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Cell Biology > Chapter 20: Cancer Overview > Flashcards

Chapter 20: Cancer Overview Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

cancer results from the breakdown of

A

normal regulatory mechanisms that govern the cell

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2
Q

in cancer what results from accumulated abnormalities in multiple cell regulatory systems?

A

loss of growth control

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3
Q

define tumor

A

any abnormal pproliferation of cells

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4
Q

characteristics of a benign tumor

A
  • remains confined to original location
  • no invading/ spreading to distant body sites
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5
Q

characteristics of a malignant tumor

A
  • capable of invading healthy tissue
  • capable of metastasis
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6
Q

what are the 3 basic types of cancer?

A
  1. carcinomas
  2. sarcomas
  3. leukemias/lymphomas
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7
Q

carcinomas are malignancies of

A

epithelial cells

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8
Q

sarcomas are solid tumors of

A

connective tissues

muslce, bone, cartilage, fibrous tissue

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9
Q

tumors are further classified according to

A
  • tissue of origin
  • type of cell involved
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10
Q

provide 2 examples of cancers that describe the type of cells involved

A
  • fibrosarcomas: fibroblasts
  • erythroid leukemias: precursors of RBCs
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11
Q

most cancers develop late in life…why?

A
  • cells become malignant
  • mutations accumulate over time
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12
Q

normal tissue is a composite of cells in which different X chromosomes have been

A

inactivated

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13
Q

as normal tissue cells proliferate each displays the same patterm of X activation…what is it?

A
  • X1: inactive
  • X2: active
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14
Q

tumors begin to develop from a

A

single initially altered cell

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15
Q

what are the 4 types of growth patterns?

A
  1. hypertrophy
  2. hyperplasia
  3. dysplasia
  4. neoplasia
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16
Q

characterists of hypertrophy

A
  • increase cell size
  • normal organization
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17
Q

characteristics of hyperplasia

A
  • increase cell #
  • normal organization
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18
Q

characteristics of dysplasia

A

disorganized growth

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19
Q

characteristics of neoplasia

A
  • disorganized growth
  • net increase in dividing cells
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20
Q

what are the 3 stages of carcinogenesis?

A
  1. initiation
  2. promotion
  3. progression
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21
Q

the initiation stage of carcinogenesis constitutes…

A

a mutation

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22
Q

as a tumor progresses it increases its

A

growth rate & malignancy

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23
Q

what is an examples of tumor progression?

A

colon carcinoma

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24
Q

the proliferation of colon epithelial cells give rise to a small benign

A

adenoma/polyp

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25
Q

colon selection leads to

A
  • adenoma growth
  • increase size
  • increase proliferative potential

malignant carcinoma

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26
Q

what are the 8 characteristics of cancer?

A
  1. density-dependent inhibition
  2. reduced dependence on GFs
  3. abnormal/blocked differentiation
  4. reduced cell adhesion
  5. angiogenesis
  6. protease secretion & metastasis
  7. resistance to apoptosis
  8. capacity for unlimited replication
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27
Q

describe density-dependednt inhibition

A
  • normal cells multiply until they reach an optimal density
  • tumor cells continue to proliferate uncontrollably
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28
Q

normal fibroblast cell migration is self-limited by

A

cell contact

tumor cells are not inhibited by cell contact

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29
Q

in leukemic cells differentiation is blocked at a stage where they still have the ability to

A

continue proliferating

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30
Q

what facilitated metastasis?

A

reduced cell adhesion

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31
Q

malignant cells secrete proteases that digest

A

extracellular matix components allowing invasion into connective tissue, blood vessels, lymphatic ducts

32
Q

resistance to apoptosis is often caused by a

A

pathway mutation

33
Q

the capacity for unlimited replication is a result of

A

telomerase expression

34
Q

focus assay takes advantage if what 3 properties of transformed cells?

