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Cancer Biology > Chapter One > Flashcards

Chapter One Flashcards

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1
Q

What is the definition of cancer?

A

The unregulated growth of cells (division)

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2
Q

What is a tumor?

A

A tumor is an abnormal growth of cells.

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3
Q

Are all tumors cancerous?

A

No

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4
Q

What is the difference between benign and malignant?

A
  1. Malignant has an abnormal look while benign looks like the parent tissue
  2. Malignant are fast growing
  3. Malignant are not encapsulated while benign are localized and encapsulated
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5
Q

What is a neoplasm?

Hint: it is a synonym for another common term.

A

It simply means “new tumor”

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6
Q

What does the term transformation mean in the context of cancer?

A

It is the changing of a normal cell to a cancer/tumor cell.

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7
Q

What is an allele?

A

It is an alternate form of a gene

Some alleles can protect you from certain cancers while others can hurt you.

Example: Everyone has the BRACO1,2 gene which is used for DNA repair.

Only the people who have a mutation in this gene are at risk

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8
Q

What is the phenotype?

A

Phenotype is the look/function/makeup at a physical level that we see given a certain genotype

Genotype determines phenotype

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9
Q

What is morphology?

A

It is the study of the changes including cells, tissue and all the way down to the molecular level of DNA and genes changing.

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10
Q

What is metastasis?

A

It is the spread of tumor cells.

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11
Q

What is the difference between a primary tumor cell and a secondary tumor cell?

A

The primary tumor cell is the cell that started it all and the secondary tumor cells are the ones that spread form it.

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12
Q

What is the incidence rate?

A

The rate at which new cases are showing up.

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13
Q

What is the mortality rate?

A

It is the death rate of those who have particular cancer.

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14
Q

What is a mutagen?

A

something that causes a mutation in DNA

mutagens are also usually a carcinogen

*not always though. for example, sodium azide is only a mutagen, but does not cause cancer

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15
Q

What is a carcinogen?

A

something that causes cancer

carcinogens are usually mutagens

*not always though. For example alcohol does not directly cause a mutation, but it is a carcinogen

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16
Q

What is carcinoma? What percent of cancers does it make up?

A

It is the cancer of epithelial cells (the lining cells of organs)

It makes up more than 90% of cancers, the reasoning for this is because there are many, many cells involved.

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17
Q

What is a hematopoietic cancer?

What percent of cancers does this make up?

A

It is cancer that arises from the blood or blood-forming cells.

It makes up around 5% of cancers.

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18
Q

What are leukemias?

A

They are cancers that involve circulating immune cells. They are liquid cancers

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19
Q

What are lymphomas?

A

They involve (solid) lymphoid tumors

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20
Q

What are myelomas?

A

They are cancers that involve the bone marrow.

B-cells (create antibodies)

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21
Q

What are sarcomas?

A

They are cancers that arise from cells of muscle, bone and connective tissue.

cells of mesoderm derivatives

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22
Q

What are neuroectodermal cancers?

A

They arise from the cells of neuronal tissues.

cells of the ectodermal derivatives

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23
Q

What is the test for myelomas?

A

Test is to check for antibodies, because showing a ton would indicate that there may be a myeloma cancer

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24
Q

What fraction of people will be diagnosed with some type of cancer in their lifetime?

A

one third of people.

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25
Q

Why has stomach cancer decreased significantly?

A

Because of the event of refrigeration.

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26
Q

What was the initial dip in uterine cancers due to?

A

It was due to the increase of pap smears.

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27
Q

What was the most recent dip in uterine cancers a result of?

A

Vaccine for HPV

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28
Q

Why has incidence in cancer not really changes in a century?

A

Because people live longer.

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29
Q

How can we distinguish a cancer cell from a normal cell under the microscope?

A
  1. Loss of contact inhibition.
  2. Growth in low serum
  3. Round morphology
  4. No Anchorage Dependence
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30
Q

Explain the loss of contact inhibition in cancer cells.

