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Medicine phase 1 > Week 4 - Cancer and signalling > Flashcards

Week 4 - Cancer and signalling Flashcards

1
Q

Neoplasm

A

tumour

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2
Q

apoptosis

A

cell programmed death

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3
Q

necrosis

A

when cells die but not by apoptosis

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4
Q

hyperplasia

A

an increase in the size of an organ as a result of cell proliferation

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5
Q

hypertrophy

A

an increase in the size of an organ due to an increase in size of consituent cells

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6
Q

criteria used to classify tumours

A

in terms of biological behaviour - benign or malignant

in terms of origin - differentiation or histogenesis

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7
Q

benign

A

will never metastasise but may grow

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8
Q

malignant

A

can spread and invade

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9
Q

compare benign and malignant nuclei

A

benign - small, regular, uniform, grow slow

malignant - larger, increased DNA content, faster growth

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10
Q

metaplasia

A

a change from one type of differentiated tissue to another - often resulting tissue is better adapted to environment

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11
Q

categories of cells or tissues that tumours are classed under

A

epithelial
connective
haematopoietic/lymphoid
neural

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12
Q

routes by which tumour cells metastasise

A

local invasion
lymphatic spread - travel to draining lymph nodes
blood spread via vessels
Transcoelomic spread

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13
Q

Describe G0 phase

A

phase when cells are not actively dividing
not always permanent
red blood cells always here

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14
Q

interphase

A

G1, s, G2

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15
Q

G1 phase

A

Growing in size
Monitoring environment
RNA and protein synthesis in preparation for S phase
Growth-factor dependent

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16
Q

S phase

A

synthesis of DNA

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17
Q

G2 phase

A

further growth
cell organelle replication
prepare for mitosis

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18
Q

M phase

A

mitosis and cytokinesis

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19
Q

order of mitosis phases

A

prophase, (prometaphase), metaphase, anaphase, telophase

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20
Q

prophase

A

chromatin condenses into chromosomes
nucleolus disappears
centrioles move to poles

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21
Q

pro-metaphase

A

nuclear membrane dissolves

chromosomes attach to microtubules and begin moving

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22
Q

metaphase

A

spindle fibres align chromosomes along metaphase plate

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23
Q

anaphase

A

paired chromosomes separate and move to opposite sides of the cell by microtubule generated pulling forces

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24
Q

telophase

A

chromatids arrive at opposite poles of cell
new membranes form around daughter nuclei
chromosomes decondense
spindle fibres disperse

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25
Q

cytokinesis

A

cleavage of cell to produce daughter cells

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26
Q

role of CDKs and cyclins

A

regulate progression through cell cycle

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27
Q

role of cyclin D in cell cycle

A

activates CDK4/6 to regulate the restriction point

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28
Q

role of cyclin dependent kinase inhibitors

A

small proteins that inactivate the CDK either by binding directly to form an active complex or by acting as a competitive ligand

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29
Q

three families that offer an extra level of controlling CDK activity

A

P21 CIP
P27 KIP
P16 INK

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30
Q

progression from G2 to M is dependent on…

A

CDK1/cyclin B also known as maturation promoting factor (MPF)
CDK1 needs to phosphorylate lamins so lamins can destroy nuclear lamina
chromosome condensation is required

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31
Q

activation of CDK1

A

cyclin B synthesis starts in G2

once there is sufficient amount, it becomes associated with CDK1 - loss of phosphorylation makes it an active kinase

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32
Q

4 checkpoints of cell cycle

A 
restriction point (G1)
DNA damage checkpoints (late G1 and G2)
metaphase checkpoint
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33
Q

define checkpoint

A

Point in the cell cycle where progress through the cycle can be halted until conditions are suitable for the cell to proceed

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34
Q

restriction point is dependent on…

A

presence of growth factors

accumulation of cyclin D

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35
Q

if growth factor is detected in restriction checkpoint…

A

cell makes cyclin D, activating CDK4/6 which phosphorylates RB protein - RB protein is then free from the inhibiting factor E2F - RB can now transcribe genes needed for S phase

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36
Q

tumour suppressor genes

A

encode normal cell proteins that inhibit cell proliferation and growth of cell
cause cell-cycle arrest in abnormally dividing cells and repair DNA damage

