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Cancer > Revision of Cancer Biology > Flashcards

Revision of Cancer Biology Flashcards

1
Q

what are the 6 hallmarks of cancer cells

A
  • Growth signals are not required for cell survival, growth and differentiation
  • unresponsiveness to growth-inhibitor signals
  • evasion of apoptosis
  • defects in DNA repair
  • limitless reproduction potential
  • ability to invade and metastasis
  • angiogenesis (blood vessel formation) is sustained and increased
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2
Q

what is angiogenesis

A

blood vessel formation

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3
Q

What is a pro-oncogene

A

a normal gene from which an oncogene is derived when mutated, it has the potential to transform a cell into a cancerous state – cacner results when activated GAIN OF FUNCTION

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4
Q

What is an oncogene

A

gene that encodes protein capable of inducing cancer, activated by gain of function

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5
Q

Give some examples of an oncogene

A

BCL-2, C-MYC, VEGF, TGF alpha, EGFR, VEGFR, B-Raf

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6
Q

What cancers does EGFR over expression cause

A
  • Colorectal cancer
  • Pancreatic cancer
  • Lung cancer
  • non-small cell lung cancer
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7
Q

what cancer does Ras mutation cause

A
  • Pancreatic cancer
  • Papillary thyroid cancer
  • Colon cancer
  • Non-small cell lung cancer
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8
Q

What cancer does EGFR mutations cause

A
  • NSCLC

- Glioblastoma

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9
Q

What cancer does B-Raf mutation cause

A
  • Melanoma
  • Papillary thyroid cancer
  • Colon cancer
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10
Q

What is a tumour suppressor gene

A
  • Tumour suppressor genes mainly act to block development of cancer, allows the cell to stop and carry on in the cell cycle
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11
Q

How do tumour suppressor genes become cancerous

A

loss of function

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12
Q

what are the 3 types of tumour suppressor gene classes

A
  • Gatekeeper
  • caretaker
  • pro-apoptotic
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13
Q

Give some examples of the three types of tumour suppressor gene classes

A

Gatekeeper

  • p54
  • pRB

caretaker

  • BRCA (1/2)
  • MMR( mismatch repair gene)

pro-apoptotic
- Bax

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14
Q

How do tumour suppressor genes restrict cell life proliferation

A
  • Control the cell cycle and cell division

- Induce apoptosis when other mechanisms have failed

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15
Q

what causes angiogenesis in cancer cells

A

vascular endothelial growth factor which can be released by cancer cells

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16
Q

give an example of photo-oncogenes and what cancers they cause

A
    • Translocation = t(14;18)(q32;q21) Bcl-2= follicular lymphoma
  • Amplification in ERBB2 or HER2 breast cancer
  • c-Fos (transcription factor)Skin/endometrial = point mtuations
  • c-H-ras (Gly)GGC- (Val)CTG = bladder = point mtuations
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17
Q

What does a gatekeeper tumour suppressor gene do

A

regulate entry into the cell cycle and the cell cycle

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18
Q

What does a pro-apoptotic tumour suppressor gene do

A
  • causes apoptosis
  • if there is a mutation in pro-apoptotic tumour suppressor gene this means that apoptosis is inhibited therefore this can lead to immortality of the cells
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19
Q

Name the main types of DNA damage that can happen

A

Single strange breaks (spontaneous mutations)
Damage DNA bases – cause of mismatch errors
UV light
Replication errors
Interstrand breaks within the DNA

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20
Q

Describes examples of

  • Single strange breaks (spontaneous mutations)
  • Damage DNA bases – cause of mismatch errors
  • UV light
  • Replication errors
  • Interstrand breaks within the DNA
A

Single strange breaks (spontaneous mutations)

  • reactive oxygen species
  • x rays
  • oxygen radicals
  • spontaneous reactions

Damage DNA bases – cause of mismatch errors
- alkylating agents (usually methylation)

UV light

  • UV light
  • Causes the Addiction of bulky adducts
  • Or causes pyrimidine dimers
  • Polycyclic hydrocarbons – see from tobacco smoke
  • Specific DNA remair mechanism within the cell to repair this

Replication errors

  • Replication errors such as depurination
  • Occur normally during the cell cycle s, G1, and G2 phases

