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UVic BIOL 360 - Fall 2019 > Cancer (ch 20) > Flashcards

Cancer (ch 20) Flashcards

1
Q

What percentage of Canadians will be diagnosed with cancer? Of that group, what percentage will die from it?

A

50% will be diagnosed and of these, 25% will die.

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2
Q

What percentage of deaths in Canada are reported to be due to cancer?

A

~30%.

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3
Q

What civilization was the first to treat cancer?

A

Ancient Egypt, treated with cauterization. Who would’ve thought?

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4
Q

Which Canadian province has the lowest incidence of cancer? What about the highest? Why might this be?

A

Lowest: BC
Highest: Nunavut
Probably due to lifestyle but maybe also a genetic component (Nunavut has large First Nations population).

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5
Q

What is an example of an environmental factor that has been shown to be causally linked to cancer?

A

Light at night (honours project woot woot).

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6
Q

Is the rate of cancer deaths projected to continue increasing in Canada?

A

No, it’s pretty much leveled off. Still increasing, but in proportion to population growth.

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7
Q

What might be a reason why cancer incidence rates are projected to increase over the next 20 years?

A

Risk of cancer increases with age, as there is a greater chance of accumulating gene mutations over time. Because we predict an ageing population, we also predict increased cancer incidence.

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8
Q

With regards to cancer pathology, what does TNM mean?

A

Tumour, Node, Metastasis.

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9
Q

Describe a Stage 0 cancer diagnosis.

A

A group of abnormal cells with the potential to develop into cancer in the future.

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10
Q

Describe a Stage 1 cancer diagnosis.

A

The cancer is small and contained within the organ it first started growing in.

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11
Q

Describe a Stage 2 cancer diagnosis.

A

The tumour is growing, but has not invaded other tissues. May have spread into adjacent lymph nodes.

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12
Q

Describe a Stage 3 cancer diagnosis.

A

The tumour is large and has invaded surrounding tissues and lymph nodes.

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13
Q

Describe a Stage 4 cancer diagnosis.

A

The cancer growth is advanced and has spread through the blood/lymph to distant sites in the body (i.e. metastatic cancer).

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14
Q

Why are some cancers detected earlier than others?

A

Some have common screening practices (breast, cervical) or are visually apparent (skin). Others are not screened for (lung) or are hard to diagnose.

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15
Q

Why is lung cancer more likely to be fatal than other cancers?

A

Because it is not screened for and often is not detected until it is in an advanced stage.

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16
Q

How many cells must make up a tumour before it is visible on x-ray?

A

10⁸ cells.

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17
Q

How many cells must make up a tumour before it becomes palpable (if possible)?

A

10⁹ cells.

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18
Q

How many cancer cells (on average) will lead to the death of a patient?

A

10¹² cells.

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19
Q

The incidence of _____ cancer has been increasing since 1985. What is this likely the result of?

A

Liver cancer. Results from chronic hepatitis infections as well as alcoholism, obesity, diabetes, smoking (obesity epidemic?).

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20
Q

How was it determined that stomach ulcers (a cause of stomach cancer) were the result of bacterial infection?

A

Cause of ulcers confirmed when Barry Marshall drank some Helicobacter pylori, developed ulcers, and then treated them with antibiotics. What a mad lad!

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21
Q

Why is it not practical to screen everyone who has stomach ulcers for cancer?

A

Because there’s a lot of people with ulcers but only a few of them will get cancer.

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22
Q

What are some viruses which are known to increase the risk of cancer?

A

Hepatitis, HIV, HPV etc.

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23
Q

What is a carcinoma?

A

A cancer arising from epithelial tissue. Common because epithelium replicates more frequently than other cell types, giving more chances for mutation.

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24
Q

What is a sarcoma?

A

A cancer arising from muscle and connective tissues.

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25
Q

What is the most common type of cancer? Why?

A

Carcinomas are the most common because epithelium replicates more frequently than other cell types, giving more chances for mutation.

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26
Q

What is a Leukemia/Lymphoma?

