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Pharmacy Y2- Exam 3 > Cancer biology > Flashcards

Cancer biology Flashcards

1
Q

Name some growth factors and their receptor?

A
  • epidermal growth factors: EGFR
  • Hepatocyte growht factros receptors-c-met receptro
  • others like FGF
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2
Q

what are benign tumours?

A

Benign tumours are abnormal growths that are no longer under

normal regulation.

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3
Q

what are malignant tumours?

A

Poorly differentiated cells, growing in a rapid, disorganized
manner and can invade surrounding tissues and are become metastatic, initiating the
growth of similar tumours in distant organs

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4
Q

how are cancers classified? what are the 4 groups?

A

classified through cell origin

  1. Carcinomas
  2. Sarcomas
  3. Lymphomas
  4. Leukaemias
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5
Q

what are cacinomas?

A

-most common type (85%)
-arise from the cells that cover external
and internal body surfaces.

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6
Q

what are sarcomas?

A

-highly malignant
-12%
-Originate from cells found in
the supporting tissues of the
body (mesenchymal layerderived) such as bone,
cartilage, fat, connective tissue,
and muscle.

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7
Q

what are Lymphomas and Leukaemias?

A
  • make up 3%
  • arise from lymph nodes and tissues of immune system
  • leukaemias are immature white blood cells that proliferate in the bone marrow and accumulate in blood stream
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8
Q

what is staging of cancers is based on?

A

1.The site of the primary tumor.
2.Its size
3.How far it has invaded into local tissues and
structures
4.Whether it has spread to regional lymph nodes.
5.Whether is has metastasized to other regions of
the body

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9
Q

what causes cancer?

A

Tumour progression is driven by a series of random
mutations and epigenetic alteration (changes in DNA
methylation) of DNA that affects the genes controlling
proliferation and survival

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10
Q

can viruses cause cancer?

A

yes

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11
Q

how can DNA viruses cause cancer?

A

they can persist in the infected cell as a circular DNA (episome) and promote the expression of proteins that promote proliferation or that inhibit tumour suppressors gens Rb and p53

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12
Q

how can RNA viruses cause caner?

A

the RNA is retro transcribed into DNA and
incorporated into the host genome (provirus)
and allows it to replicate. RNA viruses cause
carcinogenesis in two ways:
1. Providing a gene that alters growth: the
RNA viruses can contain an extra gene
additional to the sequences needed for
viral replication
2. Insertional mutagenesis: the virus
integrates into the host genome close to
a host gene that regulates growth (i.e. a
GF) and upregulates its expression

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13
Q

what are the 2 types of viral mechanisms of carcinogenesis?

A

indirect and direct

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14
Q

what is the direct mechanism of viral carcinogenesis?

A 
1. Providing a gene that alters growth: the
RNA viruses can contain an extra gene
additional to the sequences needed for
viral replication
2. Insertional mutagenesis: the virus
integrates into the host genome close to
a host gene that regulates growth (i.e. a
GF) and upregulates its expression
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15
Q

what is the indirect mechanism of viral carcinogenesis?

A

-the cell is infected by the virus so releases chemokines that causes recruitment of inflammatory cells, this is a chronic inflammation and
oxidative stress that
persistently damage
local tissues which can cause mutation
-cells infected by virus and CD8+ cell under normal function but overtime immunosuppression occurs so T cells aren’t around so tumour grows

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16
Q

what causes DNA mutations?

A
  1. Mistakes in DNA replication
    • Misincorporation of deoxynucleotides during replication
  2. Nucleotides within DNA molecules undergo chemical
    changes spontaneously
    • These changes often alter the base sequences of DNA
  3. Effect of mutagenic agents
    • Molecules generated endogenously by normal cell
    metabolism (ROS)
    • Mutagenic agents: i) physical agents X-rays), UV rays) and ii)
    chemical agents (vinyl chloride, nitrosamines)
  4. Viruses
    • HBV, EBV, HPV
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17
Q

how many mutations are required to develop cancer?

A

3-20

18
Q

what is hyperplasia?

A

when a normal cells replicates to form many cells that a normal

19
Q

what does a change from normal cells to carinoma cells show?

A

-increased genomic instability as theres an increased tendancy of genome alteration during cell division.

20
Q

what is your neoplasia?

A

after dysplasia (growth of
immature cells) and metaplasia (cells
become another less differentiated cell);
neoplastic growth is rapid and results in a
tumour, metastasis and acquisition of more
mutations

21
Q

what needs to happen for a cell to move to S phase?

A

response from external signals like GF and nutrients

22
Q

how does EGFR siginalling occur?