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37
Q

explain DNA damage checkpoints

A

p53 detects DNA damage - results in production of CKI p21 – this binds to CDK2/cyclin E or A at the G1/S transition halting progression to S
At G2/M, progression is halted by p21 binding to CDK1/cyclin A or B

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38
Q

metaphase checkpoint

A

delays anaphase until all chromosomes are correctly attached to mitotic spindle
Once all attached – inhibition removed and the anaphase promoting complex is activated which allows for the separation of sister chromatids

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39
Q

six characteristics of cancer cells

A 
uncontrolled self proliferation 
inactivation of tsg that normally inhibit growth
evasion of apoptosis
limitless replication potential
sustained angiogenesis
tissue invasion/metastasis
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40
Q

oncogene

A

mutated forms of proto-oncogene - involved in inducing cancer

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41
Q

proto-oncogene

A

a normal cellular gene that encodes for a protein normally involve in regulation of cell growth and proliferation

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42
Q

tumour suppressor gene

A

a gene whose encoded protein directly or indirectly inhibits progression through cell cycle

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43
Q

compare normal cells and cancer cells

A

cancer cells have large variably shaped nuclei, many dividing cells, variation in size and shape, loss of normal differentiated features (anaplasia), nucleus becomes bigger, accumulation of mRNAs and rRNAs in cytoplasm will make it more basophilic (appear bluer)

44
Q

tumourigenesis

A

Initiation step usually result of environmental carcinogen such as chemicals and radiation or viruses
Then the accumulation of many more mutations, some activating oncogenes and others losing tumour suppressor gene activity enhance proliferation potential
Further mutations within population of cells results in a cell that has acquired further mutations with capabilities to become malignant

45
Q

key controlling mechanisms in cell cycle

A

presence of a growth factor,

an activating signal and the RB protein

46
Q

examples of proto-oncogenes in normal cells

A

Platelet-derived growth factor (PDGF)- function: matrix formation and involved in production of proteases
RAS genes - when RAS proteins are switched on it switches on other genes which switches on genes involved in cell proliferation

47
Q

examples of tsg

A

RB - blocks entry to cell cycle in restriction point
p53 - detects DNA damage
BRCA1 - DNA repair

48
Q

mutations of proto-oncogenes forming oncogenes

A

deletion/point mutation
regulatory mutation
gene amplification
chromosome rearrangement

49
Q

result of a point/deletion mutation to proto-oncogene

A

hyperactive protein made in normal amounts

50
Q

regulatory mutation or a gene amplification to proto-oncogene

A

normal protein is greatly over produced

51
Q

result of chromosome rearrangement to proto-oncogene

A

nearby regulatory DNA sequence causes normal protein to be overproduced
or
fusion to actively transcribed gene produces hyperactive fusion protein

52
Q

example of chromosome rearrangement resulting in cancer

A

The BCR gene on chromosome 22 is brought together with abl gene on chromosome 9
Results in the Philadelphia translocation – results in the BCR-ABL hybrid which is found in Chronic Myeloid Leukaemia

53
Q

do TSGs or proto-oncogene mutations have the dominant effect

A

proto-oncogenes bc only one copy of the gene needed to be affected

54
Q

how do cancer cells invade

A

produce proteases - need to degrade the surrounding storm and ECM so they can move through it - can travel through blood

55
Q

how epithelial cells metastasise

A

e-cadherin is part of adherens junctions - loss of e-cadherin allows adjoining cells to break apart and metastasise

56
Q

why signalling is important in medicine

A

to coordinate development and to maintain normal physiological functions

57
Q

diseases from abnormal signalling

A

Diabetes type 1 – don’t produce enough insulin
Type 2 diabetes – all target tissues for insulin have lost ability to respond properly to insulin released in body
Cancer – mutated K-Ras is too active and causes cells to grow/divide/survive in the absence of growth factor signals

58
Q

3 types of signal

A

physical - sets off a chemical or electrical
electrical
(bio)chemical

59
Q

stages of cell signalling

A

signal binds to receptor in or on target cell
transduction - transmission of signal from receptor to part of cell that produces response
response

60
Q

signalling responses

A

altered gene transcription in nucleus
altered target protein activity
altered target protein binding
altered protein localisation

61
Q

signals for intracellular receptors are…

A

hydrophobic eg. steroid hormones - oestrogen and testosterone or gases

62
Q

what happens when signal binds to cell surface receptor

A

it causes a change in conformation of the receptor – alters the activity of intracellular part of receptor – change in shape/activity sets in motion the cellular response to the signal