A

A cancer of the white blood cells/lymphocytes.

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27
Q

What 2 failures of proliferation can lead to tumour growth?

A
  1. Increased cell division but normal apoptosis

2. Normal cell division but decreased apoptosis

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28
Q

What differentiates a benign and a malignant tumour?

A

Benign: localized, don’t invade other tissues
Malignant: metastatic growth, invasion

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29
Q

How can cancers subvert normal replicative cell senescence?

A

By hijacking telomerase to keep adding to the telomeres.

30
Q

What percentage of cancer deaths are the result of metastatic cancer?

A

~90%.

31
Q

What fraction of cells survive metastasis to grow in a new area of the body?

A

1/1000. Those that do have enhanced survival ability and pass that on to the new tumour and future metastases.

32
Q

What are the 2 difficult barriers to cancer metastasis? What is the 1 easy barrier?

A

Difficult:

  1. Escape parent tissue
  2. Colonize remote site

Easy:
1. Travel through circulation

33
Q

Define “cooptive growth” as it relates to cancer.

A

A tumour exploiting existing blood vessels for nourishment.

34
Q

Define “angiogenic growth” as it relates to cancer.

A

A tumour creating its own blood vessels for nourishment.

35
Q

What percentage of tumour cells have the capacity to form a new tumour?

A

~1%.

36
Q

What is a “transit amplifying cell” with regards to cancer?

A

A tumour cell which has limited self-renewal capacity and will eventually die. Contrast with cancer stem cells which propagate indefinitely.

37
Q

Approximately how many genes must have mutations before cancer is likely to develop?

A

At least 5 different genes.

38
Q

Are tumours made up of only one kind of cell?

A

No, in addition to cancerous cells they can have endothelial cells, pericytes, etc. which support growth.

39
Q

How many cell divisions happen in the human body over the course of an average lifetime? What fraction of these cause a mutation?

A

10¹⁶. Only 1 in a million cause a mutation.

40
Q

In what 3 ways might genes be heritably inactivated, giving rise to cancer?

A

Accidental…

  1. Change in nucleotide sequence
  2. DNA packaging into heterochromatin
  3. Methylation of C nucleotides
41
Q

Are epigenetic changes to the genome heritable over generations? What is a caveat to this?

A

No. However, one cell can pass them to another cell through cell division.

42
Q

With regards to cancer pathology, what best describes a “driver” mutation?

A

A mutation in the cancerous cells which confers an ability of some kind or allows the cancerous cells to bypass some constraint.

43
Q

With regards to cancer pathology, what best describes a “passenger” mutation?

A

A side effect of genomic instability. Not conferring any advantage on the cancerous cells

44
Q

What are some examples of known carcinogens?

A

Arsenic, Asbestos, Aflatoxin, Ethidium Bromide, Radiation, etc.

45
Q

With regards to cancer pathology, what is the purpose of the Ames test?

A

To test whether a substance is a potential carcinogen.

46
Q

Describe the Ames test for potential carcinogens.

A

Mix His-dependent culture, compound, and liver extract. After incubation, stronger carcinogens will have caused more cells to become His-independent.

47
Q

Why is liver homogenate added to the culture used in the Ames test for potential carcinogens?

A

Carcinogens are often not harmful until they’ve been metabolized by the liver, so we add this to simulate biological conditions.

48
Q

Give an example of a known marker for chronic myeloid leukemia (CML).

A

The Philadelphia chromosome!

49
Q

In cancer pathology, do overactivity mutations have a dominant or recessive effect?

A

Dominant. A single mutation event creates the oncogene.

50
Q

In cancer pathology, do underactivity mutations have a dominant or recessive effect?

A

Recessive. Two mutations are needed to functionally deactivate the tumour suppressor gene.

51
Q

In what 4 ways can a proto-oncogene become an oncogene?

A
  1. Deletion/point mutation in coding sequence
  2. Mutation in regulatory sequence
  3. Gene amplification
  4. Chromosome rearrangement
52
Q

How can a deletion or point mutation in a gene’s coding sequence cause cancer?