A

Normal cells will stop division when in contact with other cells, a mechanism to keep tissues organized and ovoid overcrowding.

Cancer cells lose this ability and will proliferate even when in contact with other cells.

More specifically, cancer cells will grow past confluence. Confluence is a term that describes the extent at which a petri dish or flask is filled with cells.

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31
Q

Describe what is meant when cancer cells “grow in low serum”.

A

Serum is the part of blood without the cells.
This includes things like antibodies, drugs, nutrients, and proteins.

Cancer cells will grow in low serum. “They survive on their own”.

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32
Q

What is meant by cancer cells have a round morphology?

A

Normal cells are not round in the typical sense. Cancer cells do not look like their parent cells.

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33
Q

What is meant by anchorage independence in cancer cells?

A

Normal cells need to be anchored to something in order to facilitate normal division. If they are not attached they may undergo apoptosis.

Cancer cells have anchorage independence; they can divide and they don’t need to be attached to something.

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34
Q

What is anoikis?

A

Anoikis is a form of apoptosis where cells undergo programmed cell death when they are not attached to the extra cellular matrix or lose attachment to other cells.

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35
Q

What distinguishes a cancer cell at the cellular level?

A
  1. They have unregulated cell growth
  2. They have different surface proteins
  3. They have high mutation rate of DNA
  4. They have mechanisms that inhibit apoptosis
  5. They have the ability to travel
36
Q

Growth signal autonomy is one of the hallmarks of cancer. What does it mean?

A

Cancer cells do not require a growth factor signal and they have messed up cell cycles in other ways.

37
Q

Evasion of growth inhibitory signals is one of the hallmarks of cancer. What does it mean?

A

It means even when inhibitory proteins are present the cell will continue replicating.

38
Q

Avoiding Immune destruction is one of the hallmarks of cancer. What does this mean?

A

It means that cancer cells are adept enough to avoid destruction by the immune system. Even though they are damaged “self cells” some evade destruction.

This hallmark is emerging.

39
Q

Unlimited replicative potential is one of the hallmarks of cancer. What does this mean?

A

Because cancer cells have mechanisms to replace telomeres, the chromosome never shortens and the cell can replicate indefinitely.

40
Q

Tumor promoting inflammation is one of the hallmarks of cancer. What does it mean?

A

It is inflammation that we think of that ultimately leads to the other hallmarks of cancer.

This hallmark is enabling.

41
Q

Evasion and metastasis is one of the hallmarks of cancer. What does it mean?

A

It means that cancer can move an invade other tissues.

42
Q

Angiogenesis is one of the hallmarks of cancer. What does it mean?

A

When cancer grows, the interior of tumors can become hypoxic and the cells will facilitate (by one way or another) the creation of new vessels, to provide oxygen as well as to remove wastes.

43
Q

Genome instability and mutations is one of the hallmarks of cancer. What does this mean?

A

It means that the entirety of the genome can become unstable and susceptible to mutations. It leads to other hallmarks of cancer.

This hallmark is enabling.

44
Q

Evasion of cell death is a hallmark of cancer. What does this mean?

A

It means that cancer cells have ways to avoid apoptosis

45
Q

Reprogramming energy metabolism is one of the hallmarks of cancer. What does this mean?

A

It means that cancer cells change how they harvest energy to suit their needs. One way is that they solely use glycolysis even though they are often in the presence of high oxygen levels.

It is similar to how anaerobic metabolism works.

This hallmark of cancer is emerging.

46
Q

Name and explain the three ways that DNA may be altered in tumor cells.

A
  1. Point mutations - switching the base pairs at one base within the DNA.
  2. Deletions - the elimination of a part of a gene or DNA.
  3. Translocation - switching the location of chromosome’s pieces.
47
Q

After many divisions occur, more and more mutations will be present. What does this tell you?

