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CMCB Fall > #29 Cancer 1 > Flashcards

#29 Cancer 1 Flashcards

1
Q

Where is Apoptosis most obvious?

A

Nervous system

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2
Q

What is apoptosis charcterized by?

A

morpholoical changes and cleavage of DNA to short fragments

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3
Q

What kind of specific anti0apoptotic genes can lead to ertain ancers (lymphoma) if not properly carried out?

A

bcl-2

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4
Q

what kind of apoptosis-inducing proteins

A

p53

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5
Q

portein casacades?

A

yes

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6
Q

What is the difference in cell culture/growth between neonatal cells and embryonic cells?

A

Neonatal cells (fibroblast)increase at phase I, and grow and constant rate for 50 generaltions then growth slows, and cell death occurs (phase III)

Embryonic cells- initial cell death coupled with emergence of healthy gorwing cells; lost growth potential and most cels die (crisis); very rare cells dont kdie but continue gorwing until progeny overgrows contulure –> IMMORTAL CELLS (with proper nutrients)

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7
Q

Are neonatal or embroynic cells immortal (potnetial)?

A

Embryonic

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8
Q

what is primary cell culture

A

a few days until they day

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9
Q

What is cell strain?

A

limited life
specied differences
dnumber of doublings before death

chicken<rodent

Senescence- at least partly due to telomerase

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10
Q

What is cell line?

A

IMMORTAL!

selected or trasnfeted

Variant ell takes over (difference in chromosome number?

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11
Q

what are pluripotent stem cells

A

may differentiate into various types of mature cells

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12
Q

what are exmbryonic stem cells

A

most flexible, most type so fdifferent cells

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13
Q

Cancer stem cells

A

possibiltiy of stem cells in tumors–> may be reasn why they are hard to tell

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14
Q

iPS = induced pluripotent stem cells

A

derived from differentiated or paritally differentiated adult celsl (may or may not be immortal)

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15
Q

What are the advantags of using cultured cells ?

A
  1. growth of environment can be readily controlled and maniputlaed
  2. cultures cesl provide a homogenous poplualation
  3. cultured cells can be manipulated genetically

4.

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16
Q

what are the charccterisitcs of normal cells grown in culture

What is the usual source of growth factors?

A
  1. substrate dependence for growth (collagen,ECM, polysine)
  2. serum dependence (growth factors) for growth (PDGF- platelet derived growth factors , EGF, epidermal growth factors , factors)
    cell adhesion molecules (CAMs), fibronectin, integrin
  3. Contact inhibition of growth
    monolayer on plates (compare discrete tissue formation)
  • Serum ! ; growth factors are peptdie growth factors
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17
Q

What did the experiement that shows the dependence of cell growth on serum concentration

A

Experimetn shows that factors rather than cell contacts control cell growth b/c cells are already touching one another in 20 percent serum

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18
Q

Differences in growth of cultures of normal and transformed cells revealed by studies with epidermal growth factor (EGF)

A

Equal numbers of normal and transformed cells were plated into a defined medium with or without EGF at day 0. Cell nubmers were determiend daily. T
Transformed cells in teh complete medium grew after normal cells had ceased growth. Transforemd cells grew even in teh medium without EGF]]

EGF added to some dishes of normal cellstaht were intially lacking it

cultures repsonded to teh addition of EGF by growtin, it is evident that without EGF, normal cell can remiain vialb ein the G0 state

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19
Q

What is the total cell cycle: How is it determined

A

determined by counting the number of cells present and recording the number of hours it takes for teh total number to double

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20
Q

How to determine if cell in S phase

A

Cells are incubated with H-Thymidine for a brief period. The cells are then prepared for autoradiogrpahy.

Cells wiht labeled nucleus (implies that cell was in S phase during albeling)

Once nubmer of cells with labeled nuclei is known, this value can be used to determine the length of S phase.

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21
Q

What is mitotic shake off?

A

procedure to synchornize cells
for measuremtn of M-phase or synchorizianto of culture

cells that are undergoing mitosies are rounded up adn adhere poorl to tissue culture disehs and aare easily washed off

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22
Q

What hapens when mitotic cells that are shaken off are transferred to a new dish?

