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Molecular and Cellular Processes 2 > Neoplasms > Flashcards

Neoplasms Flashcards

1
Q

neoplasm

A

new tissue, tumor, mainly cancers

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2
Q

neoplasia

A

new growth

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3
Q

cancer

A

malignant tumor

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4
Q

where do neoplasms come from?

A

normal tissue that can proliferate

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5
Q

how many mutations have to occur in a cell for a change to occur?

A

two

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6
Q

fibroma

A

from fibroblasts

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7
Q

lipoma

A

adipose

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8
Q

adenoma

A

exhibits gland patterns or from adrenal glands

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9
Q

chondroma

A

cartilaginous

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10
Q

leiomyoma

A

smooth muscle

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11
Q

myoma

A

regular skeletal muscle

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12
Q

papilloma

A

epithelial growth on surface, finger like fronds

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13
Q

how are benign neoplasms named?

A

beginning of word tells you where its coming from, and always ends in ‘oma’

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14
Q 
sarcomas, carcinomas, adenocarcinomas, teratoma, melanoma, hematopoietic 
invade adjacent tissue 
metastasize
wide range of differentiation
kills host 
not encapsulated
goes from one tissue to another
does not look like the tissue that is supposed to be there
A

malignant neoplasms

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15
Q

from mesenchymal tissue (liposarcoma, fibrosarcoma, osteosarcoma); mesoderm (middle layer)

A

sarcomas

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16
Q

from epithelial cells; ectoderm (surface)

A

carcinomas

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17
Q

glandular growth/gland association

A

adenocarcinomas

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18
Q

made of cells from more than one germ layer; come from the stem cells and can grow into anything

A

teratoma

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19
Q

coming from melanocytes (cells in your skin that give color or freckles) start to grow out of control and end up with patchy tumors

A

melanoma

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20
Q

blood cells; leukemia

A

hematopoietic

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21
Q 
remain localized, don't metastasize
grows as a cohesive unit
tend to become encapsulated
well differentiated 
not deadly
looks like the tissue cell that is supposed to be there
A

benign neoplasms

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22
Q

we have this wide arrange of differentiation or no differentiation at all

A

anaplasia

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23
Q

increase in size but not in number
still the correct type of cell
ex: pregnant, cardiovascular disease

A

hyperplasia

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24
Q

replacement of one cell type with another
better adapted to altered environment
ex. ppl w acid reflux

A

metaplasia

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25
Q 
disordered growth
loss of uniformity
loss of architectural orientation
metastasize
many different cells type show up
A

dysplasia

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26
Q

any sort of chemical that can cause cancer
can be called mutagen
but not all of _____ are mutagen and vice versa

A

carcinogen

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27
Q

what must happen for cancer to occur?

A

mutate DNA twice

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28
Q

what two types of cancers are associated with viruses?

A

cervical carcinomas (HPV) and hepatomas (liver cancers, hep C)

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29
Q

any sort of gene that’s in the DNA that will lead to the development of a cancer

A

oncogene

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30
Q

how do tumor viruses cause cancer?

A

by the interaction between carcinogen and endogenous viruses

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31
Q 
#1 on the outside, you have this extracellular domain and that's where the signal binds
#2 domain that goes through the membrane - transmembrane domain
#3 on the inside, there's kinase
A

growth factors - start of the signal cascade

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32
Q

enzyme that phosphorylates and activates the protein and changes its shape

A

kinase

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33
Q

what happens to mutated receptors?

A

changes kinase domain of growth factor so it no longer needs the signal and can activate itself

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34
Q

how many cells produce and stimulate growth factors and how are they related?

A 
two cells (epithelian and mesenchymal)
one will produce some of the growth factors and go to the other cell to be activated and/or vice versa
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35
Q

what happens to these cells in a cancer cell?

A

a cancer cell that produces the signal will also produce the receptor thus it can activate itself

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36
Q

autocrine signaling

A

self signaling

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37
Q

what is G1 preparing for?

A

S phase

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38
Q

S phase

A

synthesizes (makes two copies of) DNA

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39
Q

after S phase

A

G2

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40
Q

what is G2 preparing for?

A

mitosis (inphase)

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41
Q

how much time in G1?

A

12-15 hrs

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42
Q

how much time in S phase?

A

6-8 hrs

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43
Q

how much time in G2?

A

3-5 hrs

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44
Q

how much time inphase (Mitosis)?

A

1 hour for cell to divide into two

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45
Q

how long does it take for a cell to divide?

A

1 day

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46
Q

why do we need checkpoints?

A

stops cell from going through cycles and makes sure we have all the enzymes and proteins to go through with

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47
Q

what does the check point in S phase used for?

A

it checks for DNA damage and stops everything and causes cell to kill itself if damaged

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48
Q

what does the check point in G2 used for?