A

That mutations accumulate over time.

48
Q

What is the most studied translocation? What does it involve?

A

It is the Philadelphia chromosome.

It happens when normal chromosome 22 which contains the BCR gene breaks at this location and normal chromosome 9 which contains the ABL 1 gene and the pieces connect forming the phili chromosome.

49
Q

Are most mutations somatic, or germ-line mutations?

A

Most are somatic.

50
Q

What is obvious if a mutation is involved in the sex cells?

A

The mutation, and cancer (if that mutation causes cancer) would cause all the cells of the offspring to be highly predisposed to cancer.

51
Q

Where do all cells in a tumor come from?
What is this called?

A

They come from a single primary tumor cell that had many mutations.

This is called clonal development.

52
Q

How can clonal evolution be compared to darwinian evolution?

A

Because we have so many cells in our body, only one needs to be transformed.

The changes that occur in the transformed cell follow a similar process of darwinian evolution by which the most adapted to the cancer’s goals are the ones that survive.

53
Q

What are the processes that contribute to net cell number?

A
  1. Cell proliferation - how many are cells dividing?
  2. Apoptosis - is the programmed cell death working?
  3. Differentiation - are cells specifying into what they should become?

note cells that are completely differentiated cannot divide and enter G0

54
Q

Why is differentiation so important?

How to oncologists use these facts to help in therapy?

A

Because if differentiation of a stem cell or a precursor cell is inhibited, it can cause those cells to proliferate in excess.

They use differentiation therapy to force cells into what they should become to (in theory) avoid that mass proliferation as stem cells.

55
Q

What are oncogenes?

What is constitutive activation?

A

Oncogenes are mutated genes whose protein products are produced in higher amounts AND have increased activity.

Constitutive activation describes when proteins are constantly on ( whether that be from bypassing regulatory mechanisms or something else). It is common in oncogenes.

56
Q

Are oncogenes dominant or recessive? Describe.

A

They act in a dominant manner to initiate tumor growth. Only one of the alleles needs to have the mutation.

57
Q

What is a proto-oncogene?

A

It is a normal gene that has the potential to become oncogenic.

These are genes that are responsible for cell growth and they need to be expressed, but they must be regulated.

58
Q

What is a tumor suppressor gene?

A

It is a gene that codes for a protein that inhibit growth and tumor formation.

59
Q

Do tumor suppressors act in a dominant or recessive way? Describe.

A

They act in a recessive manner.

This means that both alleles must mutated for there to be a loss of function in these proteins.

60
Q

What is haploinsufficiency?
How did this debunk Knudson’s hypothesis?

A

It refers to the possibility that when only one of the alleles is mutated, only half the proteins are produced and this can lead to cells to function improperly.

Ex. This can lead to cancer if it is true about the tumor suppressor gene.

Let’s say that the tumor suppressor gene is responsible for regulating DNA repair, and only half the proteins are produced, well then it only has half the capacity to suppress.

It debunked the 2 hit hypothesis

61
Q

What is Knudson’s two hit hypothesis?

A

He thought that you must have a mutation on both alleles for tumors to develop.

62
Q

What is a stem cell?

A

It is a cell that is undifferentiated, can self renew, and produce differentiated progeny.

63
Q

Why may stem cells be the starting point for cancer?

A
  1. They both rely on self-renewal programs
  2. Stem cells are typically proliferating
64
Q

What are the factors that play a role in carcinogenesis?

A
  1. Environment
  2. Diet and exercise
  3. Reproductive life
  4. Smoking
  5. Others (including drinking alcohol)
65
Q

Are people doomed to get cancer?

A

NO - half of cancers are preventable

66
Q

Exposure to sun can cause cancer.
Give a specific example.

A

It damages DNA

Can cause pyrimidine dimers - Cytosine and Thymine bind covalently to their copy (T-T)

This can lead to mutations if it is not properly repaired.