A

they immediately enterd G1 phase and continue through their cycles in synchorny

Lenght of G1 is determiend b measuring the leanght of time betweent eh clletion and the first incorporatino of H-htymidine into DNA

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23
Q

How does FLOW Cytometer (fluoresence-actiated cell analyzer) work?

A

To determine cell cycle times an asynchronnously growing cell population is treated with fixative and then stianed with dye that beocmes fluoresene when it binds to DNA. Thus the intenstiy at whiha cell fluoresces is proportinal to teh amt of DNA that the cell contains

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24
Q

How can you tell results of DNA with Flow cytometry

A

Cells with the
leasg DNA are in G1,
those with double this amt are in G2, and M, those with an intermediate amt are in S
e in S phase

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25
Q

Do cells ahve to be in syncronized or asynchronzied state to determine length of G1 and G2?

HO wcan you tell lenght of G1 phase

A

synchronized

  1. Shake off mitotic cells and transfer to new dish -> immediately enter G1 phase
  2. measure length of time between collection and first incorporation of 3H-thymidine in DNA (which is start of S phase)
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26
Q

How can you detemrine lenght of M phase?

A

cells in mitosis shake off- b/c they are round and less sticky

plate them onto new cuture and count?

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27
Q

How do you determine lengh of S phase?

A

By autoradiograpy using labeled 3-H Thymidine. Thymidine will only be incorproated into htose ells that were currently in DNA sysntehsis at the time of staining

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28
Q

How can you calculate G2 phase>

A

Lenght of G2 phase by time elaspsed for label form S phase to appear in mitotic cells

  1. in an asynchronously growing cell poulation, brief pulse to label cells in autoradiography
  2. ; M-phase cells collected by mitoti “shake off” every 2 hours,
  3. time at which radioactibely lableed DNA is first found in tehse mitotic cells i determined

The “delay time” is equal to length of G2 phase

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29
Q

what phase of the cell cycle willl be fluoresced the lease in flow cytometer (which will have the least DNA)

A

G1 phase

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30
Q

Which phase will it be in if doulbe the amount of DNA than in G1

A

G2 phase and M phase

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31
Q

What about that with intermediate amount of fluoresence (immediate amount of DNA)

A

S phase

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32
Q

what is the intensity of fluoresence correpsond with>

A

The intensity at which a cell luoresces is proportional to the amt of DNA that the celll contains
G1 phase the lease DNA
G2 and M phase have double G1 phase
S phase hs intermedaite

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33
Q

What does FACS stand for?

A

Fluoresence Activeted Cell Sorter

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34
Q

Whihc phase has most cells? What does it mean?

A

G1 phase has much greater than G2

this indicateds that lenght of G1 is longer than G2

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35
Q

What are Soluble cytplasmic ffactors S-phase activator (START kinase) in yeast and M-phase promotoing factor (MPF),?

A

made up of proteins related to cdc2 kinase (p34 and cyclin) Thses factors interact in a cyclic fasion to control cell cycle

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36
Q

What are major players in teh regulation fo cell cycle (4)

A
  1. S-phase activator (start kinase)
  2. M-phase promoting factor (MPF)
  3. Cyclin
  4. Cyclin dependent kinase (CDK)
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37
Q

What can Cell diision e slowed or stopped by? (3)

A
  1. limiting nutritents
  2. depriving cells of essential growth factors (serum)
  3. adding certain durgs
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38
Q

What phases are cells in if inhibited by something?

A

G1 or in special cases G0 (quiescent phase)

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39
Q

What factors shift cells out o fG0 and G1 into S phase

A

EGF, PDGF, FGF

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40
Q

What is the deterministic hypothesis?

A

Once cells pass a certain point in the cell cycle they are committed to continue through the cycle. This is only true to a point. There are several check points thatcells will not proceed through unless the cell and its environemtn are suitable to continue

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41
Q

What is the Restriction point (R)?

A

cells normally stop deviding when they reach a point late in G2 c (called START in yeast), unless signaled to go through another whole cycle

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42
Q

What is the restirction point in late G1 in yeast called?

A

START

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43
Q

What parts of cell cycle are there checkpoints?

