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Molecular Cell Biology > Cancer > Flashcards

Cancer Flashcards

1
Q

definition of tumor

A

purposeless overgrowth of any cellular component

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2
Q

hyperplasia

A

physiological proliferative increase in number of cells

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3
Q

dysplasia

A

change in phenotype (size, shape and organization of tissue

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4
Q

neoplasia

A

abnormal proliferation, tumor

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5
Q

hypertrophy

A

increase in cell size

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6
Q

benign

A

tumors localized and of small size

Ex: warts

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7
Q

WHat delineates the extent of a benign tumor?

A

fibrous capsule

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8
Q

malignant

A

grow and divide more rapidly than normal, fail to die at the normal rate, or invade nearby tissue without significant change in proliferation rate

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9
Q

incidence of epithelial origin of cancers

A

85%

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10
Q

glandular (breast, colon, liver..)

A

adenoma, adenocarcinoma

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11
Q

adenoma

A

glandular benign

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12
Q

adenocarcinoma

A

malignant glandular

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13
Q

covering (skin, lungs, cervix…)

A

squamous cell papilloma, squamous cell carcinoma

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14
Q

squamous cell papilloma

A

benign covering

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15
Q

squamous cell carcinoma

A

malignant covering

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16
Q

epithelial b/m

A

oma/carcinoma

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17
Q

supporting tissue b/m

A

oma/sarcoma

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18
Q

bone (osteoblast)

A

osteoma/osteosarcoma

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19
Q

osteoma

A

benign bone

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20
Q

osteosarcoma

A

malignant bone

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21
Q

Striated muscle

A

rhabdomyoma/rhabdosarcoma

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22
Q

rhabdosarcoma

A

malignant striated muscle

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23
Q

rhabdomyoma

A

benign striated muscle

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24
Q

smooth muscle

A

leiomyoma/leiomyosarcoma

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25
Q

leiomyoma

A

benign smooth muscle

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26
Q

leiomyosarcoma

A

malignant smooth muscle

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27
Q

hematopoietic

A

/leukemia

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28
Q

erythrocytes

A

erythrocyte leukemia

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29
Q

erythrocyte leukemia

A

erythrocyte

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30
Q

Lymphocyte

A

Lymophocyte or lymphocytic

leukemia

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31
Q

bone marrow

A

myeloma or myeologenous leukemia

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32
Q

no benign version

A

erythrocytes, lymphocytes, BM

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33
Q

astrocytes

A

astrocytoma/glioblastoma

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34
Q

astocytoma

A

astrocytes benign

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35
Q

glioblastoma

A

astrocyte malignant

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36
Q

melanocytes

A

mole/melanoma*

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37
Q

mole

A

benign melanocytes

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38
Q

melanoma

A

malignant melanocytes

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39
Q

micro-anatomical changes

A
  1. lack of differentiation
  2. abnormal nucleus
  3. abnormal chromosome
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40
Q

anaplasia

A

dedifferentiation or lack of differentiation

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41
Q

pleomorphic

A

variation in size or shape

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42
Q

FISH

A

paints chromosome

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43
Q

Behaviorial characteristics of cancer cells

A
  • ability to proliferate indefinitely
  • resistance to apoptosis
  • anchorage-independent growth
  • loss of contact-inhibition
  • decreased requirement for growth factors
  • increased metabolism
  • form tumor in lab animals
  • loss of cell-cell adhesion
  • invasion and metastasis
  • escape from immune surveillance
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44
Q

PET scan

A

can see metabolism

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45
Q

monoclonal theory of cancer origin

A

arise from a single cell of origin

any cell could create tumor

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46
Q

cancer stem cell theory of cancer origin

A

relies on the fact that a lot of tumors are heterogenous (vary by phenotype and functions)
ONLY CSC CAN CREATE TUMOR

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47
Q

both origin theories

A

clonal evolution regulated by cancer stem cells

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48
Q

tumor cells and stem cells

A 
share many similarities
self-renewal
differentiation
active telomerase expression
anti-apoptotic
ability to migrate
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49
Q

evidence of monoclonality

A

X-chromosome inactivation patterns
Use of starch gel electrophorsis to resolve the two forms of G6PD showed that all of the cancer cells in a tumor arising in a G6PD heterozygous patient express one or the other

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50
Q

additional evidence of monoclonality

A

unusual translocation involves exchange of segments between two separate (nonhomologous) chromosomes - all of the cancer cells carry the identical rare translocation - > monoclonality

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51
Q

differences of incidence by area of the world

A

suggests strong environment involvement

52
Q

What causes cancer?

