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Cell Bio > Moss - Cancer > Flashcards

Moss - Cancer Flashcards

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Biology 101 flashcards
1
Q

what is cancer?

A

cancer is fundamentally a genetic disease, and tumors develop through a process that resembles evolution and natural selection

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2
Q

how are cancer cells able to form?

A

cancer cells escape the normal growth controls on somatic cells and may compete with their neighbors for blood supply and space

they may move from their origins and grow elsewhere in the body

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3
Q

why are cancers likely to form more often than we are aware?

A

only a few tumors grow enough of be noticed and a subset of these may become dangerous

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4
Q

what are the different types of cancer?

A

neoplasm

benign tumor

malignant tumor

metastases

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5
Q

what is a neoplasm?

A

a tumor

a growing mass of abnormal cells

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6
Q

what is a benign tumor?

A

a tumor that remains a single mass, may be possible to remove by surgery

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7
Q

what is a malignant tumor?

A

a cancer

a tumor that can invade tissues

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8
Q

what is metastases?

A

secondary tumors that are the result of spreading of the primary tumor

not possible to remove by surgery alone

must use chemotherapy, radiation, or a combo of the three

tumor established at new site

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9
Q

what do tumors consume an abundance of?

A

glucose

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10
Q

what are tumors classified by?

A

their tissue of origin

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11
Q

what are the types of tumors that can be malignant?

A

carcinomas

sarcomas

leukemias

tumors of the nervous system

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12
Q

how many types of cancer are there?

A

more than 200

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13
Q

how many organs in your body can develop cancer?

A

more than 60

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14
Q

what is a carcinoma?

A

cancers arising from epithelial cells, about 90% of all tumors

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15
Q

what are sarcomas?

A

cancers arising from muscle cells, fat cells, bone, and blood vessels, or connective tissue

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16
Q

what are leukemias?

A

cancers arising from hematopoietic (blood) cells

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17
Q

why are about 90% of all tumors carcinomas/epithelial in origin?

A

they are the most rapidly turning over cells

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18
Q

what is the difference between a benign tumor and malignant tumor?

A
  • benign:
    • can be removed
    • contained within basal lamina
  • malignant tumor
    • break through the basal lamina and leak out
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19
Q

what can a primary malignant tumor do?

A

metastasize to another organ

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20
Q

what do the characteristics of a particular cancer reflect?

A

their cells of origin

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21
Q

what cancers easily metastasize?

A

melanomas

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22
Q

what can metastases of melanomas look like?

A

they may be pigmented like the melanocytes

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23
Q

how do melanocytes develop?

A

from migrating neural crest cells

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24
Q

what must happen for cancer to form?

A

mutations must occur in proliferating cells

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25
Q

TRUE or FALSE: Terminally differentiated cells are not likely to form tumors.

A

TRUE

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26
Q

what is the estimated number of cell divisions in the life of an inidivual?

A

1016

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27
Q

what contributes to cancer development

A

spontaneous mutation rate

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28
Q

what is the average spontaneous mutation rate?

A

10-6 per cell division

this is the rate without any environmental causes

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29
Q

what is likely to have happened to every single gene?

A

every single gene is likely to have acquired a mutation on more than 109 separate occasions in one cell or another

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30
Q

why doesn’t cancer occur more frequently?

A

it is hard for a mutant cell to become cancer because the body has preventative mechanisms to detect and stop it

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31
Q

what is cancer incidence a function of?

A

age

the curve is sigmoidal

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32
Q

TRUE or FALSE: A single mutation is not enough to cause a cancer

A

TRUE

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33
Q

what is one piece of evidence that more than one mutation is needed to create a cancerous cell?

A

Cancer incidence increases with age

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34
Q

what do cancers require to be malignant?

A

multiple genetic changes

perhaps 10 or more

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35
Q

how do cancers develop?

A

gradually from increasingly aberrant cells

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36
Q

TRUE or FALSE: Cancer may not appear until long after exposure to causative agent.

A

TRUE

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37
Q

how long can cancer develop after occupational exposure to asbestos? what kind?

A

30-50 years

mesothelioma

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38
Q

how long can cancer develop after heavy smoking? what kind?

A

10-20 years

lung cancer

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39
Q

how long can cancer develop after atomic bombs at Hiroshima and Nagaskai? what kind?

A

5 years

leukemias

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40
Q

what must happen to cancer cells to progress?

A

they must accumulate somatic mutations

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41
Q

how can mutations occur?

