What Is Cancer?

Question 1

What is cancer ?

Answer 1

Cancer arises from abnormal, purposeless & uncontrolled division of cells that then invade + destroy surrounding tissues. Aka grp of diseases caused by normal cells changing so that they grow in an uncontrolled way

Question 2

What is meant by the term malignant tumour

Question 3

Normal cells need signals to survive. How about cancer cells?

Answer 3

Normal cells need signals to survive. Cancer cells can survive without them

Question 4

What is telomerase, we know mutations in telomerase can cause cancer.

Answer 4

Telomerase= enzyme responsible for maintenance of length of telomeres by addition of guanine-rich repetitive sequences i.e. it protects the ends of chromosomes

Telomeres maintain genomic integrity in normal cells, and their progressive shortening during successive cell divisions induces chromosomal instability. In the large majority of cancer cells, telomere length is maintained by telomerase. Thus, telomere length and telomerase activity are crucial for cancer initiation and the survival of tumors i.e. we must

Question 5

Describe interrupted life cycle of cancer cells

Question 6

Compare normal cells to cancer cells

Question 7

Define angiogenesis and why it’s seen in cancer cells

Question 8

What effect do growth inhibitory signals have on cancer cells

Answer 8

Cancer cells are unresponsive to growth inhibitory signals

Question 9

Define METASTASIS

Answer 9

Spread of a malignant tumour from its site of origin. This occurs 3 ways;

• through bloodstream (haematogenous)
•through lymphatic system
• across body cavities (through peritoneum)

• carcinomas generally metastasise via lymphatics, sarcomas via bloodstream

Question 10

Define proto- oncogenes

Question 11

How do proto-oncogenes become oncogenes

Question 12

Define oncogenes

Question 13

What happens when we get a mutation in the HER2 receptor (member of a tyrosine kinase receptor) on the transmembrane protein. After growth factor binds to a receptor and activates a signalling pathway

Answer 13

• a signalling protein e.g. epidermal growth factor binds and activates growth factor receptor

•if we have mutation in HER2, when the growth factor binds there’s an initiation: autophosphorylation of tyrosine, 20 different tyrosines on receptor will be phosphorylated (depending on growth factor, what other signalling proteins there are)

• tyrosine kinase HER2 receptor changes shape = activated= enhance kinase activity
=leads to uncontrolled cell growth, excess cell division leading to TUMOUR

Question 14

What does enhanced kinase activity lead to

Answer 14

Enhanced kinase activity leads to uncontrolled signalling~> tumour formation ~> excess cell division + uncontrolled cell growth

Question 15

List the 5 types of ONCOGENES

Answer 15

• growth factors (signalling proteins)
• receptors (e.g. tyrosine kinase receptors)
• intracellular signalling proteins e.g. kinases
• transcription factors
• anti-apoptotic proteins

Question 16

What is an ‘abnormal’ cell

Answer 16

A cell that carries mutations

Question 17

Define oncogenesis

Answer 17

Development of new or abnormal growth (benign or malignant tumour)

Question 18

What do tumour suppressor genes do when switched on

Answer 18

When switched on TSGs restrict cell proliferation by:

• restricting/ controlling cell cycle + division

• inducing apoptosis in cells w mutations (when other mechanisms e.g. DNA repair have failed)

• they encode proteins which INHIBIT cell growth

Question 19

What do tumour suppressor genes require to cause cancer

Answer 19

Both copies of a specific tumor suppressor gene pair need to be mutated to cause a change in cell growth and tumor formation to happen

Question 20

TSGs are deactivated as a result of _____ which leads to _______

Answer 20

TSGs are deactivated as a result of mutation which leads to cell dividing uncontrollably = may drive cell into oncogenesis

Question 21

Mutations in tumour suppressor genes

Answer 21

• mutations act recessively (both copies of TSG pair mutated) to release cells from growth control = increases probability mutant cells will become tumour cells

• increase probability of mutations in other genes

• may prevent apoptosis or allow cell devision of mutant cells

• this means cells can become immortal = cancer as DNA damage is not repaired n cell is dividing

