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Genetics of Cancer Flashcards

1
Q

Name 6 altered physiology and behaviour of cancer cells [7]

A
  1. Angiogenesis
  2. Upregulation of proteases and cytoskeletal proteins: allow invasion and migration
  3. Telomere is protected from damage
  4. Uncontrolled growth
  5. Unresponsiveness to growth-inhibitory signals
  6. Increase in anti- apoptotic pathways and decrease in pro- apoptotic pathways
  7. Defects in DNA repair proteins so mutations are not corrected
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2
Q

What are the Eight Hallmarks of Cancer

A
  • Self-sufficiency in growth signals
  • Insensitivity to anti-growth signals
  • Evading apoptosis
  • Limitless reproductive potential
  • Sustained angiogenesis
  • Tissue invasion and metastasis
  • Deregulating cellular energetics
  • Avoiding immune detection
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3
Q

What are the 3 main groups of genes implicated in cancer? [3]

A

Oncogenes

Tumour suppressor genes Two types:
* Gatekeepers (regulate cell cycle)
* Care takers (DNA repair)

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4
Q

State whether oncogenes and tumour supressor genes are activated by a single or double mutation [2]

A

Oncogene: single mutation

Tumour supressor genes: double mutation

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5
Q

Most cancer cells arise from:

  • Sporadic mutations
  • Hereditary
A

Most cancer cells arise from:

Sporadic mutations

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6
Q

Which type of genes regulate cell growth? [1]
How? [1]

A

Proto-oncogenes encode proteins which control cell growth and cell division

Tightly regulated: switched on and off

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7
Q

Explain how proto-oncogene causes normal growth [2]

A

GF bind to tyrosine-kinase receptor (transmembrane protein)

Activates cell signalling and leads to growth on / off via the activation of:

  • Growth factors (signalling proteins)
  • Receptors (e.g. tyrosine kinase receptors
  • Intracellular signalling proteins e.g. kinases
  • Transcription factors
  • Anti-apoptotic proteins
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8
Q

What are the five categories of proto-oncogenes? [5]

A
  • Growth factors (signalling proteins)
  • Receptors (e.g. tyrosine kinase receptors
  • Intracellular signalling proteins e.g. kinases
  • Transcription factors
  • Anti-apoptotic proteins
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9
Q
A
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10
Q

Name two important cell growth pathways

A

MAPK pathway
PI3 Kinase pathway

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11
Q

Explain how normal proto-oncogenes cause normal cell signalling

A
  • growth factor binds to receptor. two receptors interact (dimerization)
  • intracelllar side: phosphorylation of tyrosine
  • signalling proteins bind to P-tyrosine
  • causes cascade of phosphorylation events
  • activates two pathways: MAPK pathway and PI3 Kinase Pathway

- once pathways are activated, activate gene expression and transcription factors occur.

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12
Q

Activation of MAPK pathway causes which cell processes to occur? [2]

A

PROLIFERATION
APOPTOSIS REGULATION

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13
Q

Activation of PI3 Kinase pathway causes which cell processes to occur? [2]

A

CELL GROWTH PROLIFERATION
ANGIOGENESIS AND METABOLISM

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14
Q

HER2 Receptor is what type of receptor?

GPCR
Enzyme-linked
Nucleus binding
Tyrosine-kinase

A

HER2 Receptor is what type of receptor?

GPCR
Enzyme-linked
Nucleus binding
Tyrosine-kinase

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15
Q

What causes constitute phosphorylation of MAPK / PI3 kinase pathways? [1]

What is the effect of this? [1]

A

P added

Genes continually switched on

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16
Q

What causes constitute phosphorylation of MAPK / PI3 kinase pathways? [1]

What is the effect of this? [1]

A

P added

Continually switched on

17
Q

HER2 activates which type of receptor? [1]

A

HER2 Receptors: (Tyrosine kinase)

18
Q

Describe the consequences of the overexpresson of HER2 [4]

A

Overexpression growth factor receptors leads to uncontrolled activation of signalling pathways:

  1. Uncontrolled growth
  2. Survival of cells containing mutations
  3. Invasion of tumour cells
  4. Migration of tumour cells
19
Q

Why is HER2 receptor particularly oncogenic? [1]

A

Doesnt require simply GF to cause expression - easily overexpressed

21
Q

Tumour supressor genes work by restricting cell proliferation via which mechanisms? [3]

A
  • Controlling (restricting) cell cycle and cell division
  • Inducing apoptosis in cells carrying mutations when other mechanisms have failed e.g. DNA repair

SO: encode proteins which inhibit cell growth

22
Q

What is role of gate keepers [5] and care taker genes [1]

A

Gate keepers:
* Directly supresses growth/restricts proliferation
* Cell cycle/cell division regulator genes
* Check point control genes
* Apoptosis - related genes

Care takers:
* Maintains genetic stability: DNA repair proteins

23
Q

At which stages in cell cycle are checkpoints where cell cycle can be arrested? [2]

A

G2 / M [1]
G1 / S [1]

24
Q

In human cancers,[]is the most commonly mutated gene.

A

In human cancers,TP53is the most commonly mutated gene.

25
Explain the effect of p53 under normal function [4]
* **p53** is a **transcription factor** * DNA damage activates stimulation of p53 protein * This activates **p21**, a **cyclin-dependent kinase inhibitor**, which leads to cell **cycle arrest** * Prevents progession from **G1 to S phase** * If damage so severe, p53 can tirgger activation of **pro-apoptotic genes**
26
Explain what happens when p53 becomes mutated [2]
* Mutated p53 **does not inhibit** **cyclin B/ CDK1 complex** so cell cycle arrest at **G2/M** does not occur * Mutated p53 **does not inhibit cyclin E/ CDK2 complex** so cell cycle arrest at **G1/S** does not occur
27
What type of molecule is p53? [1] Which molecule does it activate? [1]
**p53 transcription factor**: **Increases expression of p21** (cyclin dependent kinase inhibitors)
28
Explain how Retinoblastoma occurs (and compare to normal functioning gene) [2]
**Unphosphorylated form of Rb:** binds to GF E2F - cannot bind the DNA and transcription is blocked **Phosphorylated form of Rb**: cannot bind to GF E2F - bind the DNA and transcription goes on uncontrolled growth
29
Explain the role of BRCA1 [1] Explain the role of BRCA2 [2]
**BRCA2**: * Upregulates **RAD51** * Causes repair by **homologous** **recombination** **BRCA1**: * Broader role upstream of BRCA2, participating in **various cellular processes in response** to **DNA damage.** 
30
# BRCA1/2 Explain the role of RAD51 in dsDNA repair [1]
RAD51 bridges the interaction between BRCA1 and BRCA2
31
BRCA1 & BRCA2 are involved in repairing dsDNA crosslinks at which cell cycle check point? [1]
**G2/M checkpoint**
32
Describe two genes that regulate apoptosis [2]
**Bax**: pro-apoptotic protein **Bcl2**: anti-apopotic protein
33
Name a cancer that occurs from resistance to apoptosis [1]
Bcl 2 mutatuon: **B-Cell Leukaemia/Lymphoma**
34
Which gene increases the amount of telomerase? [1] What happens if this is upregulated? [1]
**Telomerase reverse transcriptase (TERT)** If gene upregulated **allows the cancer cell to have unlimited replication**

Cancer (11 decks)

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