Mechanisms of neoplasia 1

Question 1

Definition of neoplasia

Answer 1

abnormal proliferation of cells, A neoplasm= abnormal mass of tissue that occurs as a results of abnormal cellular proliferation

Question 2

What happens in a low grade neoplasm?

Answer 2

-Cells begin to proliferate abnormally but structure of tissue is maintained

Question 3

What happens in a high grade neoplasm?

Answer 3

Structure of tissue is affected, at this stage cells have to undergo specific abnormal mutations for the tumour to begin invasive

Question 4

What happens in an invasive carcinoma?

Answer 4

Cancer cells invade neighbouring tissue. They will eventually spread to local blood/ lymph systems.

Question 5

What is the difference between monoclonal and polyclonal tumours?

Answer 5

Monoclonal= originate from a single cell. The mutations began in 1 single cell. Normally occurs in leukemia
Polyclonal= originate from mutations that occured in more than one cell. Often the case for solid tumours. Often more difficult to find effective treatments for.

Question 6

What forms the risk of an individual getting cancer?

Answer 6

Combination of genetic factors and environmental factors

Question 7

Give examples of chemical and physical carcinogens

Answer 7

• Chemical: coal tars, some hdrocarbons (PAHs), asbestos

- Physical: ionizing radiation (X-rays, UV)

Question 8

What is a point mutation?

Answer 8

change of one or several bases in DNA sequence

• Nonsense: truncated protein
• Missense: protein with altered function

Question 9

What is a chromosomal alteration?

Answer 9

change in composition of a chromosome of change in the chromosome number
-Deletion/ insertion/ translocation, amplification

Question 10

What is epigenetic regulation?

Answer 10

It occurs via different modifications of histones and methylation of DNA in the chromatin
-e.g. changes in the histone tails and other structures of how DNA is compacted. These can be caused by environmental factors.

Question 11

What is the multiple hit hypothesis?

Answer 11

That one mutation is not normally efficient enough to cause cancer. Multiple hits (alterations) are normally needed.
- However some families can carry specific genes which code for mutations that are enough to cause cancer.

Question 12

Which 2 classes of genes are involved in tumours?

Answer 12

• Oncogenes (promote cell proliferation)

- Tumour supppressor genes ( prevent aberrant cell proliferation)

Question 13

What converts proto-oncogenes into oncogenes?

Answer 13

-Gain of function such as over expression or sustained activity

Question 14

Which oncogene is caused by gain of function by mutation?

Answer 14

Ras and MAPK

Question 15

Which oncogene is cause by gain of function by translocation?

Answer 15

c-MYC

Question 16

Describe how Ras can be oncogenic

Answer 16

• Can give continuous proliferation of cells, controls the MAPk pathway.
• Can use inhibitors to stop the cancer growing

Question 17

Describe the mechanisms c-MYC uses as an oncogene

Answer 17

• MYC is the chromosome, it can translocate onto another chromosome where there is an Ig gene which is very overactive, MYC is then expressed constantly which activates non stop proliferation.
• The Ig is always active.

Question 18

How can growth signals be oncogenic?

Answer 18

• Deregulation of receptor signalling occurs
• Over expression of receptors on membrane
• Alteration in protein structure (signalling without the ligand)

Question 19

What are tumour suppressor genes?

Answer 19

They are the gate keepers of cancer, when they lose their function this induces cancer.
e.g. p53 (apoptosis), p16 and p21 (cellcycle inhibitors), DNA repair

Question 20

What does a stable/ active p53 lead to in the cell cycle?

Answer 20

Can either arrest it or trigger apoptosis if the cell is faulty. If p53 is faulty then DNA repair genes can also be tumour suppressors.

Question 21

What is the importance of telomerase enzyme?

Answer 21

-It is expressed by cancer cells, this means they maintain long telomeres and effectively become immortal.