Introduction to Cancer 2 Flashcards Preview

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Flashcards in Introduction to Cancer 2 Deck (36)
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1
Q

What are the 6 hallmarks of cancer ?

A

1) Sustaining proliferative signalling
2) Evading growth suppressors= ignore the other cells and continue to grow
3) Activating invasion and metastasis= metastasis complicates the function of the organ
4) Enabling replicative immortality= ignoring any mechanisms initiating death
5) Inducing angiogenesis= fundamental for tumours to grow
6) Resisting cell death

2
Q

What is cancer and what does it require?

A

COLLECTION of related diseases- tumours go through many of the same processes
They can start from almost any cell type
They require multiple mutations and undergo uncontrolled cell division
It is a step-wise process and can damage surrouding organs which is a key issue of the disease. They can also sometime metastasise.

3
Q

In breast tissue what is the most common cell type to develop cancer?

A

the epithelial cells within the ducts

4
Q

Where else in breast tissue can tumours occur ?

A

Within the lobules and stroma

5
Q

Why is breast tissue prone to tumourogenesis?

A

because it is very sensitive to hormonal changes

6
Q

What is the difference between ductal carcinoma and invasive ductal carcinoma?

A

ductal carcinoma= it is cancer but it is retained within the basement membrane and an operation is relatively easy because the tumour can be removed
invasive ductal carcinoma= the tumour cells break through the basement membrane and this allows them to metastasise.

7
Q

What are the different ways of classifying cancers?

A

Malignant/benign= any malignant tumour left from surgery will continue to grow leading to relapse
Pathology/histological subtype
- receptor status
Grade= level of differentiation- the more undifferentiated the worse the tumour is
Stage
- size
- spread= confined or spreading throughout the body
Molecular= gene expression- the level of improvement for treatment based on this is limited

8
Q

What are the receptor status’ in breast cancer?

A

It is one of the most important ways to classify breast cancer
estrogen receptor= use hormone eblation therapy such as tamoxifen or aromatase inhibitors to block the production of estrogen
progesterone receptors are also important

9
Q

What is the link between Her2/ErbB2 in breast cancer?

A

this is a signalling molecule which can change its gene transcription
Perceptin- monoclonal antibody that stops this molecule being activated by its ligand

10
Q

What happens to breast cancer patients that are triple negative?

A

They dont demonstrate any pathological/histological references, so they are given a horrible concoction of cytotoxic chemotherapeutic drugs

11
Q

What is a mutation ?

A

it is a changes in DNA- causes changes it how genes behave and their physiology

12
Q

Why are mutations very important ?

A

They are essential for evolution- they are the raw material of genetic variation

13
Q

What are the types of bases ?

A
Pyrimidines= cytosine, thymine and uracil
Purines= adenine and guanine
14
Q

What is nearly always true about mutations?

A

They originate in DNA but their effects are shown through proteins - it is chemical modifications that cause changes to DNA

15
Q

How many mutations occur per day ?

A

In every cell about 100 mutations occur in the body per day - most of them dont matter

16
Q

What are the different types of mutations?

A

deletions, insertions and point mutations
Synonymous= made a change to codon but no change to amino acid
Non-synonymous= change in the codon which causes a change in the amino acid
- non-sense= truncating the protein early
-missense= substituting an aa for another one

chromosome rearrangment- often occurs in leukemias
copy number variants- Her2- entire gene is duplicated more
epigenetic mutation- ER alpha- not all mutations occur in DNA

17
Q

What are the different mechanisms of mutations?

A

Spontaneous chromosome re-arrangment
Gene amplification
Random errors in replication= mistakes when DNA is replicated
Inheritance- common mutations e.g. brac-2 in breast cancer is highly inherited
Viruses- this was how oncogenes were first discovered
Environmental exposure- chemical mutagens and radiation

18
Q

What are some causes of mutations ?

A

OXIDATIVE DAMAGE of DNA by ROS
- hydrogen perioxide, hydroxyl radicals and superoxide radicals
These ROS can arise from irradiation or they can be produced by aerobic metabolism

Environmental chemicals

  • chemicals present in tobacco
  • product of industrial activity
  • resulting from metabolism of food components
  • cooking food- way food is prepared
19
Q

What are the 2 types of genomic DNA cells contain?

A

either contain 1 set of genomic DNA= germ cells

or they contain 2 sets of genomic DNA= regular diploid cells

20
Q

what can defects and ineffiences in DNA repair systems lead to ?

A

it can increase the number of mutations

21
Q

How effective are DNA repair systems ?

A

due to DNA repair systems, less than 1 incident of DNA damage in 1000 hits becomes a mutation

if mutations occur in the repair systems then this is very bad- causes cells to be prone to developing lots of mutations

22
Q

What is the base-excision repair system ?

A

this cuts out the entire base

types of damage: basic sites, free radical oxidation or deamination of cytosine/methylcytosine

23
Q

What is base mis-match repair?

A

notices irregular DNA so it replaces the base

types of damage: small adducts, free ROS, insertions/deletions

24
Q

What is the nucleotide excision repair?

A

replace sugar aswell

types of damage: large adducts and UV cross links

25
Q

What is alkyl transferase?

A

it is an enzymes

types of damage: small alkyl adducts

26
Q

What is homologous recombination?

A

this only occurs in homologous recombination

types of damage: strand breaks

27
Q

What happens if mutations are not repaired?

A

then there is an increased risk of cancer - it is proportional to mutation rate

28
Q

What are the 3 classes of genes frequently mutated in cancer ?

A

PROTO-ONCOGENES= they can become mutated forming oncogenes. Normally they are important in making cells divide and grow
TUMOUR SUPPRESSOR GENES- these stop genes dividing
GENES LINKED TO MUTATION RATE

29
Q

Define oncogene:

A

gene that has the potential to cause cancer

30
Q

Define tumour suppressor gene:

A

gene that protects cells from one step on the path to cancer

31
Q

Define mutator genes:

A

gene that increases the rate of mutation of one or more other genes

32
Q

How long does the cell cycle take ?

A

18-24 hours- it is tightly regulated

33
Q

Why are most cells not going through the cell cycle?

A

They are terminally differentiated
They are senescent
They are quiescent in G0 phase

34
Q

What happens in the G1 phase ?

A

the cell becomes responsive to growth factors - period in which cell is responsive to mitogenic growth factors and TGF-beta
TGF-beta is often mutated in cancer

35
Q

Where is the R point and what happens?

A

R point is within the G1 phase and its the point when cell stops becoming responsive to signals

36
Q

What are 2 key points about cancer cells and growth signals?

A

cancer cells are self-sufficient in growth signals and insensitive to anti-growth signals