A
  1. At end of G1 phase, is environemtnt favorable for S hase)
  2. end of G phase, in DNA all replicated, is environmental favorable?
  3. Metaphase checkpoint Aer all chrocomeoms atached to spindle
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44
Q

What are reasons that G1/S arrest?

A

cells arrest at checkpoints unless all needs are present. Arrest b/c of

  1. limiting nutritents, lack of growth fators, certain drugs
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45
Q

What is the S phase activator in mammalian cells?

A

Soluble cytoplasmic facotr (or group of factors) is responsible for signaling a cell to enter S phase and begin DNA syntehsis The S factor dissaperas after syntehsis

46
Q

What is the name of the Sphase activator in yeast??

What is it coposed ot?

A

START kinase

composed of G1 cyclin and cdc2 kinase

47
Q

What is the core of the cell-cycle control system?

A

Cdk (or diff dk’s in euk) is thoght ot asoscaite succesilvey with different cyclins to trigger didfferentdownstream processes of scycle

48
Q

what terminates Cdk activity?

A

terinated by cyclin degradation

49
Q

What is cyclin?

A

Small protein that is responsbile for regulating level so MPF (mphase promoting factors)

50
Q

Where is cyclin found?

A

in oocyte of Xenopus, increase in concntation above threshold may trigger saurge of ThMPTF

51
Q

What dos the proteolysis in cyclin that occurs abprovudly ?

A

It occurs abrublty and responsbile for decrease in MPF at end of mitosis

52
Q

How are CDK (cyclin dependent kinases) controlled?

A

by bindign of cyclin

53
Q

What happens when you expose MPF in any phase of cells?

A

Caueses cells to enter M phase

54
Q

What is the composition of MPF?

A

coposed of mitotic cyclin and cdc2 kinase and is regualted by phosphorylation

55
Q

when does CDK (cyclin dependent kinase) become associated with cyclin?

A

What cyclin levels gradually increase

enables Cdk to be phosphorylated by an activating kinase (CAK) on “activiting” stie as wella s Weel kinase of Cdc2’s catylatyic site

56
Q

What needs to phosphorylated in order to become partly activated?
What enzyme phosporyaltes cdc2
To become FULLY ACTIVE?

A

to be Fully active- When Cdk becomes acssociated with cyclin, Cdk is phosphoyrlatd by CAK (CDK-ACTIVATING KINASE)

57
Q

What does Wee1 kinase do?

A

it phosphoyrlates Cdc2’s catalyic site

this causes INACTIVATION
its phosphorylation inhibits CDk activity until phosphate gorup is removed by Cdc25 phosphatase

58
Q

What causes inactivation of Cdc2?

A

wee1 kinase by phosphorylating the catalytic site

59
Q

How do you reactivate the Cdc2 aftter it is inactivated by phosphoyrlation by wee1 kinase? what is Cdc25 phosphatase?

A

removes teh inacativating phosphate that weel kinase added to cdc2

60
Q

what is p27

A

inhibtior protein that helps regualte cell cycle and inactivtation

61
Q

what are two ways of inactiving cyclin-cdk complex?

A
  1. wee1 kinase (inactivates) by phosphorylating cdk

2. p27, inhibitory protein that binds cyclin-cdk complex

62
Q

what is the APC (anaphase promoting factor)?

A

controlls cell cycle by promoting degradation of cyclin

APC attaches ubuiquitylatin enzymes that leads to degradation of M-cyclin in proteasome

63
Q

What is SCF?

A

Controls proteolysis

IT is a ubiquitin ligase that controls cell cycle through recognition of phosphorylated CKI (cdk inhibitory protein) leading to degradatino in the proteasome

64
Q

What is p16, p21, p27 ? What is Rb?

A

family of Cdk/Cylcin complex INHIBITORS

Rb= retinoblastoma protein, a tumor suppressor protein

65
Q

what are factors that control proliferative state of (so S-phase genes is inhibited)

A

p16 binds to cdk4 so that it will be n inactive protein kinase

Active Rb inhibits E2F (a Transcription factor of S-phase genes)

66
Q

What hppaens in proliferating cells? What factors are working

A

P16 is inactive or absent so Cyclin D can bind ot Cdk4 and activate it–> Cdk4 phophoryaltes Rb and inactivates Rb –> now E2f is active and can express S-phase genes

67
Q

What are other checkpoints of at DNA?