63
Q

3 main types of cell surface receptor

A

enzyme-linked receptor
g-protein-coupled receptor
ion-channel receptor

64
Q

integration of signal response

A

multiple signals working together to produce an overall cellular response

65
Q

3 outcomes of multiple signals working at the same time

A

conflict - cell ignores one and responds to other
signals can work independently - multiple responses
integration - one overall cellular response

66
Q

classification of chemical signals

A

classified based on their chemical structure and by the distance over which they act

67
Q

four classifications of signals by distance over which they act

A

endocrine - long distance
paracrine = nearby cells
juxtacrine - neighbouring cell (direct contact)
autocrine - same cell that releases signal

68
Q

signalling pathway of enzyme-linked receptors

A

signal binds to receptor activating an enzyme in cytoplasmic side of membrane - enzyme may be beside receptor or an integral part of cytoplasmic domain of the receptor - if signal is dimeric then binding causes dimerisation - the two parts of the receptor come together and this is what activates the enzyme activity

69
Q

examples of enzyme-linked receptors

A

receptor tyrosine kinases (RTK) - enzyme is tyrosine kinase - kinase activity is intrinsic to receptor
many growth factors work via this pathway

70
Q

signalling pathway of of G-protein-coupled receptors

A

G-protein-coupled receptor is bound to a G protein - Activated g-protein activates enzyme that passes on signal into a cell

71
Q

examples of of G-protein-coupled receptors

A

adrenaline and serotonin

72
Q

example of ion-channel receptor

A

glutamate neurotransmitter

73
Q

how do ion-channel receptors work

A

Signal binds to ion-channel receptor – ion channel opens and ions can flow through that channel across the membrane, by diffusion along a concentration gradient - Ion flow into cell changes electrical properties of cell

74
Q

receptor tyrosine kinase pathway

A

ligand binding - receptor dimerisation and activation - autophosphorylation (two subunits both have kinase activity so phosphorylate each other) - relay proteins recruited to docking sites and these are what transmits the signal further into the cell (phosphorylation allows relay proteins to bind)

75
Q

example of a signalling pathway activating multiple responses

A

EGF binding to EGFR promotes cell survival, cell proliferation and cell migration

76
Q

2 main ways that a signal can be transmitted

A

kinase cascades or production of second messenger

77
Q

explain the enzyme cascade method of transmitting signal

A

Each step in a cascade is catalytic (catalysed by an enzyme)
Final enzyme in the cascade alters the function of an effector molecule which produces the cells response to the signal
Cascade system means that in addition to passing on the signal, there is amplification of the signal

78
Q

MAPK cascade (mitogen-activated protein kinase)

A

A MAP kinase kinase kinase (MAPKKK) phosphorylates and activates a MAPKK which phosphorylates and activates MAPK – MAPK phosphorylates the cascades effector proteins - this can be deactivated by dephosphorylation at the same site carried out by phosphatase

79
Q

second messenger method of transmitting a signal

A

Small molecules are produced in large quantities inside the cell after receptor activation to coordinate the cell’s response
Other second messengers work by activating other protein kinases eg. DAG activates protein kinase C

80
Q

common second messengers

A 
cyclic AMP (cAMP) produced by enzyme adenylyl cyclase
Inositol triphosphate (IP3) and diacylglycerol (DAG) – produced by the enzyme phospholipase C
Calcium ions – released from intracellular stores by IP3 or flow into cell upon ion channel activation
81
Q

how can a disfunction in the pathway of GF signalling via receptor tyrosine kinases lead to cancer

A

if the GF/RTK pathways are too activated - Can happen if the receptor is overexpressed or if specific mutations occur (Raf and Ras)

82
Q

explain how lipophilic steroid hormones elicit their effect

A

These hydrophobic hormones bind to intracellular receptor proteins in cytoplasm
Hormone-receptor complex then acts as a transcription factor, moving into the nucleus, binding to DNA and altering the transcription of specific genes
Target cell changes the genes/proteins it expresses in response

83
Q

3 main stages of life before birth and their time frames

A

week 1 - preimplantation stage
weeks 2-8 - embryonic stage (organogenesis occurs)
weeks 9-38 - fetal stage (growth and development)

84
Q

cleavage

A

As zygote starts to develop, the maternal and paternal genes start to mix and that triggers division of the zygote from one cell to two, two cells to four… this process of cell division is called cleavage