Question 22

Unlike proto- oncogenes, where _________ mutated copy of proto-oncogene can have dominant, growth promoting effect on a cell) in tumour suppressor genes_______________

Answer 22

Unlike proto- oncogenes, where SINGLE mutated copy of proto-oncogene can have dominant, growth promoting effect on a cell) in tumour suppressor genes 2 COPIES OF MUTATED GENE RESULTS IN LOSS OF FUNCTION (I.e. both copies of gene need to be mutated for effect of mutation to be seen in TSG)

Question 23

2 types of tumour suppressor genes

Answer 23

1)CARE TAKERS = maintain genetic stability. Encode proteins involved in the repair of DNA

2) GATE KEEPERS= induce APOPTOSIS or inhibit cell proliferation by restricting cell cycle + division = encode proteins that inhibit cell growth. Check point control genes

Question 24

Define proliferation (in terms of cancer)

Answer 24

rapid increase in the number of cells

Question 25

What is the function of ‘gate keeper’ tumour suppressor genes

Answer 25

GATE KEEPERS= induce APOPTOSIS or inhibit cell proliferation by restricting cell cycle + division = encode proteins that inhibit cell growth. Check point control genes

Question 26

What is the function of ‘care taker’ tumour suppressor genes

Answer 26

CARE TAKERS = maintain genetic stability. Encode proteins involved in the repair of DNA

Question 27

Define hypoxia

Answer 27

A deficiency of oxygen in the tissues

Question 28

Define hypoxaemia

Answer 28

Reduction of oxygen concentration in arterial blood, recognised clinically by presence of and peripheral cyanosis (blue blood so skin has blueish appearance)

Question 29

What are the 3 tumour suppressor genes you’re expected to know in yr1?

Answer 29

• p53
•BRCA1/BRCA2
• Rb protein

Question 30

reasons why TSGs can be mutated

Answer 30

As a result of mutation: If cell is damaged/ stressed; DNA damage
Cell cycle is abnormal
Hypoxia
High no.of free radicals (from UV light, mutagen or inherited mutation)

Question 31

p53 senses __________ and is ______

Answer 31

p53 senses DNA DAMAGE and is ACTIVATED

Question 32

What are 2 things p53 triggers

Answer 32

1) cell cycle arrest, upregulation of Rb protein, upregulation of BRCA1 + BRCA 2 = cell cycle restart

2) apoptosis of damaged cells

= cellular + genetic stability

Question 33

Why is mutant p53 a problem?

Answer 33

Mutant p53 allows cells to progress through cell cycle with DNA damage

Question 34

What happens when a child has mutant pRb

Answer 34

Mutant pRb does not prevent cell cycle progression past G1 phase so faulty DNA continues to go through cell cycle this results in a RETINOBLASTOMA (eye cancer often seen in young children)

Question 35

What does a loss of BRCA1/BRCA 2 result in?

Answer 35

A loss of BRCA1+ BRCA 2 results in strand breaks & aneuploidy after cell devision

Question 36

What is the most commonly mutated gene in human cancers

Answer 36

In human cancers TP53 is the most commonly mutated gene

Question 37

What does pRb stand for

Answer 37

Retinoblastoma protein

Question 38

State relationship between p53 and p21

Answer 38

p53 transcription factor INCREASES expression of p21

Question 39

What is p21

Answer 39

p21= cyclin dependent kinase inhibitor

Question 40

If there’s a mutation in p53, what happens to p21

Answer 40

If mutation in p53, then p21 is mutated or not synthesised. Therefore we cannot inhibit cyclins at correct checkpoint in order for DNA repair or APOPTOSIS to occur.

Question 41

If we learn how to inhibit mutated p53….

Answer 41

If we could inhibit mutated p53, we will be able to prevent cancers

• research going on rn!

Question 42

Define carcinogenesis

Answer 42

Evolution of an invasive cancer cell from a normal cell

Multi step process caused by successive genetic mutations caused by carcinogens

Question 43

define somatic cell

Answer 43

Any cell other than reproductive (gamete) cells