A
  1. ## DNA re-replication bloc
  2. Delay at mitosis (finish DNA)
  3. Chromosome spindle attached
68
Q

what is DNA re-replication block?

A

prevents genome from undergoing a second round of DNA eplication and thus ensures tha tthe genome is replicated only once in S phase

69
Q

Delay at mitosis

A

until DANN replciation si complete

70
Q

CHromosome spindle attached

A

yup

71
Q

how many cyclins and cdks are in mammales?

A

5 cyclins and cyclin dks

72
Q

How does normal cell become cancer cell?

A

it ust be tranformed into one that gros without responding to controls

73
Q

wha tis the principle type of change in cell transformation?

A

alteration of pre-existing genes to oncogenes

74
Q

what kind of treatments can be done to cultures cells that change their growth properties in cultuer?

A
  1. virus infection
  2. exposure to chemicals
  3. irradiation

These treatments can cause cells to form tumors after they are injected into susceptible animals

75
Q

What is the changes in growth properties of cells and their subsequent develpment of tumor forming cpacity?

A

malignant transformation or just transformation

76
Q

what are some changes that are commonl obseved when a normal tissue culture cel is transformed by a tumor virus?

A
  1. Plasma membrane related abnormalities
  2. Adherence abnormalities
  3. Growth and division abnormalies

***CAN CAUSE TUMORS WHEN INJECTED INTO SUSCETIBLE ANIMALS **

77
Q

What kind of plasma membrae related abnormalieis are bosered iwth transfomred tumor by virus?

A
  1. enhanced transprot of metabolites
  2. excessive blebbling of plasma membrane
  3. increased mobitliy of PM proteins
78
Q

What kind of adeherence abnormalieis are seen in transormed cells?

A
  1. diminished adhesion to surfaces, hence rounded
  2. failture of actin filaments to orgnaie into stress fibers
  3. reduced external coat of fibronectin
  4. high plasminogen activator, extracellular porteysis up
79
Q

Growth and Division Abnormaltiies

A
  1. growth unusually high cell density- no contact inhibition
  2. lowered requirement for growth factors
  3. less anchorage dependsce (can grow iwthout surfaces)
  4. “Immortal” (can proliferate indefinitely
  5. casue cause tumors when injected inot susceptible animals
80
Q

What are some agents of transformation?

A

Viruses

Chemicals

Irradiation Chromosomal

Translocations and dupications

All occur through effects of ONCOGENES

81
Q

what is the basis of oncogenesis?

A

1 Overactivity mutation (gain of function)

  1. underactivity mutation (loss of function)
82
Q

Describe overactivity mutation (gain of function)

A

single mutation eent creates oncogene –> activating mutaiton enables ONCOGENE to stimulate cell proliferation – >cells proliferate abnormally

83
Q

Describe underactvity mutation (loss of function)

A
  1. mutation event INACTIVATES TUMOR SUPPRESSOR GENE– >no effect of mutation in one gene copy
  2. 2nd mutation event, inactivates second gene copy –> 2 inactivating mutations functionally ELIMINATES THE TUMOR SUPPRESSOR GENE , stimulating cell proliferation
84
Q

What are tumor viruses? What do they cause?

A

cuase transformation of cultured cells as a consequence of their ability to integrate their genetic info into the host cell’s DNA

they cuause the chronic porduction of of one or more proteins called transforing proteins

85
Q

DNA tumor viruses, the known tranfomring genes…..

A

are integral parts of viral genome==> ONCOGENES

86
Q

For retroviruses, the tranforming genes……

A

are normal or slighlty modified cellular genes that are expressed with hyperactivity in the host cells ==> ONCOGNENES

87
Q

What is Human T-lymphotropic virus Type I (HTLV-1)

A

human RNA retrovirus that is known to cause a type of cancer, referred to as adult T-cell leukemia and lymphoma and a demyleinating diseased caleld HTLV-1 assocaitaied myelopathy’/Tropial spastic paraparesis (HAM/TSP)

88
Q

What does human t-lymphtropic virus Type I cause?

