Cancer Flashcards

1
Q

Adenocarcinoma:

A

cancer arising from ductal or glandular structures

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2
Q

Anaplasia

A

absence of differentiation

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3
Q

Cancer

A

refers to a malignant tumor and is not a term used to refer to benign growths

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4
Q

Carcinogens

A

are substances that, when introduced into a cell, cause changes in the
structure and function of the cell that lead to cancer.

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5
Q

Carcinogenesis

A

production of cancer

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6
Q

Carcinoma

A

cancer arising from epithelial tissue

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7
Q

Leukaemia

A

Cancers from blood forming cells

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8
Q

Oncogene

A

Derived from a mutated porto-oncogene which now results in excessive and uncontrolled cell growth

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9
Q

Proto-oncogene

A

Normal gene that promotes cell growth

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10
Q

Sarcoma

A

Cancer from connective tissue

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11
Q

Tumour suppressor gene

A

Inhibits cell replication

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12
Q

What are the characteristics of benign neoplasms?

A

Resemble normal cells, don’t infiltrate, grow slowly, don’t metastasize, don’t recur after removal, localized issue, doesn’t cause tissue damage, and don’t cause death

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13
Q

What are the characteristics of malignant neoplasms?

A
  • cells often bear little
    resemblance to the normal
    cells of the tissue
  • infiltrates and destroys the
    surrounding tissue
  • rapidly growing
  • gains access to blood lymph to make mets
  • tends to recur when removed
  • generalized effects: anemia, fatigue, weightloss
  • causes death and tissue damage
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14
Q

What are the 3 basic units of DNA that make up nucleotides?

A
  1. Pentose sugar molecule (deoxyribose)
  2. Phosphate molecule
  3. Nitrogenous bases
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15
Q

What is the codon?

A

The protein coding DNA = are successive triplets of bases

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16
Q

What is the malignant transformation of cells?

A

An accumulation of mutations in a particular class of genes

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17
Q

What are the 2 gene classes that when mutated account for most controlled cell proliferation seen in cancer?

A
  1. Proto-oncogenes
  2. Tumour suppressor genes
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18
Q

What are the characteristics of cancer cells?

A
  1. Loose shape and boundaries
  2. Stop responding to growth-inhibiting signals
  3. Replicate uncontrollably
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19
Q

What does a tumor descend from?

A

A single precursor cell that has been transformed

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20
Q

What other carcinogens are hits that can cause normal cells to mutate?

A
  1. Hormonal
  2. Viral
  3. Occupational
  4. Environmental
  5. Behavioural
  6. Other/random
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21
Q

What are the 4 types of gene mutations that can occur to result in cancer?

A
  1. Point mutation
  2. Chromosome translocation
  3. Gene amplification
  4. Frame-shift mutation
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22
Q

What is a point mutation?

A

A single change to one base group?

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23
Q

What is a frame shift mutation?

A

a) An addition is added into a base group resulting in an inappropriate number of bases, no longer in triplets

b) OR a deletion occurred which makes it an inappropriate number of triplets

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24
Q

What is chromosome translocation?

A

A piece of one chromosome that is relocated to or swapped with a different part of the chromosome

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25
Q

What is an example of chromosome translocation?

A

Burkett’s lymphoma (B cell cancer)

  • Ig gene on chromosome 14 and MYC photo-oncogene on chromosome 8 are swapped

This results in HIGH rate of B cell proliferation

=

Increase chance of transcription error and development of cancer

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26
Q

What is gene application?

A

Over-expression or duplication of a piece of chromosome

27
Q

What is an example of gene amplification?

A

Breast cancer: Human epidermal growth factor 2(HER-2) gene becomes over expressed

=

cells in breast ducts grow and replicate outside of their normal boundaries

28
Q

What 3 factors contribute to gene mutation?

A
  1. Hereditary genetic error
  2. Exposure to carcinogen
  3. Exposure to a virus
29
Q

What is a hereditary genetic error and what are the 2 types?

A

An inheritance of altered gene from parent that passes on an increased risk but not guarantee of developing cancer

  1. Autosomal dominant
  2. Autosomal recessive
30
Q

What is autosomal dominant inheritance?

A

NO carriers, only one copy of allele is mutated for condition to result.

Gender dependent

31
Q

What is autosomal recessive inheritance?

A

Person can be a carrier and not be affected

32
Q

What are examples of viruses that can cause genetic mutations?

A
  1. Epstein Barr - burrito’s lymphoma
  2. HPV - cervical
  3. Hep B - liver
  4. Human T-cell leukaemia virus
33
Q

What are the two basic control systems to prevent a single cell from becoming cancer?

A
  1. Promotion of cell growth
  2. Safeguard systems`
34
Q

Describe the “promoting cell growth” system and what happens when it fails?

A

Proto-oncgenes are normal genes that encode proteins for cell growth and development

Damage or mutation of these genes results in ONCOGENES which flood cells to keep mutating inappropriately

35
Q

What are the 4 safeguard systems that help prevent a single transformed cell from becoming cancer?

