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MBChB - year 2 > Week 2 P&I Lectures > Flashcards

Week 2 P&I Lectures Flashcards

1
Q

What is metastasis?

A

The multi-step process by which tumour cells move from a primary site to colonise a secondary site

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2
Q

What is a neoplasm?

A

new cellular growth – can either be benign or malignant

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3
Q

What are the 6 biological capabilities acquired during the multistep development of human tumours?

A
  • Sustaining proliferative signalling
  • Resisting cell death
  • Evading growth suppressors
  • Inducing angiogenesis
  • Activating invasion and metastasis
  • Enabling replicative immortality
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4
Q

What is the acquisition of the 6 biological capabilities for the development of tumours enabled by?

A
  • The development on genomic instability in cancer cells

- Inflammatory state of premalignant and frankly malignant lesions

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5
Q

How does genomic instability lead to the acquisition of the 6 biological capabilities for the development of tumours?

A

which generates random mutations including chromosomal rearrangement

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6
Q

How does the Inflammatory state of premalignant and frankly malignant lesions lead to the acquisition of the 6 biological capabilities for the development of tumours?

A

It is driven by cells of the immune system, some of which serve to promote tumour progression.

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7
Q

How is metastasis the leading cause of cancer related death?

A
  • Physical obstruction
  • Compromise organ function
  • Compete with healthy tissue for nutrients and oxygen
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8
Q

What is the metastatic cascade?

A

the steps that a tumour needs to take to be able to metastasise and set up in a new location

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9
Q

What are the steps of the metastatic cascade? (6 steps)

A
  1. Invasion
  2. Intravasation
  3. Transport
  4. Extravasation
  5. Colonisation
  6. Angiogenesis
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10
Q

What are the 7 key characteristics involved in the metastatic cascade?

A
  1. Reduced cell-cell adhesion
  2. Altered cell-substratum adhesion
  3. Increased motility
  4. Increased proteolytic ability
  5. Angiogenic ability
  6. Ability to intravasate and extravasate
  7. Ability to proliferate (locally and ectopic sites)
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11
Q

What is the epithelial-mesenchymal transition (EMT)?

A

The process in which epithelial cells lose their characteristic polarity, disassemble cell-cell junctions and become more migratory

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12
Q

What are stress fibres?

A

Long strands of actin that are important for movement

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13
Q

What maintains Adherens junction?

A

E-cadherin

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14
Q

What is the importance of the adherens junction?

A

It is important in maintaining sheet like structure of epithelial cells

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15
Q

What can cause aberrant E-cadherin expression in tumours? (5 examples)

A
  • somatic mutations
  • chromosomal deletions
  • silencing of the CDH1 promoter by methylation
  • mutations in proteins that interact with E-cadherin
  • mutations in transcription factors (Slug, Snail, & Twist) that regulate E-cadherin expression
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16
Q

what can E-cadherin be turned into?

A

N-cadherin - functionally is very different to E-cadherin

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17
Q

What are integrins?

A

Transmembrane receptors that bind to and respond to the ECM

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18
Q

What type of signalling can integrins do?

A

bidirectional signalling – can receive signals from inside the cell and from the ECM

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19
Q

How many possible heterodimers of Integrins are there?

A

24

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20
Q

What are examples of where integrins are found?

A

Basal epithelial cells and in focal adhesions in migrating cells

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21
Q

What are focal adhesions?

A

focal adhesions are little attachment sites. Stress fibres attach to focal adhesions

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22
Q

What is the role of integrins in cancer?

A
  • support oncogenic growth factor receptor (GFR) signalling – can augment it
  • cell migration and invasion
  • extravasation from blood vessels
  • colonisation of metastatic sites
  • survival of circulating tumour cells
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23
Q

what is HGF?

A

Hepatocyte growth factor (or scatter factor)

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24
Q

What are the functions of HGF (in terms of a tumour)?

A

A mitogen and motogen

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25
Q

What produces HGF in a tumour?

A

Stromal cells

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26
Q

What does HGF bind to in the tumour?

A

C-met (a RTK on tumour epithelial cells)

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27
Q

What does activation of C-met lead to?

A

Increased tyrosine phosphorylation if B-catenin (involved in the structure and binding of e-cadherin)

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28
Q

What is the result of C-met activation?

A

disrupted E-cadherin-mediated cell-cell junctions

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29
Q

What are morphogens?

