Cancer EOYS1 Flashcards

1
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name two important cell growth pathways

A

MAPK pathway
PI3 Kinase pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

PROLIFERATION
APOPTOSIS REGULATION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

CELL GROWTH PROLIFERATION
ANGIOGENESIS AND METABOLISM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is HER2 receptor particularly oncogenic? [1]

A

Doesnt require simply GF to cause expression - easily overexpressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

In human cancers,TP53is the most commonly mutated gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What type of molecule is p53? [1]

Which molecule does it activate? [1]

A

p53 transcription factor:

Increases expression of p21
(cyclin dependent kinase inhibitors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain how Retinoblastoma occurs (and compare to normal functioning gene) [2]

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain the effect of p53 under normal function [4]

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Explain what happens when p53 becomes mutated [2]

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Explain the role of BRCA1 [1]

Explain the role of BRCA2 [2]

A

BRCA2:
* Upregulates RAD51
* Causes repair by homologous recombination

BRCA1:
* Broader role upstream of BRCA2, participating in various cellular processes in response to DNA damage.

20
Q

BRCA1 & BRCA2 are involved in repairing dsDNA crosslinks at which cell cycle check point? [1]

A

G2/M checkpoint

21
Q

BRCA1/2

Explain the role of RAD51 in dsDNA repair [1]

A

RAD51 bridges the interaction between BRCA1 and BRCA2

22
Q

Describe two genes that regulate apoptosis [2]

A

Bax: pro-apoptotic protein

Bcl2:anti-apopotic protein

23
Q

Name a cancer that occurs from resistance to apoptosis [1]

A

Bcl 2 mutatuon: B-Cell Leukaemia/Lymphoma

24
Q

Which gene increases the amount of telomerase? [1]

What happens if this is upregulated? [1]

A

Telomerase reverse transcriptase(TERT)

If gene upregulated allows the cancer cell to have unlimited replication

25
Malignant neuroectodermal tumours are called what? [1]
Glioma/ neuroblastoma
26
Malignant embryonic tumours are called what? [1]
Blastoma
27
Describe tumour development from initiation to metastasis [6] (of epithelial cancers)
**Initiation** **Hyperplasia**: cells divides more rapidly than normal **Dysplasia**: Altered cells with increased grwoth potential **In situ cancer** **Invasive** **Cancer**: cells enter blood and lymph **Metastasis**: forms at different sites
28
What is the yellow arrow pointing at in this prostate slide? [1]
Basal cell
29
Describe the changes seen in malignant prostate glands [4]
* Note size of nucleus: cytoplasm * **Prominent nucleoli** (green arrows) * **Absence of basal cell layer** * **Hyperchromasia** (blue arrows) * Glands **lost** regular **tubuloalveolar** arrangement
30
Grading of cancer is based on which two factors? [2]
1. Degree of anaplasia (degree of differentiation) 2. Rate of growth
31
Staging of cancer is based on which two factors? [2]
1 Size of tumour 2 Extent of growth (or spread)
32
What are the two types of staging? [2]
Two types: 1 Tumour Nodes Metastasis (TNM) 2 Number system
33
Explain TNM staging of tumours [3]
**T** - size of the cancer and how far it has spread into nearby tissue * **T1, T2, T3, T4**: Refers to the size and/or extent of the main tumor. The **higher the number after the T**, the **larger the tumor** or the more it has grown into nearby tissues. T's may be further divided to provide more detail, such as T3a and T3b. **N** refers to whether the cancer has spread to the lymph nodes – it can be between 0 (no lymph nodes containing cancer cells) and 3 (lots of lymph nodes containing cancer cells) * N1, N2, N3: Refers to the number and location of lymph nodes that contain cancer. The higher the number after the N, the more lymph nodes that contain cancer. **M** refers to whether the cancer has metastasised – it can either be 0 (no spread) or 1 (the cancer has spread)
34
# Abnormal mitosis What is the yellow arrow pointing at? [1]
Tripolar Spindles
35
# Abnormal mitosis What is the red arrow pointing at? [1]
Quadripolar Spindles
36
Describe process of metastatic niche creation [1]
Once lodged into area for secondary tissue growth: create environment called **metastatic-niche**. Get different cell types arriving so that tissue can grow
37
Colon cancer commonly metastasises to the Brain Bone Kidney Liver Prostate
Colon cancer commonly metastasises to the Brain Bone Kidney **Liver** Prostate
38
Metastatic breast cancer: Which genes are downregulated? [2] Which genes are upregulated? [1]
Downregulated: * **BRCA1** * **E-cadherin** Upregulated: * **VEGF**
39
Describe the differences in Grade I - IV of cancer grading [4] (what % is each grading?)
**Grade – I**: Well differentiated (< 25% anaplastic cells) **Grade – II**: Moderately differentiated (25-50% anaplastic cells) **Grade – III** : Moderately differentiated (50-75% anaplastic cells) **Grade - IV**: Poorly-differentiated or anaplastic (>75% anaplastic cells
40
What is the histopathological slide depicting? Hyperchromatic karyokinesis Hypochromatic karyokinesis Asymmetrical bikaryokinesis Trikaryokinesis Karyokinesis of chromatin in disorders
What is the histopathological slide depicting? Hyperchromatic karyokinesis Hypochromatic karyokinesis Asymmetrical bikaryokinesis Trikaryokinesis **Karyokinesis of chromatin in disorders**
41
Stage IIIC breast cancer is a cancer in how many lymph nodes? >6 >7 >8 >9 >10
Stage IIIC breast cancer is a cancer in how many lymph nodes? >6 >7 >8 >9 **>10**
42
'Radioactive tracer and a blue dye are administered near site of tumour' What does this describe
**Sentinel node biopsy**
43
'Radioactive tracer and a blue dye are administered near site of tumour' What does this describe [1]
**Sentinel node biopsy**
44
Which cancers do we screen for in the UK? [4]
Retinoblastoma Bowel-FiT Cervical Breast
45
Which cancer screenings do not fulfil Wilson’s criteria? [2]
Prostate Ovarian
46
Name 5 red flags in a patient that would indicate cancer in patients [5]
**Weight Loss** **Lumps**: * Anywhere * Throat/mouth/neck * Primary or secondary Symptoms of **Anaemia** and/or Infections **Unexpected Bleeding:** PU, PV, PR, Resp, Bruises **Changes**: voice; stamina/SOB; moles; back pain, bone pain, swallowing; bowels; complexion (jaundice/pallor); itching