Interstrand breaks within the DNA

  • UV lights
  • Hydroxyurea
  • X rays
  • Anti -tumour agents
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21
Q

describe the features of benign tumours

A
  • Generally slow growing but progressive.
  • Mitotic figures rare - this is the ability to see cells going through mitosis on the slide
  • Non-invasive
  • Non- metastasising.
  • Well differentiated.
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22
Q

Describe the features of malignant tumours

A
  • Fast growing
  • Mitotic figures may be numerous and abnormal.
  • May ulcerate on the surface
  • Local invasion – clinical cardinal feature
  • May metastasise –cardinal clinical feature.
  • More common with large undifferentiated primary tumours
  • May see weight loss, anorexia and anaemia
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23
Q

What is the main clinical cardinal feature of malignant tumours

A

metastasises

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24
Q

Describe what the normal prostate gland look like

A

Tubuloalvolar glands

basal cells

25
Q

describe what BPH looks like

A
  • Crowded tubules
  • columnar arrangement near gland
  • nucleoli not typically seen
26
Q

describe the difference between a high grade and low grade PIN - (Prostatic intraepithelial neoplasia)

A

Low grade PIN

  • Nucleoli not prominent
  • Tissue appears almost normal
  • Intact basal layer

High grade PIN

  • Large nuclei,
  • hyperchromasia
  • prominent nucleoli,
  • scattered basal cells periphery
27
Q

What does a malignant prostate gland look like

A
  • note size of nucleus: cytoplasm = high nuclei to cytoplasm ratio
  • prominent nucleoli
  • absence of basal cell layer
  • hyperchromasia
28
Q

What are the common sites of metastases for breast

A

bone and lung and liver

29
Q

What are the common sites of metastases for ovarian

A

liver

30
Q

what are the common sites of metastasis for pancreas

A

liver and lung

31
Q

what are the common sites of metastasis for lung

A
  • adrenal gland

- bone

32
Q

where are the common sites of metastasis for colon

A

liver

33
Q

What does a mesenchymal cell phenotype allow the tumour to do

A
  • enhanced migratory capacity
  • invasiveness
  • elevated resistance to apoptosis
  • > ECM components.
34
Q

What is a epithelial cell polarised

A

-when the basement membrane is on the basal surface

35
Q

What is MAT(mesenchymal–amoeboid transition)

A

the acquisition of amoeboid motility by mesenchymal cells is often associated with enhanced metastasis.

36
Q

what are the two types of changes that cancer cells undergo in order to allow them to metastasise

A

epithelial cells to mesenchymal amoeboid cell - this means that they have an enhanced ameboid movement and metastasis

the cell loses epithelial characteristic and gains a mesenchymal – start to produce proteases so they can pass through the basement membrane and enter the blood stream

37
Q

what can be used as an early marker of cancer

A

the cell loses epithelial characteristic and gains a mesenchymal – start to produce proteases so they can pass through the basement membrane and enter the blood stream = this can be an early marker of cancer

38
Q

what are the 4 main phases of the cell cycle

A
  • G1
  • S
  • G2
  • M
  • GO – non dividing, fully differentiated or quiescent stem cells, or not going through the cell cycle
39
Q

How long does each part of the cell cycle take

A
  • 23 hours spent in interphase

- 1 hour spent in mitosis

40
Q

what is interphase made up of

A

G1
GO
S
G2

41
Q

what is mitosis made up of

A

Prophase
Metaphase
Anaphase
Telophase

42
Q

describe what happens in G1 and G2

A
  • Gap (growth) phases – need to grow so they can make two cells out of one cell
  • Longest phases
  • No synthesis of DNA
  • Cell has checkpoints and the cell will not progress unless they are met
  • Replication of organelles happen in G1 and production of proteins, cytoplasm and nucleotides
  • G2 – cell double checks DNA has been copied properly and checks for errors, if they are unable to repair errors then the cell undergoes apoptosis
  • G1 - Cell checks the environment both internally and externally – make sure that the external environment is correct around the cell so it can receive the daughter cell
43
Q

what happens in S phase

A
  • Synthesis phase
  • DNA is duplicated
  • 2n to 4n – sister chromatids, each chromosome replicates
  • chromosome are held at the centromere, so they are not mixed up at this point
  • need 4N for two of the daughter cells
  • semi-conservative replication
  • this is where mutations can occur
44
Q