A
  1. altered morphology
  2. loss of contact inhibition
  3. loss of density-dependent inhibition
35
Q

list some examples of carcinogens

A
  • UV radiation
  • chemical toxins
  • mutagens
  • tumor promoters
  • viruses
36
Q

UV radiation is likely to cause

A

skin cancer

37
Q

list 4 examples of chemical toxins

A
  1. tobacco
  2. asbestos
  3. benzenes
  4. aflatoxin
38
Q

mutagens damage

A

DNA

39
Q

list examples of tumor promoters

A
  • phorbol esters
  • endocrine disruptors
  • hormones
40
Q

what are the steps of tumor viruses in permissive cells

A

virus replication
cell lysis
release of virus particles

41
Q

what are the steps of tumor viruses in non-permissive cells

A

virus replication
some cells are permanently transformed

42
Q

80% of human cancers are NOT induced by

A

viruses

43
Q

what is considered the prototype of a highly oncogenic retrovirus

A

RSV

44
Q

studies of RSV lead to the

A

identification of the first viral oncogene

45
Q

what are the 4 things found in RSV genones?

A
  1. virion structural proteins
  2. reverse transcriptase integrase
  3. envelope glycoproteins
  4. Src tyrosone kinase
46
Q

what are the 3 genetic sources of cancer?

A
  • oncogenes
  • tumor suppresor genes
  • DNA repair genes
47
Q

what are known as the accelorators in cancer

A

oncogenes

48
Q

what are known as the brakes in cancer?

A

tumor suppresor genes

49
Q

what are known as the mechanics of cancer?

A

DNA repair genes

50
Q

oncogenes are normally

A

growth promoting

51
Q

oncogenes as a normal gene is called

A

proto-oncogene

52
Q

oncogenes when mutated induce

A

transformation

53
Q

oncogenes can be

A

viral or cellular

54
Q

tumor suppressor genes when mutated can NOT arrest

A

proliferation

Rb, p53

55
Q

human oncogenes are usually homologous of

A

viral counterparts

56
Q

oncogenes result from

A
  • single point mutations
  • chromosomal translocations

genes of regulatory mechanisms Ras

57
Q

DNA extracted from human bladder carcinoma induced the

A

transformation of transfected mouse cells in culture

58
Q

Ras mutants cannot carry out

A

GTP hydrolysis

results in constitutively active protein

59
Q

what is the single point mutation of Ras

A

Gly is substituted for Val

60
Q

oncogenes proteins act as

A
  • GFs (EGF)
  • GF receptors (ErbB)
  • intracellular signaling molecules (Ras/Raf)
61
Q

Ras/Raf oncogenes constitutively activate the

A

ERK MAP kinase pathway

62
Q

describe the translocation of c-myc

A

proto-oncogene is translocated from C8 to the IgH on C14

63
Q

the translocation of c-myc results in

A

Burkitt’s lymphoma

malignancy of antibody producing B cells

64
Q

Tel/PDGF oncogene encodes a fusion protein where the extra-cellular domain of the normal receptor is replaced by the

A

Tel transcription factor

65
Q

in Tel/PDGF oncogene activation the helix-loop-helix induces

A

dimerization of PDGFr & continuous activation of the protein kinase

66
Q

what is the prototype of a tumor suppressor gene

A

Rb

67
Q

tumor suppressor genes target

A

cyclin D/Cdk4,6

68
Q

tumor suppresor genes where first identified as the product of a gene responsible for

A

retinoblastoma

69
Q

unphosphorylated Rb binds to the

A

E2F transcription factor

70
Q

Rb binding to the E2F transcription factor prevents

A
  • transcription of genes for DNA replication
  • passage through the G1 checkpoint into S phase
71
Q

phosphorylated Rb cannot bind

A

E2F

72
Q

E2F then activates

A

gene transcription triggering the onset of S phase

73
Q

when retinoblastoma is hereditary the 1st mutation is already present in the

A

germ line

74
Q

when retinoblastoma is nonhereditary the 1st mutation is present after the

A

first somatic division

75
Q

what are characteristics of retinoblastoma?

A
  • thickening of optic nerve
  • displaced retina

Cell Biology (12 decks)

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