A

By creating an abnormally hyperactive or constitutively expressed protein product.

53
Q

How can a mutation in a gene’s regulatory sequence cause cancer?

A

By greatly overexpressing the protein product.

54
Q

How can a gene amplification event cause cancer?

A

By greatly overexpressing the protein product.

55
Q

In what 2 ways can chromosome rearrangement cause cancer?

A
  1. Overproduction due to nearby regulatory region

2. Overproduction due to fusion with actively transcribed gene

56
Q

How are cancer cells most easily identified in culture?

A

They lost contact inhibition and start to grow all on top of one-another.

57
Q

How can we differentiate the energy production method of normal differentiated cells and cancer cells?

A

Normal: prefer oxidative phosphorylation for energy
Cancer: strongly favour lactate for energy

58
Q

What does the Warburg effect stipulate with regards to cancer pathology?

A

That cancer cells prefer to derive energy from lactate rather that the more efficient oxidative phosphorylation.

59
Q

Why is it far less common for people to develop a retinoblastoma in only one eye as opposed to both? Answer in terms of hereditary cancers.

A

Requires a double knockout (rare). However, many people who inherit a knockout of one gene will have retinoblastoma in both eyes because it only took one more knockout.

60
Q

If a maternal copy of a gene is already non-functional, what are some ways in which the paternal copy can be eliminated?

A
  • Nondisjunction (chromosome loss)
  • Loss then duplication (2 mutant copies)
  • Mitotic recombination
  • Gene conversion
  • Deletion
  • Point mutation
61
Q

Just know that the loss of tumour suppressor gene function can be from a combination of genetic and epigenetic changes.

A

Couldn’t think of a question, just know that it could be 2 epigenetic changes, 2 genetic changes, or a combination of both.

62
Q

When was the human genome sequence performed?

A

2000.

63
Q

From cancer genome sequencing, what comparisons can be made between oncogenes and tumour suppressor genes in terms of susceptibility to mutation?

A

Oncogene: many missense mutations in a few key areas

Tumour Suppressor: truncating mutations all over, missense mutations localized around regulator binding site

64
Q

What cancer does Imatinib (Gleevec) treat? How?

A

Chronic Myelogenous Leukemia (CML). Inactivates oncogenic kinase, preventing it from phosphorylating target.

65
Q

What intracellular signalling pathway is a common target for inhibitory anti-cancer drugs? What parts of this pathway are targeted?

A

The Ras-MAP kinase pathway. Almost all parts of the pathway are targeted (Receptor, Ras, Raf1, Mek, Erk, etc.)

66
Q

Why is multidrug treatment a common approach in cancer therapy?

A

A cell may be resistant to drug A or drug B. The cells have the potential to become resistant to A and B unless both are given simultaneously.

67
Q

How can immunological therapy be used to treat cancer?

A

By injecting antibodies that selectively target and poison cancer cells. Can also remove the immunosuppressive tumour environment.

68
Q

What can a sequence of a genome show us with regards to cancer pathology?

A

Whether there are gene amplifications (of new oncogenes) or gene deletions (of tumour suppressors).

69
Q

What will a DNA microarray show when used to identify cancer? What else is required?

A

Need to fluorescently label the normal and tumour tissue. Then on a microarray we can see distinct fluorescence in parts of the genome corresponding to cancerous or normal DNA.

70
Q

What are some examples of oncogenes?

A
  • Myc
  • IDH1 (isocitrate dehydrogenase 1)
  • FOXL2 (transcription factor)
71
Q

What 2 methods are most often used to identify tumour suppressor genes?

A
  1. Microarray analysis of healthy vs tumour tissue

2. Studying rare hereditary cancers

72
Q

What is the Philadelphia chromosome?

A

An aberrant chromosome associated with CML which is the result of faulty chromosomal translocation between chromosomes 9 and 22.

UVic BIOL 360 - Fall 2019 (10 decks)

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