67
Q

Why did nuns get breast cancer more frequently?

A

Could be for a variety of reasons, but one major reason is because people who have children experience changes in their breast tissue to produce milk.

This differentiates cells, which means in nuns there is a higher proliferation of cells that are not differentiated.

68
Q

How is diet correlated with cancer?

A

Local risk for cancer is strongly correlated with diet.

Example is that Japanese men can reduce their risk for stomach cancer when they move to the US.

Could have to do with salt consumption or preserved foods.

69
Q

What is an example of how environment can cause cancer?

A

Exposure to UVB rays can cause damage in DNA - pyrimidine dimers - Adenine to Adenine Thymine to Thymine. This causes a distortion in the DNA helix, and if not repaired properly, can result in mutation.

70
Q

It is known that both chronic alcohol consumption as well as smoking can increase your risk for cancer. What is the synergistic effect of cancer incidence with drinking and smoking?

A

The risk is not additive.
If smoking and chronic alcohol consumption each increase your risk for certain cancers by 10%, the new risk is not 20%, but 40!

71
Q

What are other factors that increase the risk for cancer?

A
  1. DNA replication errors.
  2. By products of metabolism (reactive oxygen species)
72
Q

What are the four ways in which cancer is typically treated?

A
  1. Surgery
  2. Radiation
  3. Chemotherapy
  4. Immunotherapy (new)
73
Q

Taxanes are a class of drugs used in chemotherapy. What do they do?

A

They mess with microtubules, preventing cell division. This will force the cell to hopefully undergo apoptosis.

74
Q

What are the basic problems with chemotherapy?

A

They have effects on other cells as well.

Ex. Wound healing goes down.

75
Q

What are some other ways that cytotoxic chemotherapy target dividing cells to eventually induce cell death?

A

They can damage the DNA so badly that replication/division cannot happen.

They can interfere with the production of purine nucleotides

They can form covalent intra-strand bonds that prevent division

They can target growth signal pathways.

76
Q

Give some basic examples of how immunotherapy works.

A
  1. Could mess with the hormone levels for cancers that are hormone specific. (certain cancers grow in response to hormone levels)
  2. They can target proteins that act as important receptors for the tumor. This is known as monoclonal antibodies MAB
  3. They can be prophylactic meaning they are given to prevent cancer, as well as therapeutic for cancers that are currently there.
77
Q

What is the therapeutic index?

A

It is the value of the difference between the minimum effective dose and the maximum tolerated dose.

When the value is large, it can be very effective.

78
Q

In the most basic way, how do clinical trials work?

A

phase 1: safety
phase 2: efficacy and safety
phase 3: efficacy against conventional treatments

number of participants goes up with each phase.

79
Q

What are protein kinases?

A

They add a phosphate to a hydroxyl group on specific amino acids like serine, threonine and tyrosine

80
Q

What are protein kinases involved in?

A
  1. Cell cycle progression
  2. Signal transduction
  3. Transcription
81
Q

What is the Ras family of genes?

A

They help transmit signals from receptors to the inside the cell - involved in cell cycle regulation (PDGF involved)

Seen in proto-oncogenes and are mutated in more than half of certain cancers.

82
Q

What is tumor protein p-53

A

It is responsible for tumor suppression. It arrests the cell cycle when cell is stressed (DNA gets damaged) to give the cell time to re-cooperate

When it is mutated, DNA repair can be inhibited and that is a big issue.

83
Q

What is Rb (retinoblastoma) gene?

A

it is also a tumor suppressor gene that inhibits the cell cycle’s progession.

84
Q

How has the human genome project created the need for personalized medicine?

A

Because we can identify and treat mutations in certain genes, one therapy for someone will be completely useless for someone else.

85
Q

What are genome-wide association studies?

A

Studying the entire genome, for common variants to determine if there is a link between changes in one letter of the sequence and cancer.

It is really hard to determine causality.

Cancer Biology (11 decks)

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