A
  1. chemical agents
  2. radiation (UV, ionizing)
  3. infectious agents (virus)
  4. heredity
53
Q

carcinogens vs mutagens

A

carcinogens are mutagens

54
Q

test mutagens

A

Ames test

55
Q

Ames test for gauging mutagenicity

A

liver is homogenized - releasing the enzymes that can metabolically activate a chemical to mutagenic form

  • mixed with test compound
  • add to Salmonella bacteria unable to grow w/o histidine in culture
  • count colonies
56
Q

Rous’s protocol for inducing sarcomas in chickens

A

Removed sarcoma from breast muscle of chicken
- pass through fine pore filter
- filtrate into wing web of a young chicken
- sarcoma*
Therefore, VIRUS.
RSV

57
Q

transformation

A

conversion of a normal cell into a tumor cell could be accomplished with RSV

58
Q

three major types of viral proteins

A

env - glycoprotein spike (adsorb to cell surface)
gag - protein coat of core proteins
pol - specify reverse transcriptase molecules

59
Q

temperature sensitive mutant and the maintance of transformation by RSV

A
  • infected at permissive temp (transformed)
  • shifted to non permissive (normal)
  • back to permissive temp (transformed again)
    Thus, temp sens viral protein must be active to transform cell.
60
Q

viruses containing DNA molecules

A

are also able to induce cancer

61
Q

Important discoveries of viruses and cancer

A
  1. transformed cells integrate viral genome
  2. Some viral genomes have genes that can transform cells (these have no function in viral replication)
  3. transforming genes have counterparts in host cells
  4. often viral oncogenes are mutated and hyperactive
  5. cellular proto-oncogenes can also be activated by insertion of slowly transforming retrovirus lacking oncogenes (insertional mutagenesis)
62
Q

nude mice in testing tumorigenicity

A
  1. lack thymus/immunocompromised; receptive to engrafted cells
  2. hairless - easy to monitor closely the progress of tumor formation
63
Q

oncogenes

A

gene with the potential to cause cancer

gain of function drives toward cancer

64
Q

proto-oncogene

A

gene that can become an oncogene if mutated or expressed at high levels

65
Q

insertional mutagenesis

A

cellular proto-oncogenes can also be activated by insertion of slowly transforming retrovirus lacking oncogenes

66
Q

tumor supressor gene

A

loss of function

67
Q

two categories of cancer-critical mutations

A

dominant (oncogene)/recessive (tumor suppressor gene)

68
Q

conversion of protooncogene to oncogene

A
  1. deletion or point mutation - hyperactive protein made in normal amounts
  2. regulatory mutation - normal protein overproduced
  3. gene amplification - normal protein overproduced
  4. chromosome rearrangement
    a. normal protein overproduced
    b. hyperactive protein
69
Q

Screening of oncogenes

A

transfection

  • DNA extracted from cancer cells
  • DNA uptake by cells
  • if has oncogene, result in tumor formation
70
Q

Cloning of transfected oncogenes

A

Southern blotting
Alu sequence probe, ones that were transfected successfully were oncogenes in the mouse
-genomic library and DNA clone could be identified

71
Q

cloned proto-oncogene

A

no transfection

72
Q

cloned oncogene

A

transfection

73
Q

localization of an oncogene-activating mutation - point mutation - Ras

A

endonuclease with a protooncogene

until you get a fragment that transfects the proto-oncogene

74
Q

activating mutant of Ras…

A

fails to hydrolyze GTP

75
Q

Sos

A

Ras GEF

76
Q

Grb2

A

bridging protein of Sos to ligand-activated growth factor receptors due to two SH3 domains
bind to proline rich domains of Sos

77
Q

Two bridging proteins of Sos

A

Grb2 and Shc

78
Q

Ras/Raf/MAP kinase pathway

A

Ras->Raf->MEK->ERK (MAPK)

- Fos and Jun Tx factors, associate with one another to form AP-1, found in hyperactive cancer cells

79
Q

translocation

A

fuse a region from one chromosome with another region from a second, unrelated chromosome

80
Q

ongenic activation of myc

A
  1. gene amplification
  2. insertional mutagenesis (WT mys locus, but under foreign promoter
  3. chromosomal translocation
81
Q

myc driven under

A

IgH promoter - Burkitt’s lymphoma

82
Q

truncated growth factor receptor causing

A

deregulated firing

Ex: truncated EGF receptor in breast

83
Q

structural changes in protein

A

can also lead to oncogene activation

84
Q

conceptualized existence of tumor suppressor genes by

A

cell fusion

  • tumorigenic - dominant
  • not - recessive
85
Q

Rb (retino blastoma)