A

signalling molecules that emanate from a restricted region of a tissue and spread away from their source to form a concentration gradient

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30
Q

What does the gradient of a morphogen signal determine?

A

The pattern of development of the cells

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31
Q

What can HGF/scatter factor induce?

A

Epithelial cells to dissociate and scatter

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32
Q

What else can have a similar effect to HGF?

A

EGF

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33
Q

What does the increased proteolytic activity of tumours facilitate?

A
  • Invasion of the ECM at primary and secondary sites
  • Digestion of the endothelial BM
  • Angiogenesis
  • Activate proteases
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34
Q

What is the function of Urokinase plasminogen activator?

A

Plasminogen –> plasmin

Plasmin activates MMPs and degrades the ECM

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35
Q

What do MMPs do?

A

MMP2 - degrades type IV collagen (the type found in the BM)

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36
Q

What does Cathepsin K collagenolytic activity do?

A

Matrix degradation

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37
Q

What is an example of a serine protease?

A

Urokinase plasminogen activator (uPA)

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38
Q

What is an example of a cysteine protease?

A

Cathepsin K

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39
Q

What are the different mechanisms of cell motility?

A
  • Mesenchymal migration
  • Cluster/ cohort migration
  • Ameboid migration
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40
Q

What is mesenchymal migration?

A

send out stress fibre driven processes to push the membrane out and make new contact through the integrins and the focal adhesions. At the leading edge of the cell there is also proteases being made.

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41
Q

What is cluster/ cohort migration?

A

Cells at the leading edge drag others along. The cells at the leading edge are making new contacts (integrin mediated) and making proteases at the front to degrade as they move along

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42
Q

How are cells connected in cluster/cohort migration?

A

by cadherins and gap-junctional communication

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43
Q

What is ameboid migration?

A

They send processes out in every way until they find the favourable way to move through the ECM

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44
Q

What type of tumour cells tend to move using Ameboid migration?

A

Lymphoma cells

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45
Q

What are the modes of tumour spread?

A
  • Lymphatic
  • Haematogenous
  • Transcoelomic
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46
Q

Why is lymphatic spread easier than haematogenous?

A
  • the lymphatic capillaries are thin-walled single layers of endothelial cells - they lack inter-endothelial tight junctions
  • They are not covered by smooth muscle
  • no basement membrane
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47
Q

What is commonly spread through haematogenous spread?

A

Sarcomas

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48
Q

What is Transcoelomic spread?

A

Across the peritoneal cavity

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49
Q

What are the three steps of a tumour moving through a capillary?

A
  1. Intravasation
  2. Transport
  3. Extravasation
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50
Q

What is intravasation?

A

The movement of the tumour cells from their primary sites into the capillary

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51
Q

What is extravasation?

A

The movement of the tumour cells from the vessel to its new site

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52
Q

Why do most tumour cells not survive transport?

A
  • Shear stress of blood flow can destroy them
  • Cells must avoid immune detection
  • Anoikis
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53
Q

What is an emboli and how can it help the cancer avoid immune detection?

A

White blood cells and platelets attach to the tumour cells so the body may not recognise it as a threat

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54
Q

What is anoikis?

A

a form of apoptosis for cells that are meant to be attached to the ECM – if they detach they go through a process to apoptose but since it is slightly different it is called anoikis.

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55
Q

What are the steps of intravasation?

A
  • Attachment
  • Degrade BM
  • diapedesis
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56
Q

What are selectins?

A

carbohydrate-binding transmembrane molecules

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57
Q

Where is P-selectin found?

A

Platelets and endothelial cells

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58
Q

Where is E-selectin found?

A

endothelial cells

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59
Q

What are E-selectins important for in cancer?

A

the attachment of cancer cells to endothelium

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60
Q

Where is L-selectin found?

A

leukocytes

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61
Q

What is the main physiological function of all selectins?

A

to mediate leukocyte recruitment to sites of inflammation or to lymphoid tissues

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62
Q

What happens when VEGF is transcripted?

A
  • Endothelial cell proliferate, penetrate basement membrane & migrate.
  • Formation of invasive endothelial tips (angiogenic sprouting) is followed by stabilisation of some and regression of other vessels.
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63
Q

What happens in angiogenesis in cancer?

A

Prolonged increase of angiogenic activators which doesn’t turn off and there is no increase of angiogenic inhibitors which means it just continues on.

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64
Q

What is the “seed and soil” theory?

