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pbl week 2 Flashcards

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1
Q

what is invasion

A

growth by infiltration and destruction of surrounding tissues

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2
Q

metastasis

A

spread of tumour to -and growth at - ectopic sites , via blood, lymphatics , intra-epithelial route or transcoelomic route.

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3
Q

info on the basement membrane

A

it delineates the epithelial or endothelial tissues
it is secreted by basal epithelial cells/endothelial cells
it is a layer of the extracellular matrix
contains fibronectin , type 4 collagen and laminin
it acts as a barrier to spread *carcinoma cells

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4
Q

the metastatic cascade steps

A 
local invasion 
neovascularisation/angiogenesis
detachment
intravasation
transport
lodgement/arrest
extravasation 
growth at ectopic site
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5
Q

what are properties of metastatic tumour cells

A
  1. reduced cell to 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
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6
Q

for carcinomas (and melanoma), the cancer cells acquire the
ability to escape the ‘glue’ that binds them together, via mutations
(or epigenetic alterations) in

A

E-cadherin, or in molecules that
regulate or interact with it.
•mutations in transcription factors that regulate E-cadherin
(snail, slug, twist
•mutations in proteins that interact with ECD (b-catenin, APC)
• ECD promoter methylated (inactive) in some carcinomas

•‘exon-skipping’ in diffuse-type gastric tumours ~ lacking exons that
encode Ca2+
-binding domain

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7
Q

what are cell adhesion molecules

A

integral to plasma membrane and bind to ECM molecules / they are found in basal epithelial cells and in focal adhesions of migrating cells.

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8
Q

what are integrins

A

Integrins are proteins that function mechanically, by attaching the cell cytoskeleton to the extracellular matrix (ECM), and biochemically, by sensing whether adhesion has occurred. The integrin family of proteins consists of alpha and beta subtypes, which form transmembrane heterodimers

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9
Q

example of an integrin

A

alpha 5 beta 1 which is the fibronectin receptor so it binds fibronectin

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10
Q

what specific integrin promotes invasion and metastasis

A

vitronectin receptor (integrin alpha v beta3) on invasive front of melanoma

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11
Q

the possible mechanisms by which integrins encourage cancer

A

decreased adhesion to basement membrane surrounding epithelium

increased migration through stroma

increased adhesion to basement membrane or endothelial cells of blood vessels which is a binding site for proteolytic enzymes

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12
Q

what is HGF

A

is the same as scatter factor and it can induce epithelial cells to dissociate and scatter in culture . HGF is a mitogen (GF) a motogen (motility factor) and a morphogenic with a development role .

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13
Q

where is HFG produced

A

produced by stromal cells in a tumour (cells in the tumour micro-environment

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14
Q

what is c-met `

A

a receptor tyrosine kinase on tumour epithelial cells

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15
Q

what happens when HGF binds with c-met

A

activation of c-met leads to increased tyrosine phosphorylation of b-catenin
in tumour epithelial cells which disrupts ECD-mediated adhesion.
HGF/c-met - example of tumour-stroma interaction

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16
Q

what cells are in a tumour microenvironment

A 
cancer-associated fibroblasts (CAFs)
immune cells that have infiltrated the tumour *
myofibroblasts
tumour-associated vasculature
pericytes

And these secrete - growth factors , chemokines and enzymes

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17
Q

what are pericytes

A

contractile cells that wrap around the endothelial ells that line the capillaries and venules throughout the body

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18
Q

what does the tumour microenvironment facilitate ?

A

tumour-stromal interactions

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19
Q

what is the stromal component of the tumour component c-met?

A

HGF

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20
Q

what is the stromal component of the tumour component chemokine receptor (CKR)

A

chemokine

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21
Q

what is the stromal component of the tumour component protease receptor

A

protease

22
Q

what is the stromal component of the tumour component integrin alphavbeta3

A

MMP2

23
Q

what is the stromal component of the tumour component TGF

A

stromelysin

24
Q

what is the stromal component of the tumour component VEGF

A

VEGFR

25
Q

example of serine protease

A

urokinase plasminogen activator (uPA) , plasmin binds to receptors on tumour cell surface (uPAR)

26
Q

examples of matrix metalloproteinases - MMPs

A

collagenases, gelatinases , stromelysins , membrane-tupe MMPs

soluble forms with ECM homology can bind to integrins e.g. MMP-2 binds to alphavbeta3

produced by white blood cells and are associated with tissue/wound repair

27
Q

what leads to MMP expression

A

tumour-stromal interaction

28
Q

what does HIF do

A

hypoxia inducible factor .
promotes expression of VEGF .
the newly formed vessels are weak and leaky thus allowing fibrinogen to leak which is then converted to fibrin by pro coagulants.
fibrin forms a clot which is a good surface for endothelial cell growth

29
Q

steps to extravsation

A

rolling, activation , adhesion and diapedesis

30
Q

how does VEGF work

A

the VEGF binds to VEGFRs on near by endothelial clls causing the endothelial cells to migrate towards the tumour and start forming new blood vessels