A

may occur due to the inherent error rate of copying DNA as cells divide

may run in families

Increased exposure to agents that cause mutations

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42
Q

what causes genetic instability in cancers?

A

point mutations

small insertions and deletions

chromosomal rearrangements

chromosomal translocations

duplications or deletions of while chromosomes (aneuploidy)

43
Q

what factors contribute to the genetic instability in cancers?

A

defects in DNA replication

defects i DNA repair

defects in cell-cycle checkpoints

errors in mitosis

44
Q

what do DNA maintenance genes do?

A

they affect DNA repair, fidelity of replication, chromosome alignment during mitosis, and chromosome stability

45
Q

what happens if a cell has a mutation in DNA maintenance genes?

A

cancers can develop

46
Q

what are DNA maintenance genes that people tend to have mutations in?

A

BRCA½

47
Q

what is the mutation rate in some cancer cells?

A

10-20 times the mutation orate of normal cells

48
Q

Cancer cells are characteristically…

A

genetically unstable

49
Q

what can be used to show the chromosomal abnormalities of cancers?

A

karyotyping

50
Q

what does tumor progression involve?

A

successive rounds of mutation and selection

51
Q

TRUE or FALSE: in cancer cells, each mutation increases chance of more mutations to to occur

A

TRUE

52
Q

what does sequencing more than 10,000 genes in a set of breast and colorectal cancers reveal?

A

that cancer cells have accumulated enough mutations to cause an amino acid change in the proteins of roughly 100 genes

53
Q

what does a subset of genes found to be repeatedly mutated in a particular type of cancer suggest?

A

that alterations in as many as 20 genes are needed to drive tumor progression

54
Q

what can cancer critical mutations cause?

A

increase rate of division

disables programmed cell death (apoptosis/autophagy)

decrease propensity for differentiation

prevent senescence due to stress and damage

affect any of the other characteristics of cancer cells

55
Q

what are the characteristics of cancer cells?

A
  1. reduced dependence on signals from other cells for survival growth and division
  2. increased tolerance for stress and internal derangement
  3. indefinite proliferation
  4. genetic instability
  5. increased invasiveness
  6. High need for nutrients
  7. survival and proliferation in abnormal locations
  8. ability to modify surrounding tissues
  9. escape from immune surveillance
56
Q

what does it mean that cancer cells have reduced dependence on signals from other cells for survival, growth, and division?

A

mutations activate these pathways inappropriately

57
Q

what does it mean that cancer cells have increased tolerance for stress and internal derangement?

A

the pathways for apoptosis are almost always defective

58
Q

what does it mean that cancer cells have indefinite proliferation?

A

normal cell shave limitations on the number of divisions thy undergo (cell senescence due to telomere shortening)

cancer cells don’t

59
Q

what does it mean that cancer cells have genetic instability?

A

once DNA repair mechanisms are damaged, mutations become more frequent

60
Q

what does it mean that cancer cells have increased invasiveness?

A

The loss of cadherins and other adherence molecules and the signals that they generate allows them to move

61
Q

what does it mean that cancer cells have high need for nutrients?

A

Cancer cells use glycolysis over OxPhos to make ATP

this is less efficient, but can work in oxygen-deprived tumor microenvironments

62
Q

what does it mean that cancer cells have survival and proliferation in abnormal locations?

A

the independence on extracellular signals and the lack of apoptosis remove the primary barriers from growth out of place

63
Q

what does it mean that cancer cells have ability to modify surrounding tissues?

A

Highly progressed cancers can remodel surrounding tissues and cause non-tumor cells to further support the tumor’s growth

uses blood vessels and growth factors as collaborators

64
Q

what does it mean that cancer cells escape from immune surveillance?

A

The immune system requires certain molecular markers to recognize and destroy aberrant cells, markers that the tumor cells suppress or eliminate

they are no longer recognized as aberrant cells

65
Q

what does cancerous growth often depend on?

A

defective control of cell death, cell differentiation, or both

66
Q

what do cancer-critical genes regulate?

A

cell proliferation

cell growth

DNA repair

cell death and survival

as well as other processes like (apoptosis, immune response, regulation of gene expression

67
Q

what are cancer critical genes?

A

mutated genes that continuously occur

not necessarily cancer causing

68
Q

what are oncogenes?

A

genes that actively cause cancer, usually a mutant form, genetically dominant (hundreds of different oncogenes)

69
Q

what are protoncogenes?

A

genes that when mutated can become oncogenes

not necessarily cancer

70
Q

what are tumor suppressor genes?