A

• erbB2 family of receptors
• In the presence of ligand (EGF, TGFa),
EGFR come together and form homodimers
(EGFR) or heterodimers (HER1,2,3)
• Receptors are then phosphorylated (*) in the
intracellular tyrosine kinase domain
• Specific adaptor molecules (yellow) permit
Ras/Raf/MAPK and PI3K pathway to proceed
and activation of target genes
• PI3K can also bind directly any of the erbB
partners of EGFR heterodimers. Cell growth
• Activated receptors undergo endocytosis and
follow two possible routes: lysosomal
degradation or importin-mediated nuclear
translocation. And it can act as a transcription
factor (for cyclin D1 up-regulation) or as
coregulator of other gene transactivators.
• Result in nuclear activation of genes related
with cell proliferation, survival, invasion, and
metastasis.

23
Q

what is Ras and what does it do?

A 
• The product of the ras protooncogene are ras proteins
• Small G-proteins
• Involved in GTPase reaction cycles
• Relay a growth signal from a
growth factor receptor on the cell
membrane to a cascade of tyrosine
kinases
24
Q

what happens when Ras is mutated?

A

-Point mutation G to T i.e. Glycine to Valine
-Just one single amino acid substitution affected the function of Ras to
convert it from a proto-oncogene to an oncogene!
• Mutations in the Ras gene are found in 30% of human cancers

25
Q

what is a constitutive signal?

A

when the pathway signal keeps happening regardless of if there is a ligand present

26
Q

what types of mutations can occur in GFR signalling pathways?

A

Gene amplification: too many copies of a gene so too much of a product (1,2 & 5)
• Gene rearrangements: promoter in wrong place so normally a weakly expressed gene
can be expressed at high levels (5)
• Large structural deletions: deletions in receptors sequences e.g. truncated EGFR (2)
• Subtle mutations: a single nucleotide change e.g. Ras (3)

27
Q

what is the chronic myeloid leukaemia (CML)?

A

-accounts for 15-20 percent
of all leukaemias
- CML was the first malignancy in which a specific chromosomal
abnormality (the Philadelphia chromosome) was identified.
• Characterization of the molecular consequences of this
chromosomal abnormality identified an activated oncogene, BcrAbl, as the cause of this disease.

28
Q

what are 3 oncogenes implicated in a named cancer?

A
  • Ras
  • BCR/ABL
  • EGFR
29
Q

How do healthy cells control proliferation?

A
  1. Through checkpoints or external
    signals- favourable environment,
    nutrients, enough GF / mitogen
  2. By internal signals- DNA damage
30
Q

what are the 3 main tumour suppressor genes?

A
  • cyclin/cyclin dependant kinase
  • retionoblastoma protein
  • p53
31
Q

mutations in what phase checkpoints genes are common in tumours?

A

-G1

32
Q

what is Rb?

A

-acts as a brake here keeping the cell in G1 to prevent mutations or breaks
-Inhibits the genes
necessary for
progression into S
phase
• Phosphorylation of Rb
releases the brake

33
Q

what does deletion or mutation of retinoblastoma do?

A

encourages cell division

34
Q

what does deletion or mutation of retinoblastoma do?

A

encourages cell division because they result in E2F mediated transcription of S phase genes

35
Q

How can mutant Rb, which is a

recessive gene cause cancer?

A

-Retinoblastoma requires the loss of both functional copies of the Rb gene
- People inherit one mutated gene, later
the other mutates
• Retinoblastoma patients are on the
way to developing cancer
• They require two “hits” or mutational
events:
• Random chance mutation
• Chromosomal loss

36
Q

what is a sporadical cancer?

A

Most cancers are sporadic; no known cause, by chance with no relatives with a
similar cancer

37
Q

what does mutations of p53 do?

A

Mutations in this tumour suppressor gene causes
dysregulated cell growth and proliferation and
cancer

38
Q

what is p53 and where does it work?

A 
p53 acts as a brake
keeping the cell in G1
if there is DNA
damage until there is
either repair or
apoptosis
-interacts with CDK inhibitor p21
39
Q

what is the normal pathway for p53 if there is no DNA damage?

A

-p53 will be sat in the cytoplasm bound to MDM2 which is a E3 ubiquitin
ligase that constantly degraded by the protesome

40
Q

what is the normal pathway for p53 if there is DNA damage?

A
  • it becomes phosphorylated and interacts with p21

- then we get an inactive cdk complex and give cell cycle arrest and DNA repair

41
Q

what are the 2 main cancer genes?

A

tumour suppressor genes and proto-oncogenes

42
Q

what is a tumour suppressor gene?

A

normally block mitosis and must be knocked out for cancer to occur

Pharmacy Y2- Exam 3 (22 decks)

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