A

it makes sure that the DNA is replicated

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49
Q

what is the R point?

A

restrictive point will determine whether cell cycle will go all the way through or not

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50
Q

what do CDKs depend on?

A

presence of kinase

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51
Q

why are cyclins important and how many are there?

A

this is how the cell knows it should be in a specific cycle; 4 (DEAB)

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52
Q

around G1 then it goes away

A

D

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53
Q

at the end of G1 and beginning of S phase after that it goes away

A

E

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54
Q

middle of S phase and goes away towards beginning of G2

A

A

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55
Q

is around in G2

A

B

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56
Q

CDK 4/6

A

D and G1

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57
Q

CDK 2

A

E

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58
Q

CDK 1

A

A and B

59
Q

where is the R point?

A

at the end of CDK 4/6 and D and this is the point that will determine whether the DNA will be synthesized

60
Q

what is the protein that controls the R point?

A

retinoblastoma, Rb

61
Q

what does Rb do?

A

it causes CDK 4/6 to go away and process continues

62
Q

guardian of the genome - makes sure that there are no other mutations in the DNA
initiates cell death

A

p53

63
Q

a cell that is cancerous we say that the cell has been ______

A

transformed

64
Q 
contact inhibition loss
foci development
altered shape
ability to grow in low serum
immortal
anchorage independence
tumorigenicity
A

transformed characteristics

65
Q

how can cancer make new blood vessels form?

A

through angiogenesis)

66
Q

first line of defense
second line of defense
defenses against any pathogen
not specific

A

innate immunity

67
Q

third line of defense
immunity or resistance to a specific pathogen
specific response –> going to be a lot stronger
has memory
slower to respond

A

adaptive immunity

68
Q

intact skin
mucous membranes and their secretions
normal microbiota

A

first line of defense

69
Q

phagocytes (neutrophils, eosinophils, dendritic cells, macrophages)
inflammation
fever
antimicrobial substances

A

second line of defense

70
Q

specialized lymphocytes: T cells and B cells

antibodies

A

third line of defense

71
Q

ability to ward off disease

A

immunity

72
Q

keratinized epidermis (consists of tightly packed cells)
replaced every 4-5 days
dry environment
no blood vessels

A

skin

73
Q

sebum (oil)
sweat (viscous)
organic acids (lowers pH)

A

glands

74
Q

transports microbes trapped in mucus away from lungs

A

ciliary escalator

75
Q

washes eye

A

lacrimal apparatus

76
Q

dilutes and washes microbes off

A

saliva

77
Q

flows out

A

urine

78
Q

flow out and low pH

A

vaginal secretions

79
Q

in perspiration, tears, saliva, and urine

an enzyme that breaks down bacterial cell wall

A

lysozyme

80
Q

microbial competition (competing w pathogens)

A

normal microbiota

81
Q 
one organism (microbe) benefits, the other (host) is unharmed
may be opportunistic pathogens
A

commensal microbiota

82
Q

part of the immune system, a series of proteins made to fight bacteria/infections

A

complement system

83
Q

increased in numbers at start of infection, most abundant

A

neutrophils

84
Q

present in all tissues, important in presenting antigen to adaptive immune

A

dendritic cells

85
Q

10-15% of lymphocytes in peripheral blood
lack antigen specific receptors
attack whatever but kill tumor cells and virally infected cells

A

natural killer cell

86
Q

10-15% of lymphocytes in peripheral blood
lack antigen specific receptors
attack whatever but kill tumor cells and virally infected cells

A

natural killer cell

87
Q

redness, swelling, pain, heat, loss of function

A

inflammation

88
Q
  1. destroy injurious/infecting agent, remove it and its products - vasodilation
  2. limit the effect of agent by confining - not letting it spread - phagocytose
  3. repair or replace damage tissue - start the repair process - repair
A

inflammation steps

89
Q

in fever, which endotoxin does gram negative bacteria cause phagocytes to release ?

A

IL-1 and TNF a ; they instruct the hypothalamus to increase internal temperature

90
Q

what does the hypothalamus release that resets the hypothalamus to a high temperature

A

prostaglandins

91
Q

increases transferrin
increases IL1
produces interferon

A

advantages of fever

92
Q

tachycardia
acidosis (pH of blood goes down)
dehydration
106 dg C

A

disadvantages of fever

93
Q

cause cell to produce antiviral proteins that inhibit viral replication

A

IFNa and IFN b

94
Q

causes neutrophils and macrophages to phagocytize bacteria; puts a little tag on bacteria

A

IFNy

95
Q

IFNa IFNb IFNy

A

interferons

96
Q

binds iron

A

transferrin

97
Q

inhibits microbial growth by inhibiting cell wall, forms pores in membranes and destroys DNA and RNA
non-antibody proteins that attack and destroy bacteria

A

antimicrobial peptides (pt of complement system)

98
Q

what are the two complement proteins?