A
  1. Tumour suppressor gene
  2. Mismatch repair gene
  3. Apoptosis
  4. Immune system
36
Q

Describe what occurs with the inactivation with the TSG

A

Tumour suppressor gene normally inhibits cells growth

Inactivation or damage prevents inappropriate cell growth

*TSG is a recessive gene

37
Q

What happens when the mismatch repair gene is inactivated?

A

Mismatch repair gene usually reads DNA sequences and repairs errors from replication

If this gets damaged/doens’t occur, errors don’t get fixed = mutation

38
Q

What happens when apoptosis fails?

A

Normal cell remove doesn’t occur and old damaged cells are allowed to continue replicating

39
Q

What happens with immune system dysfunction?

A

Cancer cell replication outpaces the immune system

Cancer cells will change their appearance and display self antigens

Cancer cells lose contact inhibition and start growing all wacky

40
Q

What 3 factors influence the local manifestations of cancer?

A
  1. Location of the tumour
  2. Size and distend ability of the space the tumour is occupying
  3. Surrounding structures
41
Q

What affects systemic manifestation of cancer?

A
  • If the cancer is a systemic or local type
  • Is a local type metastasized
42
Q

5 Steps of tumour spread

A
  1. Transformation of cell
  2. Growth of transformed cell
  3. Local invasion (mechanical pressure, lytic enzymes, motility)
  4. Dissemination into lymphatics and bloodstream
  5. Metastasis
43
Q

What happens during the transformation of an individual cell during tumour spread?

A

Individual cell undergoes mutation

44
Q

Explain the growth of the transformed cell step of tumour spread

A

The transformed cell starts to replicate immortally

Change in number but not in appearance

45
Q

What is replicative immortality?

A

Normal cell replicates through life cycle and dies. Cancer cells don’t die and keep replicating because the express the telomerase enzyme which prevents the telomere caps from falling off in older cells (telomeres get shorter and thats part of what kills a cell)

46
Q

What are the 3 components of local tissue invasion?

A
  1. Mechanical pressure
  2. Release of lytic enzymes
  3. Motility of the cancer cells`
47
Q

Explain the role of the ECM

A

The basement membrane (extracellular matrix) is critical in keeping tissue boundaries and cell to cell communication

Chemical signals from the ECM to the cells above let the cells know they are on home ground. If these cells inappropriately detach from the ECM, a cytokine message is sent resulting in apoptosis

48
Q

Explain mechanical pressure in local invasion?

A

Pressure builds up in local area (finger like projection), moves along the line of least mechanical resistance, increase in pressure will block capillary blood flow to local tissue

49
Q

Explain the lytic enzyme involvement in local invasion

A

Cancer cells secrete lytic enzymes to digest physical barriers to facilitate movement within a tissue or organ

Type IV Collagenase and plasminogen activator are the MOST important

50
Q

What is Type IV collegenase’s role?

A

Digests type IV collagen in the ECM in vascular and epithelial basement membranes

51
Q

What is plasminogen activator’s role?

A

Convert serum proenzyme plasminogen into protease plasmin which will degrade a variety of proteins

52
Q

Explain motility in local invasion

A

Cancer cells produce a cytokine called autocrine motility factor and produce a invadopodia that facilitate movement of cancer cells through basement membrane of tissues by grabbing onto fibronectin (like a fibronectin rock wall)

53
Q

Explain the dissemination of cancer cells into the lymphatic system and bloodstream

A

Cells will relocate through lymphatic or circulatory system

Tricks for travelling:
* clump together = harder to phagocytose
* Cover themselves in platelets so they don’t look foreign

Challenge for travelling:
* Turbulent blood flow which is why they clump together to increase chance of survival
* They have to encounter lots of immune cells in their journey

54
Q

Explain the metastatic establishment step

A

Local invasion tactics are re-used to leave the lymph or circulatory system (enzymes, motility, pressure)

Vascular endothelial growth occurs
- once tumour is bigger than 2cm it needs its own blood supply

Nutrition
- anorexia-cachexia syndrome: tumour induced starvation

Hormonal support:
- tumour uses body’s own hormones to stimulate growth

55
Q

Where does breast cancer usually metastasize?

A

Brain, lungs and bone

56
Q

Where does colon/bowel cancer metastasize?

A

Liver, bone

57
Q

Where does lung cancer usually metastasize?

A

Brain and bone

58
Q

Why is grading tumours important and what is it based on?

A
  • Grading and staging sets paramedics of the clinical gravity of the disease
  • Grading is based on the degree of differentiation of the cancer in comparison with tissue of origin
59
Q

Explain differentiation

A

process of a cell becoming progressively more specialized in function and
structure

60
Q

Explain poorly differentiated cancer cells

A
  • Mutated early in cell division
  • Little resemblance to tissue of origin
  • Harder to treat, more unpredictable, more AGG cancer
61
Q

Explain well differentiated cells

A

Look like tissue of origin, more predictable treatment wise and in their growth pattern

62
Q

What does the TNM system stand for?

A

Primary tumour and it’s extent
Regional lymph node involvement
Metastases

63
Q

What are tumour markers and what are they used for?

A

Proteins, enzymes and antigens in blood. Not all cancers have tumour markers.

They are used to screen high risk people for presence of cancer

Used for diagnosis and to identify primary origin of cancer

Monitor effectiveness

Check for recurrence