31
Q

principle sites of metastasis

A

breast -bone, bone, lungs, liver , brain

lung adenocarcinoma - brain, bones , adrenal gland , liver

skin melanoma - lungs , brain, skin liver

colorectal - liver and lungs

pancreatic - liver and lungs

prostate - bones

sarcoma - lungs

32
Q

what is lymphocyte homing

A

lymphocytes have the ability to intravasate and extravasate because they need to carry out immune surveillance . they are about to transiently bind to endothelial cells via selectin molecules allowing them to bind and roll onto endothelial cells and start intra/extravasation

33
Q

organ tropism

A

Clinical studies have identified a specific pattern for the metastatic spread of cancer

34
Q

Possible mechanisms for organ tropism

A

Selective adhesion to endothelium of target organs (selectins , CD44
variants)
• Selective response to GFs at ectopic site – e.g.,
PTHRP and IL-11 allow breast cancer cells to establish
osteolytic metastases
• Selective migration to CK source (differential CKR expression)
• Factors released by tumour / other cells cause changes in prospective
TME at secondary sites, creating pre-metastatic niche
• Balance of local angiogenic factors versus systemic anti-angiogenic
factors (angiostatin & endostatin)

35
Q

what is ecadherin

A

is a structure that is used to connect adjacent epithelial cells together. the e-cadherin is attached to the cytoskeleton intracellularly via alpha and beta catenin . E-cadherin is calcium dependent.

36
Q

what is exon skipping

A

when the axons encoding for the calcium binding domain in ecadherin are missing . the less ecadherin in tumour cells the more aggressive the tumour is .

37
Q

what is BRAF

A

IT is a member of the raf kinase family which are a family of growth signal transduction protein kinases .
it plays a role in the MAP kinase / ERKs signalling pathway .

38
Q

what is psychiatry

A

= medical specialty concerned with diagnosis, treatment

& prevention of mental health disorders

39
Q

clinical features of depression

A

core :
decreased mood , and or anhedonia and or fatigue

associated :
diurinal variation , insomnia, decreased appetite , decreased weight, decreased libido , constipation , amenorrhoea

decreased concentration, slow negative thinking , guilt, loss of self esteem, hopeless, suicide

Psychosis:
Delusions – mood congruent (‘nihilistic’)
Guilt, poverty, hypochondriasis, persecutory
Cotard’s syndrome – self / part of self is dead
Hallucinations – auditory 2nd person
”You’re stupid, you’re rubbish, you should die.”

40
Q

Cognitive distortions in depression

A

Minimizing, magnifying, arbitrary inference,
selective abstraction, personalization,
overgeneralization, catastrophizing

41
Q

severity of depression

A

Mild – >2 core + >2 associated, function ok
Mod – >2 core + >4 associated, function ↓
Sev – >2 core + >6 associated, function ↓↓
+/- psychosis

42
Q

bIPOLAR DISORDER diagnosis

A

more than two mood disturbances (hypomania and mania) , depression

43
Q

neurochemical pathogensis of depression

A

DECREASED levels of serotonin, NA and Dopamine

44
Q

Vemurafenib

A

Attacks the BRAF protein directly - it is reversible , ATP competitive inhibitor of the kinase domain of BRAF

These drugs shrink the tumours in about half of the people with metastatic melanoma with a BRAF gene change

45
Q

Immune surveillance

A

Elimination - immune system recognises and destroys potential tumour cells before they start to metastasise - cytoxic T cells (CD8) kill the tumour cells. APC. cells usually ingest tumour cells or theirbantigens present to T cells via MHC I

Equilibrium - when elimination isn’t completely successful. A process known as cancer immunoediting continuously shapes the properties of the tumour cells that survive

Escape - rumour cells have accumulated diffident mutations Elide the attentions of the immune system and grow unimpeded to become clinically detectable

46
Q

imatinib

A

tyrosine kinase inhibitor - blocks signals in cancer cells that helps them divide . Imatinib works by inhibiting the action of the abl-gene.

47
Q

Ipilimumab

A

is a monoclonal antibody.
CD-28 is an on switch for cytotoxic t cells
CTL4 is an off switch for cytotoxic t cells
ipilimumbad blocks the CTL4 antigen and enhances inflammation. also increases number of T cells

48
Q

Nivolumab

A
  • Nivolumab is an anti-PD-L1 monoclonal antibody.
  • The pathway includes two proteins called programmed death-1 (PD-1), which is expressed on the surface of immune cells, and programmed death ligand-1 (PD-L1), which is expressed on cancer cells. When PD-1 and PD-L1 join together, they form a biochemical “shield” protecting tumour cells from being destroyed by the immune system. • If cells display this, then the PD-1 receptor on the T cell gets activated and it will initiate programmed cell death of the T cell. However Nivolumab blocks this, and allows the T cell to function
49
Q

monoamine theory of depression

A

that depression is due to reduced activity of monoamines (dopamine, NA,serotonin).

50
Q

types of depression

A

reactive and endogenous

51
Q

selective seritonin reuptake inhibitors SSRIs

A

fluoxetine - selectively blocks 5-HT reuptakwe, usually first line of treatment.
• Nausea, vomiting, agitation, sexual dysfunction, hyponatremia, sweating

52
Q

tricyclic antidepressants

A

reduce noradrenaline and 5HT from the synaptic cleft , elavtes mood through increasing monoamine levels .
amytiptyline .
Anticholinergic effects, sedation, weight gain, sweating, hyponatremia, cardiotoxic effects, hallucinations

people and illness (5 decks)

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