNA damaging compounds
  • balance between Bax (anti-apoptotic) and Bcl-2 (pro-apoptotic) required for normal apoptosis as form a dimer
  • mutation within Bax = apoptosis
  • increased Bcl-2 = cells immortalised
  • In B cell lymphomas translocation of Bcl-2 occurs using stronger promoter of immunoglobulin gene to evade apoptosis
32
Q

How do tumour suppressor genes work?

A
  • act to block development of cancer
  • mutations enable loss of function of these genes and therefore lose restriction of cell growth enabling tumour survival
33
Q

How do tumour suppressor genes restrict cell proliferation?

A
  • control cell cycle and division

- induce apoptosis when other mechanisms have failed

34
Q

What do mutations of tumour suppressor genes do?

A
  • act recessively releasing cells from growth control
  • greatly increase probability of mutations
  • may prevent apoptosis or allow or allow cell division of mutated cells
35
Q

What are gatekeeper genes?

A
  • type of tumour suppressor genes
  • stop cell cycle progression when DNA damage is detected
  • p53 TF mutations are most common genetic alteration in cancer
  • pRB transcription inhibitor

(both examples of gatekeeper genes)

36
Q

What is the function of p53?

A
  • TF
  • activated by DNA damage, hypoxia or cell injury
  • activates p21 to inhibit cyclin complex preventing cell leaving G1 and entering S phase
  • cell cycle arrest/DNA repair/entry to apoptotic pathway
  • mutant p53 = cells progress through cycle with DNA damage and so mutations accumulate becoming cancerous
37
Q

What is the function of pRB?

A
  • prevents cell cycle progression past G1 phase by inhibiting S phase genes
  • mutant pRB = retinoblastoma
38
Q

What are caretaker genes?

A
  • maintain genomic stability
  • repair DNA damage during cell cycle arrest
  • BRCA (DNA repair protein) (breast and ovarian cancer)
  • MMR (mismatch repair genes)
39
Q

What are BRCA1 and BRCA2?

A
  • breast cancer
  • repair damaged dsDNA crosslinks at G2/M checkpoint
  • loss = strand breaks and aneuploidy after cell division
40
Q

What is BRCA1?

A
  • interacts with cyclins and CDKs triggering CDK inhibitor, p21 and p53 = controls cell cycle
  • involved in DNA repair
  • if BRCA1 deficient = genomic instability
41
Q

What is BRCA2?

A
  • facilitates homologous recombination

- if deficient = cannot recruit ssDNA binding proteins to repair double strand breaks from homologous recombination

42
Q

What are the physiological factors of cancer cells?

A
  • growth signals not required for survival, growth and differentiation
  • unresponsive to growth inhibitory signals
  • evasion of apoptosis
  • defects in DNA repair
  • cells become immortal
  • ability to invade and metastasise
  • angiogenesis sustained and increased

Cancer Week (12 decks)

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