A

secondary growth of cancer cells (the “seed”) is dependent on the microenvironment of the distant organ (the “soil”)

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65
Q

What is the mechanical theory of metastasis?

A
  • Mechanical factors influence the initial fate of cancer cells after they have left a primary tumour.
  • Blood-flow patterns from the primary tumour determine which organ the cells travel to first.
  • The relative sizes of cancer cells and capillaries lead to the efficient arrest of most circulating cancer cells in the first capillary bed that they encounter.
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66
Q

What makes up the tumour microenvironment?

A

various cell types including endothelial cells forming lymph and blood vessels, pericytes, stromal fibroblasts and bone marrow derived cells such as macrophages, neutrophils, mast cells and mesenchymal stem cells

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67
Q

How does the tumour microenvironment contribute to tumour progression?

A
  • secretion of growth factors, cytokines and chemokines

- by the rearrangement of ECM3 preparation of the “soil” at the putative distal site of metastasis

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68
Q

What are M1 macrophages?

A

Tumoricidal

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69
Q

What do M2 macrophages do?

A

Promote tumour growth

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70
Q

How do macrophages promote tumour growth?

A
  • chronic inflammation – increased risk of cancer
  • immune suppression – recruit immunosuppressive cells
  • angiogenesis - secrete angiogenic factors
  • invasion/ metastasis - CSF1/EGF paracrine loop
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71
Q

What is a delusion?

A

fixed false belief held despite evidence to contrary, out with sociocultural norms

72
Q

What is a hallucination?

A

sensory perception in the absence of external stimuli – seeing things that aren’t there

73
Q

What is an illusion?

A

misperception of real external stimuli – seeing a face in a cloud – no face but your brain interprets the shapes as a face

74
Q

What is mood?

A

subjective feeling of sustained emotion (happy, sad)

75
Q

What is affect?

A

objective immediate conveyance of emotion (blunt, flat, labile)

76
Q

What is pathological depression?

A

“a biochemical disorder with a genetic component and early exposure experiences make it so someone can’t appreciate sunsets.” (Prof Sapolsky)

77
Q

What are the chances someone will develop depression if a close family member has depression?

A

60% if an identical twin has it

40% if a primary relative has it

78
Q

What are medical comorbidities for depression?

A

Thyroid conditions, Heart failure, MS

79
Q

What is an example of a medication that can cause depression?

A

steroids - usually cause mania but can also cause depression

80
Q

What are the neurochemical causes of depression?

A

decreased serotonin, dopamine and noradrenaline

81
Q

What is used to set the clinical features required for depression diagnosis?

A

ICD-10

82
Q

What are the biological features of depression?

A
  • Diurnal variation
  • Insomnia
  • ↓ appetite
  • ↓ weight
  • ↓ libido
  • Constipation
  • Amenorrhea
83
Q

What are the core symptoms of depression?

A

↓ mood +/- anhedonia +/- fatigue.

Every day >2 weeks

84
Q

What are the cognitive symptoms of depression?

A
  • ↓ concentration
  • Slow - Very slow speaking etc.
  • Loss of self esteem
  • Hopeless
85
Q

When someone is manic how will you feel talking to them?

A

They are very funny and you often find yourself laughing with them

86
Q

What is it like talking to someone who is psychotic?

A

Hard to follow what they are saying (e.g. speaking about aliens and stuff)

87
Q

How is the severity of depression ranked?

A
  • Mild - >2 core + >2 associated, function ok
  • Moderate – >2 core + >4 associated, function ↓
  • Severe – >2 core + >6 associated, function ↓↓ +/- psychosis
    (if someone has psychosis automatically severe)
88
Q

What happens in psychosis associated with depression?

A

Delusions and hallucinations

89
Q

What can delusions of someone with psychosis associated with depression be?

A

Mood congruent (‘nihilistic’):

  • Guilt – believe they’re bankrupt
  • Poverty
  • Hypochondriasis
  • Persecutory
  • Cotard’s syndrome
90
Q

What is Cotard’s syndrome?

A

self / part of self is dead – seen in really severe depression

91
Q

What can hallucinations of someone with psychosis associated with depression be?

A

auditory 2nd person – address the person as you (e.g. “You’re stupid, you’re rubbish, you should die.”)

92
Q

What are the potential outcomes of depression?

