Tumour Pathology 2

Question 1

Define “pleomorphism”.

Answer 1

This refers to cancer cells being of many different shapes and sizes (cells and their nuclei).

Question 2

Define “hyperchromatic”.

Answer 2

This is the useful feature of cancer cells where their nuclei stain more deeply.

Question 3

Define “coarse chromatin”

Answer 3

This refers to irregular clumping of cancer cells that vary in size and shape.

Question 4

List the physical properties of cancer cells.

Answer 4

Pleomorphic
Hyperchromatic
Coarse chromatin
Highly mitotic and abnormal functions
Disorganised structure

Question 5

Explain the difference in behaviour of cancer and normal epithelial cells.

Answer 5

Cancer cells undergo unregulated growth, whereas normal cells only replicate when required.
Cancer cells have less cohesion than normal cells and are more singly dispersed in tissues.
Cancer cells are forever immature, whereas normal cells progress and specialise to a certain role.
Cancer cells are immortal as they are able to “switch off” apoptosis”, whereas normal cells die when instructed.

Question 6

Define “carcinogenesis”.

Answer 6

Carcinogenesis is the formation of cancer (from normal cells).

Question 7

Describe tumour angiogenesis.

Answer 7

Tumour angiogenesis is required to sustain the growth of the tumour (oxygen).
Also allows an escape route, where the tumours can exit through the vessels and spread to other parts of the body.

Question 8

Define “apoptosis”.

Answer 8

Apoptosis is regulated cell death and it is an active process. It requires energy.
The release of harmful intracellular content is avoided.

Question 9

Define “necrosis”.

Answer 9

Necrosis is premature/unregulated cell death.
This is a passive process.

Question 10

List some factors that can cause necrosis.

Answer 10

Infection
Trauma
Hypoxia
Toxins

Question 11

Describe the process of necrosis.

Answer 11

There is a loss of cell membrane integrity: cells swell and burst.
Uncontrolled release of intracellular contents or the interstitum.
This initiates an inflammatory response, which may be collateral damage.
Usually large areas of tissue and cell death.

Question 12

Define “proto-oncogene”.

Answer 12

Normal cells molecules that turn into oncogenes once mutated.

Question 13

Define “oncogenes”.

Answer 13

Oncogenes stimulate the cell cycle or prevent cell death.
They may be inherited or sporadic.

Question 14

Define “tumour suppressor genes”.

Answer 14

Tumour suppressor genes regulate/suppress cell cycle.

Question 15

Define “metastasis”.

Answer 15

The spread of cancer cells, either by direct invasion or metastasis is the hallmark of malignancy.

Question 16

List the 4 ways that metastasis.

Answer 16

Local spread
Lymphatic spread
Haematogenous spread
Trans-coelomic spread

Question 17

Describe the process of lymphatic spread.

Answer 17

(Each step requires mutations, as normal cells lack these capabilities).
Usually only able to detect metastasis clinically at the end of the pathway.
- Invade connective tissue
- Enter lymphatic
- Travel through lymphatics
-Exit lymphatics
-Enter lymph node
-Grow in lymph node

= lymph node metastatic deposit.

Question 18

Describe trans-coelimic spread.

Answer 18

Process where cancer can spread to a distant site, without having developed the capacity for vascular space invasion.
Spreads through body cavity.

Question 19

Define “metastatic niche”.

Answer 19

The tumour and host factors both define the “metastatic niche” for a particular tumour.

Question 20

State some uncommon sites of metastasis.

Answer 20

Kidney
Spleen
Skeletal muscle
Heart

Question 21

Explain the ability of cancer cells to deregulate cellular energetics.

Answer 21

Instead of aerobic metabolism.
Aerobic glycolysis can occur.
Much less efficient and requires more glucose for same amount of ATP.
Beneficial as it protects against a low oxygen environment.

Question 22

Describe the ability of cancer cells to avoid immune destruction.

Answer 22

Avoid detection (first of all) by not presenting their antigens on their surface.
They then produce proteins/ligands on the surface of cells, which, when attached to lymphocytes, inactivate them and the immune system as a whole.

Question 23

Describe the ability of cancer cells to enable replicative mortality.

Answer 23

They avoid the usual mechanisms for senescence, by attacking telomeres (ends of chromosomes that protect the chromosome from being frayed or tangled).