Cancer Cell Biology Flashcards

1
Q

What is a carcinogen?

A

A substance capable of causing cancer in living tissue

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

What are some way carcinogens react with DNA and cause mutations?

A

Chemically modify bases-point mutation

Strand breaks-deletion, chromosome translocation

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

What are some causes and risk factors of lung cancer?

A

Air pollution, asbestos, radon, smoking, second-hand smoking

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

What is a polyp?

A

An encapsulated abnormal outgrowth

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

What is Wnt and where is it produced?

A

Wnt (Wingless Integrated 1) is a secreted glycoprotein

Produced by the stromal cells at the bottom of the colonic crypts

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

What is the function of Wnt?

A

To drive proliferation

It is a growth stimulatory pathway

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

Explain the wnt signaling pathway?

A
  • Wnt binds to the frizzled receptor
  • This causes the phosphorylation of LRP, inducing the translocation of the destruction complex towards the receptor.
  • This releases Beta-catenin which translocates into the nucleus and acts as a transcription factor (increased cell prolideration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain what happens in the absense of the wnt signaling pathway?

A
  • Wnt dosent bind
  • Destruction complex remains together and activates
  • GSK-3 phospharylates Beta-catenin
  • Beta-catenin undergoes ubiquitination and breaks down ( inhibition of proliferation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the destruction complex in the wnt signalling pathway made up of?

A

GSK-3
Axin
Beta-catenin
APC

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

How does the mutation of APC in the destruction complex lead to cancer?

A
  • loss of function of APC prevents the ubiquination and degredation of the Beta-catenin
  • So can function as transcription factor and increase cell proliferation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is meant by the multi-steps of cancer?

A

That it is a series of mutations and not just one

Starts off as a small adenoma, then leads to a large adenoma and then cancer

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

What is sporadic cancer?

A

Cancer due to a random chance/enviromental exposure

-accounts for around 70% of cancers

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

What is familial cancer?

A

Cancer that occurs in families
-from shared enivromental exposure
-similar genetic background
Accounts for around 20% of cancers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is hereditary cancer?

A

Cancer due to a inherited genetic mutation
Increased risk of cancer development
-Accounts for around 10% of cancers

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

What are the 3 main categories of cancer?

A

Sporadic
Familial
Hereditary

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

What do the hallmarks of cancer represent?

A

They outline the possible biological capabilities that can be aquired during the multistep process of cancer development

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

What is clonal evolultion in cancer?

A

Where with each mutation the abnormal cell gains selective advantage (heterogeneity) over neighboring cells giving rise to a clonal population

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

What is tumour heterogeneity?

A

The observation that different tumour cells can show different mutations and morphological profiles

19
Q

What are cancer critical genes?

A

All genes whose mutation contributes to the causation of cancer

20
Q

What are the 2 main classes of cancer critical genes?

A

Proto-oncogenes

Tumour suppressor genes

21
Q

What are proto-oncogenes?

A

Normal genes within our cells that promtoes cellular proliferation
-the accelerator

22
Q

What occurs when a proto-oncogene mutates?

A

Proto-oncogenes when mutated, become over activated or overexpressed

  • become an oncogene
  • leads to increased/uncontrolled proliferation
23
Q

What are the 3 mechanisms that produce oncogenes?

A

Translocation -new promoter region
Gene amplification-multiple copies
Mutation- within control region or within the gene

24
Q

What is the Philadelphia chromosome?

A

A changed chromosome 22, containing part of chromosome 9 (reciprocal translocation)

25
Q

What is the other name for the Philadelphia chromosome?

A

The BCR-Abl fusion gene

26
Q

What does the Philadelphia chromosome cause?

A

Produces increased levels of tyrosine kinase activity

-leads to increased cell proliferation

27
Q

What cancers is the Philadelphia chromosome found in?

A

Found in Chronic Myeloid Leukaemia (CML)

And in Acute Lymphoblastic Leukaemia (ALL)

28
Q

Are oncogenes dominant or recessive?

A

Dominant

29
Q

What is the significance of oncogenes being dominant?

A

There only need to be a mutation in one of the alleles to produce the uncontrolled cell growth
-higher chance of loss of function

30
Q

What are tumour suppressor genes?

A

Normal genes that negatively regulate (supress) cell proliferation
-the brakes

31
Q

What occurs when a tumour supressor gene mutates?

A

Results in a loss of function of the corresponding protein

Cell proliferation not regulated- leads to uncontrollable cell proliferation

32
Q

Is a tumour suppressor gene usually dominant or recessive?

A

Recessive

33
Q

What is the significance of a tumour suppressor gene being recessive?

A

A mutation in one allele doesn’t result in a loss of function
Loss of function requires a mutation in both alleles
-less chance of loss of function

34
Q

What is retinoblastoma and how is it caused?

A

The most common eye cancer in children

-caused by the mutation of the retinoblastoma (Rb) gene

35
Q

What theory did Knudson propose?

A

The 2 hit hypothesis ( the Knudson hypothesis)

36
Q

What is the 2 hit hypothesis?

A

That most tumour supressor genes require both alleles to be inactivated, either through mutation or epigenetic silencing, to cause a phenotypic change

37
Q

What are the different mechansims of how a tumour suppressor gene can be inactivated?

A

-Epigenetic silencing
-deletion of both alleles- homozygous deletion
-loss of function to both alleles
-loss of function to one allele and deletion of another
(loss of heterozygosity)

38
Q

What is a germline mutation?

A

A germline mutation is mutations in germ cells (reproductive cell in the body). These mutations are the only mutations that can be passed to offspring

39
Q

What is a germ cell?

A

A germ cell is a reproductive cell of the body. Found in egg cells of females and sperm cells of males

40
Q

What are examples of a germline mutation?

A
Retinoblastoma (Rb gene)
Breast/Ovary cancer ( BRAC1 and BRAC2 gene)
Colorectal cancer (APC)
41
Q

What are the different types of point mutation?

A

Silent
Missense
Nonsense

42
Q

What is a silent point mutation?

A

Change in single base

- same amino acid coded for, dosen’t affect the function of the protein

43
Q

What is a missense point mutation?

A

Change in single base

-results in a codon that codes for a different amino acids therefore could or could not affect function of protein

44
Q

What is a nonsense mutation?

A

Change in base that produces a stop codon

- stops transcription of protein therefore changes the fucntion of that protein