A
  • Recurrent depressive disorder (60%)
  • Substance misuse (40%)
  • Anxiety (40%)
  • Suicide (attempted 9%), x8 mortality
  • Cardiovascular disease
93
Q

How can depression cause CV disease?

A

long standing depression has physical effects that can lead to obesity etc.

94
Q

What are potential differential diagnoses for depression?

A
  • Dysthymia
  • Atypical depression
  • Adjustment reaction
  • Grief
95
Q

What is Dysthymia?

A

↓mood, chronic >2yrs but not enough depression

96
Q

What is cyclothymia?

A

alternating ↓mood (mild), ↑ mood (mild)

97
Q

What is atypical depression?

A
  • ↓mood, reversed associated symptoms (sleeping too much eating too much etc.)
  • SAD – winter
98
Q

What is an adjustment reaction?

A
  • Adaptation to significant recent stressor
  • Can include low mood
  • Onset <1 month from stress
  • Duration <6 months max
99
Q

What is abnormal grief?

A
  • intense, prolonged (>6 months)
  • delayed (2 weeks)
  • absent (inhibited).
100
Q

What is the Kübler-Ross Model for grief?

A

(DABDA)

  • Denial
  • Anger
  • Bargaining
  • Depression
  • Acceptance
101
Q

How is depression assessed?

A
  • Clinical history
  • Risk assessment – post- partum depression (risk to mother and baby), risky jobs – pilot, driver etc.
  • MSE (mental state exam)
  • Physical exam
  • Baseline blds
102
Q

What are the biological (meds) treatment options for depression?

A
  • SSRIs
  • TCAs
  • MAOIs
103
Q

What are SSRIs?

A

Selective serotonin reuptake inhibitors

104
Q

What are some examples of SSRIs?

A

Citalopram and sertraline

105
Q

What are TCAs?

A

Tricyclic antidepressants

106
Q

What are some examples of TCAs?

A

Amitriptyline, Doxepine, nortriptyline

107
Q

What are MAOIs?

A

Monoamine oxidase inhibitors

108
Q

What are some examples of MAOIs

A

Isocarboxid, Moclobermide

109
Q

What is the mechanism of action of SSRIs?

A

They block the reuptake of serotonin by the presynaptic cell, increasing the amount present in the synapse and magnifying its effect

110
Q

what are the potential side effects of SSRIs?

A

Nausea, vomiting, weight gain, dizziness, discontinuation syndrome, anxiety, suicidality, mania (ensure there is no undiagnosed bipolar) , serotonin syndrome, cardiac effects (QTc prolongation)

111
Q

What is responsiveness of people to SSRIs?

A

33% response rule (a third get better immediately, a third take a while to respond, a third don’t respond at all)

112
Q

What are the potential side effects to TCAs?

A
  • Anti-adrenergic (↓BP)
  • Anti-cholinergic
  • ECG changes (arrhythmia, QTc prolongation)
113
Q

How do MAOIs work?

A

Block MAO-A, MAO-B which breaks down 5HT, NA, DA in CNS

114
Q

What are the potential side effects of MAOIs?

A
  • Hypertensive crisis; ‘cheese reaction’ (cant eat cheese on these)
  • MAO-A also in GI tract; breaks down tyramine
  • If blocked, ↑ ↑ BP
115
Q

What is ECT?

A

Electroconvulsive therapy

116
Q

How does ECT work?

A

Patients under anaesthesia and a seizure is induced
Altering seizure threshold increases neurotransmitters, redirects blood blow to different areas of the brain, and increases neurogenesis.
EXTREMELY EFFECTIVE

117
Q

What are the risks/ potential side effects of ECT?

A

generally just the risks of anaesthesia, but very rare side effect of memory issues

118
Q

What are the core principles of psycho treatment of depression?

A
  • talk
  • keep active
  • eat well
  • sleep well

There are no quick fixes

119
Q

What is a mental state examination?

A

An assessment of a person’s current state of mind

120
Q

When is a mental state examination carried out?

A

When you are taking a psychiatric history

121
Q

What is the purpose of a mental state examination?

A

To allow someone else to imagine the person from your description

122
Q

What is a mental state examination used for?

A

Alongside a psychiatric history in assessment and diagnosis of a patient , and, to assess progress during/ after treatment

123
Q

What are the stages of the mental state examination?

A
  • Appearance & Behaviour
  • Speech
  • Mood & Affect
  • Thought Form & Content
  • Perception
  • Cognition
  • Insight
124
Q

What is the first thing that kills cancer when it begins to develop?