85
Q

define zona pellucida

A

tough glycoprotein coat around the outside of embryonic cells - stops embryo getting bigger and also stops it sticking to uterine wall (premature implantation)

86
Q

define morula

A

embryo forms a cluster of cells - tight junctions between cells for communication - after morula stage, embryo moves into uterus and the formation of a blastocyst stage embryo starts

87
Q

blastocyst formation

A

inner cell mass forms embryo and extra embryonic tissues
trophoblasts contibute to placenta
embryo enters uterine cavity, fluid enters via zona pellucida into spaces of inner cell mass
fluid filled blastocyst cavity forms

88
Q

what happens at about 5-6 days when embryo starts to run out of nutrients?

A

blastocyst hatches out of zona pellucida
fluid inside blastocyst starts to build up until blastocyst cavity expands and causes holes to form in zona pellucida
eventually bursts - sticky trophoblast cells make contact with uterine lining and attach and implant

89
Q

2 layers of bilaminar disk

A

epiblast and hypoblast

90
Q

during implantation the cells closest to inside of embryo differentiate to…

A

a single layer of cells called cytotrophoblast

91
Q

syncytiotrophoblast

A

outer layer that forms during implantation - more extensive and is the invasive layer

92
Q

implantation of embryo process

A

blastocyst makes contact with the endometrium of uterus and decidualisation occurs in the stromal cells of the uterus - triggers production of several molecules and promotes trophoblast cells to become invasive - implanting sysncytiotrophoblast cells communicate with maternal side of placenta and establishes a connection to enable diffusion of oxygen, waste and nutrients via blood supply

93
Q

trophoblast layer differentiates to form…

A

two placental layers - cytotrophoblast and the invasive syncytiotrophoblast

94
Q

ectopic implantation

A

implantation occurs at an abnormal site - can be due to slow transit in uterine tube or premature hatching of a blastocyst

95
Q

name the four extra embryonic membranes/fetal membranes

A

amnion, chorion, yolk sac and allantois

96
Q

describe an amnion membrane

A
  • continuous with the epiblast
  • lines a structure called the amniotic cavity which is filled with fluid and acts to protect the developing embryo
  • present up until birth
97
Q

describe a chorion membrane

A

double layered
formed by trophoblast and the extra embryonic membranes
lines a structure called the chorionic cavity (seen in early pregnancy but disappears due to expansion of the amniotic cavity
forms the fetal component of placenta

98
Q

describe a yolk sac

A

continuous with hypoblast
important in nutrient transfer in weeks 2-3 but disappears completely by week 20
important in blood cell formation and formation of the gut

99
Q

describe an allantois membrane

A

forms as an outgrowth of the yolk sac

contributes to the umbilical arteries and connects to the fetal bladder

100
Q

gastrulation

A

process in cell division and migration resulting in the formation of three germ layers
formation of epiblast into trilaminar embryo

101
Q

three germ layers

A

ectoderm
mesoderm
endoderm

102
Q

describe the invagination process

A

Primitive streak appears and it encourages migration of the cells of the epiblast
Cells migrate towards primitive streak and move down through embryo to create a new layer called mesoderm
More cells push even further down, pushing past hypoblast cells, displacing them to create a new bottom layer called endoderm
Cells left on the top (where epiblast was) become ectoderm

103
Q

which tissues and organs do cells in the ectoderm give rise to

A 
epidermis of skin 
epithelial lining of mouth and anus
cornea and lens of eye
nervous system
sensory receptors in epidermis
adrenal medulla
tooth enamel
epithelium of pineal and pituitary glands
104
Q

which tissues and organs do cells in the mesoderm give rise to

A 
notochord 
skeletal system
muscular system
muscular layer of stomach and intestine 
excretory system
circulatory and lymphatic systems 
reproductive system 
dermis of skin
lining of body cavity
adrenal cortex
105
Q

which tissues and organs do cells in the endoderm give rise to

A 
epithelial lining of digestive tract
epithelial lining of respiratory system
lining of urethra, ulinary bladder and reproductive system
liver
pancreas 
thymus
thyroid and parathyroid glands
106
Q

teratoma

A

tumour with tissue or organ components resembling derivatives of the germ layers
germ cell teratomas are usually found in the gonads

Medicine phase 1 (14 decks)

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