A

genes whose absence causes cancer

they normally prevent the formation of a cancer

genetically recessive

p53

71
Q

what are examples of genes whose function or expression is altered in cancers?

A

DNA repair genes

cell death genes

differentiation genes

cell cycle regulators

microRNAs

immune system function genes

72
Q

what are examples of cancer critical genes?

A

oncogenes

protooncogenes

tumor suppressor genes

73
Q

what mutated cancer gene is a dominant (gain-of-function) mutation?

A

oncogene

activating mutation enables oncogene to stimulate cell survival, proliferation, or both

74
Q

what mutated cancer gene is recessive (loss-of-function)

A

tumor suppressor

two activating mutations functionally eliminate the tumor suppressor gene, promoting cell survival, and proliferation

75
Q

what are the different ways to activate oncogenes?

A

mutation in coding sequence

gene amplification

chromosome rearrangement

76
Q

what is heterozygosity?

A

the possession of two different alleles of a particular gene or genes by an individual

77
Q

what is loss of heterozygosity (LOH)?

A

a cross chromosomal event that results in loss of the entire gene and the surrounding chromosomal region

78
Q

what are the different ways a tumor suppressor could be inactivated?

A

heterozygosity

loss-of-heterozygosity

79
Q

what are the possible ways of eliminating Rb Gene?

A

nondisjunction, causing chromosome loss

chromosome loss, then duplication

mitotic recombination

gene conversion

deletion

point mutation

80
Q

what happens if a healthy cell with only one normal Rb gene copy is mutated?

A

mutation of single healthy copy can cause total loss of healthy genes

81
Q

what is the important of APC to the inhibition of Wnt signaling?

A

when Wnt is off, the APC complex is active and Beta-catenin is degraded

(APC inhibits Wnt pathway)

when Wnt is on, APC complex is inactive and Beta-omega-catenin is released

(no APC Wnt pathway is overactive)

82
Q

what is familial adenomatous polyposis coli?

A

an inherited disease that predisposes someone to colon cancer

issue with APC gene

83
Q

how do colorectal cancers evolve?

A

slowly via succession of visible changes

84
Q

what is the progression from normal cell to metastasis?

A
85
Q

what can the steps of tumor progression often be correlated with?

A

specific mutations

86
Q

how is each case of cancer characterized?

A

by its own array of genetic lesions

87
Q

what do some colorectal cancers have defects in?

A

DNA mismatch repair

88
Q

what is a primary tumor?

A

the original tumor that gives rise to metastases

89
Q

when is a primary tumor normally detected?

A

usually not detected until it contains 109 cells

90
Q

what may be associated with a primary tumor?

A

non-cancerous cells like fibroblasts and blood vessels

91
Q

who discovered the Philadelphia Chromosome in CML?

A

Peter C. Nowell

David A. Hungerford

92
Q

how do we know tumors arise from single cells?

A

because they can have unusual mutations

93
Q

if all the cancer cells share the same unusual mutation…

A

they are very likely to be a clone

94
Q

what is the Philadelphia Chromosome Translocation?

A

found in patients with Chronic Myelogenous Leukemia (CML)

it is a translocation between chromosomes 9 and 22

95
Q

what do casual genetic changes in cancers mean?

A

they are more subtle and indicate clonal origin on most clonl

96
Q

what is the molecular result of the translocation of the Philadelphia Chromsome?

A

the generation of the Bcr-Abl fusion protein

97
Q

what is BCR-Abl?

A

it resembles Abl and Src

its primary cancer-causing feature is its unregulated expression

98
Q

what is Gleevec?

A

treatment for several tumors

development of the drug was dependent on a deep understanding of the molecular biology underlying the disease

99
Q

what can small molecules be designed to do?

A

inhibit specific oncogenic proteins

100
Q

How does Gleevex affect the action of Bcr-Abl and othert kinases?

A
101
Q

what is Gleevec effective against?

A

leukemias

melanoma

certain sarcomas

102
Q

what do immunotherapies that targetT cells do?

A

immunotherapies that target inhibitory regulation of T cells such as anti-PDI antibodies can cure otherwise incurable cancers

103
Q

what do anti-immune-checkpoint antibodies do?

A

they disinhibit cytotoxic T cells that recognize novel parts of proteins on cancer cells

104
Q

what does treatment with a monoclonal antibody (ipilimumab) on a patient with advanced metastatic melonoma do?

A

it binds the T cell protein CTLA-4

after 16 weeks, the tumors were smaller

by 72 weeks, they had essentially been eliminated

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