A

The innate immune system - NK, NKT and gamma-delta T cells

125
Q

What happens when the innate immune system recognises something foreign?

A

they drive an immune response mainly through inferin-gamma that stimulates macrophages and pulls in dendritic cells

126
Q

What drives the adaptive immune response?

A

Dendritic cells

127
Q

What do dendritic cells pull in?

A

T and B cells

128
Q

What are cancers seen in children associated with?

A

developmental aspects of the body (osteosarcoma, glioblastoma, leukaemia’s) these are all developmental abnormalities

129
Q

What are the cancers seen in adults (organ cancers) associated with?

A

Exposure (and long term exposure) to carcinogenic factors drive the cancer

130
Q

What happens to tumours when the is immunoediting?

A

The immune system kills of everything is can in terms of the tumour but some cells, known as low antigenicity tumour cells are left which forms the seed for the cancer developing

131
Q

What are the three E’s of immunoediting?

A

Elimination
Equilibrium
Escape

132
Q

What is equilibrium in terms of tumours?

A

the cancer and the immune system reach a balance which is dynamic but can last for long periods of time even decades

133
Q

What is a tumour known as when it is in an equilibrium?

A

An occult tumour.

134
Q

Why are immunosuppressed patients more likely to develop cancer?

A

There has been an occult tumour in their body that due to their immunosuppression has been able to break free and Gr0w. (THIS IS ESCAPE)

135
Q

What happens at the end point of carcinogenesis? (end stage cancer)

A

Loss of immune control

136
Q

What are the three options for cancer treatment?

A

Surgery
chemo/radio therapy
Immunotherapy

137
Q

When is surgery particularly useful in cancer treatment?

A

Primary tumours

138
Q

Why is chemo/radio therapy damaging to patients?

A

it has an effect on fast growing cells that are normal. The cells that are damaged by these treatments are fast growing cells so follicular cells and cells of the gut mucosa are particularly effected, so this is why patients undergoing chemotherapy lose their hair and get mucositis.

139
Q

Why is the immune system further compromised in chemo/radio therapy?

A

Immune cells are fast growing and these therapies damage fast growing cells

140
Q

What are the different approaches to immunotherapy?

A
  • Vaccination strategies
  • Non-specific therapies
  • Antibody therapies
  • Cell based therapies
141
Q

What are non-specific therapies?

A

they are not trying to drive something specific against the cancer, but are generating a response which also has the benefit of killing cancer.

142
Q

Why is T cell therapy not very effective?

A

when you put it back in the patient after growing it up it has lost the cues that got it to the tumour in the first place so it isn’t as effective

143
Q

What did Dr William Coley discover?

A

that in patients who had infections and cancer at the same time the cancer wasn’t as severe

144
Q

What did Dr William Coley’s discovery lead him to try?

A

he used bacterial preps to treat patients with severe facial cancers and injected it into the site which caused inflammation and drove the immune response to destroy the cancer

145
Q

What is Aldara?

A

a drug used for precancerous conditions that follows a similar theory to Dr William Coley

146
Q

What does Aldara do?

A

it’s a tolite receptor agonist. It is a viral mimic that contains a molecule that the immune system sees as a viral attack and when it is painted on you get a huge immune response. If it works, it then clears, and you get resolution of the precancerous condition

147
Q

What is the issue with Aldara?

A

it is very difficult to gage if the patient will respond, one person could only get a mild rash which wouldn’t do much to the cancer but another person could have a very extreme reaction to the treatment which can become very hard to control

148
Q

What does IL-2 therapy do?

A

a T-cell growth factor that is used to drive T-cell growth in the body. The idea is that the immune system recognises the cancer but isn’t powerful enough to destroy it.

149
Q

What is the issue with IL-2 therapy?

A

IL-2 is very toxic and is very difficult to administer. You can treat patients with large doses but there is a very narrow therapeutic window. Very narrow window between the therapy being curative and so toxic it can kill the patient.

150
Q

What is the issue with monoclonal antibody therapy?

A

it requires a target. Most are aimed at blood cancers and target things only expressed on blood cells and nowhere else which can be quite challenging

151
Q

What are the 4 mechanisms of MAB therapy?

A
  • Apoptosis induction
  • Complement mediated cytotoxicity
  • ADCC
  • Conjugated to toxin/ isotope
152
Q

How do MABs induce apoptosis in targets?