A
  1. adult T cell leukemia dn lymphoma

2. demyelinating disease caleld HTLV-I assocaitely myelopathy/Tropical spasptic paraparesis (HAM/TSP)

89
Q

What is HIV?

A

lentivirus (member of tretrovirus family ) that causes acquired immunodeficiency syndrome (AIDS)

90
Q

How many CD4+ T cells until cell-mediated immunity is lost?

A

200 cells per uL

91
Q

what are first symptoms of HIV

A

recurring respiratry tract infections, prostatite,s skin rashes, oral ulceration, oporutnitstic infections, resistance to oral Candida species and Mycobafcterium TB is lost

92
Q

What is the oncogene src?

A

induces a cancer in chickens, is part of the small RNA genome of Rous Sarcoma Virus (a retrovirus)

93
Q

What happens when a retrovirus infects a cell

A

Viral RNA is copied into ds DNA by enzyme reverse transcriptase which is supplied by virus

DNA then becomes integrated into host cell’s DNA

When host cell’s DNA is transcribed into RNA by cellualr enzymes , the viral DNA is also transcribed

Some viral RNA provides copies of viral genomes for inclusion in new virus partile and some of it is processed to make mRNA –> translated by cell’s protein-synthesizing machinery into viral proteins

94
Q

What is the product of src gene?

A

NOT A COMPETENT virus particle

it is an enzyme caleld a protein tyrosine kinase, which binds to inner surface of cells PM and phosphorylates cellular proteins –> thereby converting cell to cancerous growth

95
Q

What is difference between life cycle of DNA virus?

A

Viral DNA is not usually integrated into host genome, but it can

Oncoproteins are produced that take over regulation of cell (form oncogene)

96
Q

What is the difference between c-src and v-src

A

c-src = cellular src is normal oncogene

v-src is a oncogene of Rous Sarcoma Virus

97
Q

What is the difference in structure of vsrc and csrc

A

v-rsrc has no introns that are present in scrc

v-src contains mutaitons tha splice our of v-src over eolutionary time

v-src contains mutations that alter amino acid sequence of protein making hypeactive and unregulated as a tyrosine-specific protein kinase

98
Q

What is the difference between direct carcinogens and indirect carcinogens?

A

Direct carcinogens ACT DIRECTLY on a process in the cell

Indirect carcinogesn HAVE TO BE CHEMCIALLY MODIFIED in THE animal/human, frequencyly by CYP 450 system, before damage is caused

99
Q

What is an example of a direct carcinogen?

A

methyl nitrosuria, acts on DNA

100
Q

What is example od indirect-acting Carcinogen?

A

Dimethylnitrosamine and

AFLATOxIN B1

101
Q

Where can you get the indirect carcinogen AFFLATOXIN?

A

from mold onpeanuts/grain

invovled in liver cancer , acts on p53

102
Q

what does Aflatoxin act on? What is activation of aflatoxin by Cyp450.

A

involved in liver cancer and acts on p53 tumor suppressor preotin

103
Q

What is the most important site of reactivity for chemical carcinogens?

A

DNA!

104
Q

Do cells that are transformed by treatment with chemical arcingoens have activated oncogenes?

A

Yes!

105
Q

what is irradiation?

A

xrays, gamma rays, act on human DNA and lead to cancer

this is also related to alteration in proto-oncogene expression

106
Q

What agent of transformation cause Burkitt’s lymphoma?

A

Chromosomal Translocations and Duplications

107
Q

What is an example of chromosomal translocation and dupliation type of cancer?

A

Burkitt’s lymphoma

108
Q

Describe mehanism of Burkitt’s lymphoma. What is it’s clinical presentaiton

A

Reciprocal translocation between chromosme 8 and 14. A malignancy of ells in human immune system

Mechanism that enhanes production of antibodies in normal B cells then activates teh oncogene myc

109
Q

Which oncogene does Burkitt’s lymphoma activate?

A

oncogene myc- overexpression of it

110
Q

How does EBvirus promote oncogenesis in Burktit’s?

A

by inhibiting apoptosis in B cells- syntergistic with this translocation

111
Q

Which chormosomes are involved in the reciprocol translocation in Burkitt’s lympoma?

A

Chromosome 8 and 14

CMCB Fall (17 decks)

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