A

first identified tumor suppressor gene

86
Q

genetic mech that cause Rb

A

hereditory - every one has one missing

nonhereditory - all cells contain functional…both are lost or inactivated

87
Q

elimination of WT Rb gene copies

A

LOH

88
Q

loss of heterozygosity

A

from mitotic recombination/crossing over

89
Q

p53

A

tumor suppressor

suppresses Ras induced transformation of fibroblasts

90
Q

mutant p53

A

has dominant negative function

91
Q

accumulation of p53

A

cell-cycle arrast, DNA repair, block angiogenesis, apoptosis

92
Q

p53 controlled by

A

Mdm2 - causes p53 proteolysis

93
Q

p53 targets

A

p21 (cell cycle inhibitor)

PUMA (pro-apoptotic)

94
Q

ARF

A

binds to Mdm2 and blocks p53 degradation

95
Q

loss of p53 function

A

excessive proliferation, inhibition of apoptosis and DNA damage repair

96
Q

loss of function of tumor suppressor genes caused by

A

genetic and epigenetic factors

methylation!

97
Q

How do you search for tumor suppressor genes?

A

LOH analyses by RFLP (restriction fragment length polymorphism)
rationale: chromosomal region flanking tumor-suppressor gene is likely to undergo LOH

98
Q

Tumor Progression

A

growth and dissemination

99
Q

new blood vessel generation…

A

is critical for primary tumor growth

100
Q

hypoxic cells

A

die

101
Q

distance from blood vessel

A

100-200 mm

102
Q

hypoxia triggers

A

angiogenesis

103
Q

angiogenesis aids…

A

survival of tumor cells

104
Q

metastatic dissemination requires

A

new blood vessel generation

105
Q

leaky tumor vasculature promotes

A

intravasation

106
Q

metastatic colonization requires

A

angiogenesis

107
Q

4 ways to recruit blood vessels to tumors

A
  1. sprouting angiogenesis (predominant)
  2. vasculogenesis
  3. vascular mimicry
  4. Csc differentiation
108
Q

sprouting angiogenesis

A

new vessel generation from pre-existing vessels

109
Q

VEGF signaling promotes

A
  • junctional disruption
  • proliferation
  • survival
  • migration
  • recruitment of EPCs
110
Q

VEGF upregulation

A

in cancer

111
Q

major triggers of VEGF

A

hypoxia, oncogenic signaling

112
Q

H1F1-alpha

A

regulated by oxygen

113
Q

major oncogenic signaling

A 
PI3K, Ras
PI3K mutation
Activated EGFR
AKT mutation
PTEN loss
RAS activation
114
Q

multicellular interactions in the tumor microenvironment

A

promote tumor angiogenesis

115
Q

key players in tumor angiogenesis

A

tumor cells, EC, matrix remodeling, secretion of pro-angiogenic factors, myeloid cells (macrophages ECM deg)

116
Q

block VEGF signaling

A

block progenitor cell recruitment

117
Q

vascular mimicry

A

channel formation

118
Q

CSC differentiation into

A

Endothelial cells

119
Q

epithelial to mesenchymal transition

A

promotes tumor invasion

E-cad staining (loss of E-cadherin)

120
Q

reciprocal stimulation

A

promotes tumor invasion/intravasation

121
Q

macrophages and fibroblasts secrete

A

mmps

122
Q

Treatments

A

surgery
radiation
chemotherapy
adjuvants

123
Q

chemotherapy treatments

A
  1. antimetabolite (analogs)
  2. microtuble stabilizing (taxol)
  3. DNA cross-linking agents (cisplatin)
  4. antibiotics (doxorubicin
  5. hormone therapy (tamoxifen)
124
Q

adjuvent

A

anti-angiogenic drug (VEGF antibody)

growth-factor receptor blocker (EGFR antibody)

125
Q

Problems with therapy

A
  • side effects
  • delivery issues
  • redundancy of mol players and pathways (single line adjuvant therapy is not often sufficient)
  • increased drug resistance (over expression of transporter proteins)
  • resistance offered by cancer stem cell
126
Q

Tumor vessels are abnormal

A
  1. leaky
  2. tortuous
  3. heterogeneous
  4. poor pericyte coverage
  5. thin basement membrane

Molecular Cell Biology (5 decks)

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