A

They block a receptor or a target that the tumour cell needs to grow and it will apoptose

153
Q

How do MABs use complement mediated cytotoxicity?

A

the complement binds to the antibody as normal and destroys the tumour

154
Q

How do MABs use ADCC?

A

ADCC - antibody dependent cytotoxicity -

mark the tumour cell so that other immune cells can come and attack it like macrophages and NK cells

155
Q

What is the issue with using MABs that are Conjugated to toxin/ isotope?

A

it’s hard to get the antibody on the tumour without it sticking somewhere else and causing toxicity

156
Q

what can happen if a cancer becomes sneaky to MABs?

A

It can downregulate the receptor that is being targeted by the MAB

157
Q

What are the main drugs that target PD-1?

A

Nivolumab and pembrolizumab

158
Q

What was the first drug used to target the immune system rather than the cancer?

A

Ipilimumab

159
Q

What does PD-L1 do?

A

It protects cancer from immune attack

160
Q

What happened when it was trialed using more than one checkpoint inhibitor?

A

It didn’t work much better but the toxicity was so high the patients came off the trial early and died

161
Q

What is needed for antibodies to work effectively?

A

A functional immune system

162
Q

What approaches can be taken to give the immune response back in cancer?

A
  • Haematopoietic stem cells
  • Tumour-Infiltrating T cells (TILs) – Tcells already killing cancer and make more
  • Dendritic Cell Vaccines – the guide and coordinate the adaptive immune response
  • NK cells – involved in early stages of cancer so could try them again
  • Gamma-delta T cells – involved in early stages of cancer so could try them again
163
Q

How is cell therapy carried out?

A
  • High dose chemo or radio therapy is used to completely destroy the immune system.
  • The haematopoietic stem cells are then re-infused into this ‘clean system’ then hopefully the innate immune system recovers quickly
  • slowly the adaptive immune system comes back.
  • Hopefully the cancer has already been completely destroyed in the bone marrow (usually used on blood cancers) and you are looking at a cure.
164
Q

What is autologous stem cell therapy?

A

Using the patients own cells

165
Q

What is allogeneic stem cell therapy?

A

Putting someone else’s bone marrow in

166
Q

How is autologous stem cell therapy done in a patient with cancer?

A

What can be done is try to remove the cancer from the bone marrow before you put it back in

167
Q

What is the advantage of autologous stem cells?

A

No graft vs host disease

168
Q

What is the disadvantage of autologous stem cells?

A

There may still be cancer in the cells so the chance of relapse is higher

169
Q

What are CAR-T cells?

A

Genetic modification of the patient’s own T-cells

CAR - chimeric antigen receptor

170
Q

What doe CAR-T cells do?

A

rather than trying to use HLA or T cell receptors they have made an entirely new receptor completely from scratch

171
Q

What is the new receptor on CAR-T cells made up of?

A
  • a molecule that contains the end of an antibody which is attached to a spacer
  • an intracellular component
  • an intracellular signalling component which is taken from a few different signalling molecules
172
Q

What is an issue with most cancer treatments?

A

COST

173
Q

What is PTLD?

A

post-transplantation lymphoproliferative disease

174
Q

How does Epstein-Barre Virus-driven B cell lymphoma occur in transplant patients?

A

If you get Epstein barre you never get rid of it, it stays in your body. Normally this has no consequence but this has become an issue in transplant patients as they will be immunosuppressed so there is a chance the virus can come back and reactivate. This transforms B cells into cancer.

175
Q

What are the first line treatments against PTLD?

A

Chemotherapy - not preferred because chemo on top of a transplant can be very toxic
Rituximab - works well

176
Q

What happens if PTLD relapses?

A

There are not many treatment options - the mortality rate is 80-90%

177
Q

What is the new treatment option for relapsed PTLD using SNBTS T cell bank?

A

When blood is donated it is broken up into its components and usually the WBCs are gotten rid of. Within these WBCs will be T cells and roughly 50% will be carrying Epstein barre virus and will be able to kill it so these can be used as an allogeneic treatment for patients with PTLD. These are isolated and frozen for when someone comes in with PTLD and these can be used to treat them. It can be curative but it doesn’t need to be all it needs to do is protect the patient for a year till the immunosuppression can be lightened and their own immune system can take over protecting against EBV.

MBChB - year 2 (25 decks)

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