Cancer Flashcards

1
Q

Define benign

A

Non cancerous, remains encapsulated and the same cell type that it began as. Doesn’t invade surrounding tissues.

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

Define adenocarcinoma

A

Cancer that starts in glandular tissues that make fluid or mucus eg breast

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

Define proliferation

A

rapid reproduction of cells

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

Define angiogenesis

A

new blood vessels form from pre existing ones

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

Define oncogenes

A

Gene in certain circumstances can transform a cell into a tumour cell

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

Define neoplasm

A

Abnormal cells (tumour). Excessive, uncoordinated and persistent.

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

Define malignant

A

Cancerous. Neoplasm that is capable of invading surrounding tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define replicative immortality

A

Normal human cells can only grow and divide a number of times and undergo apoptosis when they are no longer needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define telomeres

A

compound structure at the end of chromosome

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

Define metastasis

A

development of secondary malignant growths at a distance from primary cancer site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Define proto oncogenes and oncogenes

A

Set of genes that normally code for proteins to start the cell cycle and cell proliferation. Oncogenes - activation on, in cancer cells oncogenes have been mutated to be constantly turned on to replicate cells, these are called oncogenes.

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

Define sarcomas

A

rare form of cancer which grows in connective tissues like bones

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

Define chemotherapy

A

cancer treatment used to kill cancerous cells

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

Define leukaemia

A

blood cancer

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

Define lymphoma

A

Group of blood and lymph tumours that develop from lymphocytes

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

What are the 6 stages of the pathophysiology of cancer

A

Unlimited proliferation, evading growth suppressors, resistance to cell death, replicative immortality, angiogenesis, invasion and metastasis

17
Q

Explain unlimited proliferation

A

Cell division without growth stimulatory factors (proto oncogenes), so continuous growth.

18
Q

Explain evading growth suppressors

A

Cancer cells do not respond to growth inhibitory signals, tumour suppressor gene is off

19
Q

Explain resistance to cell death

A

Evading cell death - evade apoptosis signals

20
Q

Explain replicative immortality

A

replicative potential of cancer cells, telomeres maintained

21
Q

Explain angiogenesis

A

Cancerous cells have alot of new mutations making the cell increase in size, so it will quickly run out of nutrients, oxygen and glucose and will have alot of waste to get rid of. The cells need new method of obtaining nutrients so cells encourage new blood vessel formation and triggers vascular growth.

22
Q

Explain invasion and metastasis

A

Cancer cells can move to other parts of the body

23
Q

Explain why benign tumours can cause problems

A

By compression of structures, blood vessels and nerves. Affects organs that secrete hormones that disrupt normal homeostasis.

24
Q

Where do haematological malignancies arise from ?

A

Blood and bone marrow cells

25
Q

Why are cancerous cells resistant to apoptosis ?

A

Mutational change in the genes that prevents apoptosis from naturally occurring.

26
Q

Explain replicative immortality

A

Normally when cell copies DNA you have protective ends on the DNA (telomeres) every time a cell copy is made, telomeres are shortened. Cells usually only have a certain amount of time they can be copied. In cancer mutations telomeres do not shorten or they are constantly getting longer which results in immortality of these cells.

27
Q

What is a risk of angiogenesis ?

A

Cancerous cells have a rich blood supply so there is a high risk of bleeding.

28
Q

Explain invasion and metastasis

A

Cancer cells can break away from primary tumour and be carried on the blood and lymphatic system. Cells must pass through the basement membrane. Move through the extracellular space and penetrate the basement membrane of blood or lymphatic vessel. Involves loss of adhesion between cells and release of enzymes that digest the basement membrane. Reaches new tissue and moves through basement membrane. In new tissues cancer cells go through angiogenesis.

29
Q

What are the risk factors for gene damage ?

A

Mutations occur in the normal process of cell division. The older we are the more cell division we made. Some tissues have more frequent cell division or constant replacement for eg GI tract. Therefore age and certain tissue types put us naturally at a higher risk

30
Q

What are some evidence based risk factors for cancer ?

A

Over 65, smoker, alcohol, UV, asbestos, radon, diet, physical activity

31
Q

What is the involvement in viruses and bacteria in cancer ?

A

Thought to influence development of cancer, causing genetic changes.

32
Q

Explain hereditary cancer, giving examples from TP53, BRCA1, BRCA2 and APC genes

A

Researchers have associated mutations in specific genes with more than 50 hereditary cancers which are disorders that may predispose individuals to developing certain cancers. Most commonly mutated gene in all cancers is TP53 which produces a protein that suppresses the growth of tumours. Inherited mutations in BRCA1 and BRCA2 genes are associated with hereditary breast and ovarian cancer syndrome, these genes are tumour suppressor genes when either of these genes acquire mutations cells are more likely to develop cancer
* BRCA1 and BRAC2 are inherited from either a mother or a father
* APC gene produces a protein that helps control how often a cell divides APC gene mutation can occur in colorectal cancer

33
Q

Explain Gleason’s pattern scale

A

Describe neoplasm in terms of cell abnormality, cancer cells exhibit degrees of differentiation, how well developed cancer cells are and how they are organised in the tissue

34
Q

Explain the difference between well and poor differentiated

A

Well - if cells and tissue structures are similar to normal
Poor - cells look abnormal and are more likely to invade surrounding tissue

35
Q

What are the 4 differentiating characteristics of cancerous cells ?

A

Staging - location and pattern of spread
Tumour - size and how far it has spread
Lymph nodes - whether it has spread to lymph nodes
Metastasised - spread to other parts of the body

36
Q

Explain chemotherapy process

A
  • Drugs act on different phases of the cell cycle
  • Directly interfere with DNA
  • Inhibit enzymes related to DNA synthesis
  • Destroy cell proteins
  • Cell cycle-specific – acting on cells undergoing division within the cell cycle
  • Mitotic poisons prevent spindle formation
  • Cell cycle non specific – cells in either dividing or resting phases
  • Alkylating agents that bind to DNA molecule disabling cell division
37
Q

What are the hallmarks of cancer ?

A

Acquired capabilities that allow cancer cells to survive, proliferate and spread.

38
Q

Explain cancer as a disease of dividing cells

A

All of our cells divide at different rates. In order for a cell to divide, cell needs signals to tell the other cell when to divide and when to stop. Every cell has DNA, parts of this DNA are called genes and these code for proteins. For a cell to become abnormal then something has to have grown wrong in the DNA. In cancer cells they have to have multiple genetic mutations