A

C3 and C5

99
Q

what causes pores to be formed in the membrane, part of the flagging mechanism so that macrophages and neutrophils find the offending agent

A

C3B

100
Q

activates other sorts of neutrophils and WBC to hunt down microbes present in the area; need to be cut in half

A

C3

101
Q

is activated via C3 in order to bring those macrophages and neutrophils to kill offending agent

A

C5

102
Q

coats microbes for phagocytosis and complement activation
elevated plasma levels
beginning of an infection
tagging mechanism

A

c-reactive proteins

103
Q

releases antibodies in order to do something; pathogens outside of the cell

A

humoral; B cells

104
Q

specifically use cells to attack things with antibodies; trying to control antibodies by attacking cell; pathogens inside the cell

A

cellular; T cells

105
Q

where do B and T cells mature?

A

B in bone marrow, T in thymus

106
Q

a substance that causes the body to produce specific antibodies or sensitized T cells

A

antigen

107
Q

what do antibodies interact with?

A

epitopes

108
Q

globular proteins called immunoglobulins

number of antigen-binding sites determines valence (how many epitopes present)

A

nature of antibodies

109
Q

protein with 2 heavy chains and 2 light chains
constant region
variable region

A

antibody structure

110
Q

how many immunoglobulins are there?

A

5 )GAMED)

111
Q 
monomer
2 epitope binding site
80% of serum antibodies
neutralize toxins
23 days
A

IgG

112
Q 
dimer 
4 epitope binding sites
10-15% of serum antibodies
secretions, mucosal protection
6 days
A

IgA

113
Q 
pentamer
10 epitope binding sites
5-10% of serum antibodies
agglutinate microbes
5 days
first to show up in adaptive immune response
A

IgM

114
Q 
monomer
2 epitope binding site
0.2% of serum antibodies
B cells, innate immune response
3 days
A

IgD

115
Q

monomer
0.002% of serum antibodies
allergic rxn, lysis of parasitic worms
2 days

A

IgE

116
Q

where are B cells sitting?

A

lymph nodes

117
Q

antigen presented Th cell

Th cell produces cytokines

A

T dependent antigens

118
Q

stimulate the B cell to make antibodies

antigen/epitope randomly bumps into a cell and causes activation to occur

A

T independent antigens

119
Q

what do B cells differentiate into?

A

plasma cells and memory cells

120
Q

what eliminates harmful B cells?

A

clonal deletion

121
Q

what do B cells do?

A 
agglutination
opsonization
activation of complement
neutralization
antibody dependent cell mediated cytotoxicity
122
Q

macrophages, Tc Cells, natural killer cells

A

T Helper (1) cell

123
Q

eosinophils, IgM and IgE

A

T helper (2) cell

124
Q

destroys target cell on contact

A

cytotoxic T lymphocyte

125
Q

regulates immune response and helps maintain tolerance

A

T regulatory cell

126
Q

attacks cancer cells

A

activated macrophage

127
Q

destroys target cells (virus infected, tumor cells)
participates in antibody dependence
cell mediated cytotoxicity
granular leukocytes destroy cells that don’t express MHC I

A

natural killer cells

128
Q

what are the three antigen presenting cells ?

A

dendritic
macrophage
B cell

129
Q

viral pathogens and allergens; all throughout the body

A

dendritic

130
Q

intracellular and extracellular pathogens; mainly bacteria

A

macrophage

131
Q

recognize viruses and pathogens

A

B cell

132
Q

what is the pedestal where the bacteria is presented?

A

MHC II

133
Q

CD4+
TCR recognize antigens and MHC II
produce cytokines and differentiate

A

T Helper Cells

134
Q

CD8+
endogenous antigens
releases perforin and granzymes
carry their own antigens

A

T cytotoxic cells

135
Q

stops autoimmune responses

A

T regulatory cells

136
Q

situation where we have a foreign thing inside of us that is too big to be phagocytosed - coat it with antibodies

A

antibody dependent cell mediated cytotoxicity (ADCC)

137
Q

amount of antibody in the serum

A

antibody titre

138
Q

occurs after initial contact with the antigen

A

primary response

139
Q

occurs after second exposure

A

secondary (memory or anamnestic) response

140
Q

adaptive immunity resulting from infection

A

naturally acquired active immunity

141
Q

adaptive immunity resulting from transplacental or via colostrum

A

naturally acquired passive immunity

142
Q

adaptive immunity resulting from injection of antigen (vaccination) itself

A

artificially acquired active immunity

143
Q

adaptive immunity resulting from injection of antibody to take care of something

A

artificially acquired passive immunity

Molecular and Cellular Processes 2 (1 decks)

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