what is the interphase phase the cell spends most of the time in

A

G1 and G2

45
Q

what happens in prophase

A
  • DNA condenses to form chromosomes that are joint at the centromere
  • Nucleoli disappears
  • Nuclear envelope breaks down – chromosomes need to go into the main part of the cell,
  • Centromere is a specialisation of the histones, this is an attachment point onto the microtubules
  • Centrioles are special hollow structure that organise the microtubule assembly, organise mitotic growth spindles
  • Centrioles separate and move apart towards opposite poles and organise the production of microtubule filaments
  • Mitotic spindles start to appear and grow towards the equator of the cell
  • Microtubules form a radiating array
  • Chromosomes are attached to the microtubules by kinetochore
46
Q

describe the process of metaphase

A
  • Chromosomes are lined up in the metaphase plate
  • Centrosomes are at polar ends
  • Microtubules and centromeres bind together to form kinetochores
  • Kinetochore/microtubules are used to pull chromosomes apart, one from each pair of sister chromatids pulled towards opposite ends
  • Cohesion are now only present in centromere to hold sister chromatids together
47
Q

Describe the process of anaphase

A
  • When chromosome reaches centrosome, the poles separate further by elongation of the polar microtubules
  • Cohesin is hydrolysed and it is not functional anymore this allows separation
  • they are pulled to polar ends
48
Q

describe telophase work

A
  • Uncoiling of chromosomes
  • Reformation of nuclear envelope
  • Contractile ring forms of actin and myosin pinches the cell until it splits into 2 daughter cells , cytoplasm is dividing and division is completed
49
Q

where does crossing over take place

A
  • Takes place in prophase 1 between homologous pairs of non-sister chromatids
  • Crossing over of tails which is called chiasmata
50
Q

How do we regulate cell cycle progression

A
  • Cyclin dependent kinases (Cdks)
  • Cdks are activated by cyclins
  • Specific cyclin-Cdk complexes act at different parts of the cell cycle
  • The combination of cyclins and CDKs produce energy required for the cell to progress to the next stage
51
Q

how is an cDK activated

A

Cdk

  • Breaks down ATP and releases a phosphsate
  • phosphate given to substrate that binds to cyclic and activates Cdk
  • CKIs inhibit CDKs
52
Q

What proteins block the G1/S phase transition

A
  • CKI proteins (p16, p21, and p27) primary act to block the entry into the cell cycle and the G1/S transition
53
Q

what are the cell cycle checkpoints

A

1st - end of G1 - restriction point G1/S
2nd - end of G2(finished by end of G2) G2/M
3rd - metaphase - spindle checkpoint M

54
Q

what are the 3 types of chemotherapy drugs (drugs used to control the cell cycle)

A
  • Anti-mitotics
  • biologics
  • anti-hormonal drugs
55
Q

describe how anti-mitotic work

A
  • tradition chemotherapy drugs
  • Anti-microtubule agents
  • Affect all the dividing cells either tumour cells or human cells - non selective
    There are two main classes
  • Vinca alkaloids prevent the formation of the microtubules therefore metaphase cannot occur
  • Taxanes prevent the microtubule disassembly , chromsooems do not dissociate from the spindles and the cell cannot enter telophase
56
Q

Describe check point 1

A

1ST check point (restriction checkpoint) Cell growth checkpoint (G1/S)

  • Occurs at the end of G1
  • Checks cell size, growth factors, DNA damage, nutrients
  • Controlled by CKI, p16, which inhibits CDK4/6 so it cannot bind to cyclin D
  • If not cell goes through resting phase until it was ready to divide
57
Q

Describe check point 2

A

2nd check point - DNA synthesis checkpoint – completed by the end of G2 (G2/M)

  • Occurs end of G2
  • Checks cell size, DNA damage, and DNA replication
  • Uses a phosphatase to remove a phosphate from cyclin B/CDK 1 complex as the phosphate is acting as an inhibitor
  • If there is damage to DNA, or incorrect replication the cell cycle would be stopped
  • Cell continues onto mitosis
58
Q

Describe check point 3

A

Mitosis checkpoint – occurs during metaphase

  • Spindle checkpoint
  • Checks whether chromosomes are attached to spindles
  • Tension in microtubules causes the initaiton of anaphase

Cancer (13 decks)

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