Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Tissue Pathology > Cancer > Flashcards

Cancer Flashcards

1
Q

Role of beta catenins in Wnt

A

Central transducer of canonical Wnt singles => enter the nucleus => relief of TCF/LEF mediated transcriptional repression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Beta catenin is found in 3 complexes

A

Cadherin
TCF/LEF
APC, axin, GSK3, CK1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Beta catenin is located at which junction

A

Cell-cell adherens junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Beta catenin is located at which junction?

A

Cell-cell adherens junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Beta catenin is regulated by ________________ in adherens junctions.

A

Tyrosine kinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Beta catenin is regulated by ___________________ such as ______ in cytoplasm

A

Serine kinases
GSK3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What three pathways do Wnt target genes activate? And what do all pathways begin with?

A

[1] Wnt/Beta-catenin
[2] Wnt/CA2+
[3] Planar cell

Binding of Wnt to Frizzld and recruitment of dishevelled family proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Repression of _________ expression has a key role in pathological EMT

A

E-cadherin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Downregulation mechanisms of E-Cadherin [6]

A

Transcriptional regulators
Genetic mutations of gene CDH1
Proteolytic degradation
Receptor tyrosine kinases -> phosphatase
Oncogenes -> Fos
TCF/Beta-catenin complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outcomes of down regulating E-Cadherin [4]

A

Reduction of strength of cellular adhesion
Increase cell motility
Cancer cells to cross basement membrane and metastasise
Interaction in Wnt/Beta-catenin pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Loss of E-cadherin has two effects on cancer

A

Alters signalling of beta-catenin/wnt
Modulates cell-cell adhesion

=> development of epithelial derived tumour types
Tumour progression - invasion or metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

loss of cadherin from adherens junctions results in….

A

Release of its partner beta-catenin, into cytosol which activates Wnt pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Oncogenes

A

Mutated proto-oncogene becomes oncogene => loss of growth control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Tumour suppressor genes

A

Copies of the TSG on both homologues are mutated => loss of growth control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Factors influencing invasion by cancer cells [3]

A

Abnormal or increased cell motility
Secretion of proteolytic enzymes
Decreased cellular adhesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Two types invasion

A

Single cell invasion
- mesenchymal
- amoeboid

Collective cell migration
- coordinated
- cohort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Increased cellular motility indicates abnormalities in the regulatory mechanism enabled by:

A

Autocrine growth stimulation
Reduced apoptosis
Telomerase activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the three families of matrix metalloproteases?

A

[1] interstitial collagenases
- degrade collagen type I, II and III

[2] gelatinases
- degrade type IV collagen and gelatin

[3] stromelysins
- degrade type IV collagen and proteoglycans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

VEGF angiogenesis

A

Tumour cannot grow beyond 1-2mm in diameter due to hypoxia
Secretion of VEGF
Formation of new vascular system that provides nutrients and oxygen
Tumour growth and proliferation
Potential escape to metastasise

20
Q

Podosomes and invadopodia ECM degradation through:

A

Zinc-related MMPs
Cathepsin
Cystein protease
Serine protease

21
Q

Podosomes

A

Found in epithelial cells, smooth and cardiac muscle and macrophages
Actin centre and integrins
Form bridges with cytoskeleton and ECM

22
Q

Invadopodia

A

Found in carcinoma cells, fibroblasts
Larger actin centre
Lead invasion via degradation of ECM

23
Q

6 steps in cancer progression

A

Local invasion
Intravasation
Dissemination
Extravasation
Micrometastasis
Macroscopic metastasis

24
Q

Paget’s seed and soil hypothesis

A

1889

25
Q

What is the cancer metastasis target?

A

Generation of permissive micro environment in target organ
- VEGFR1 expressing progenitor cells go to pre-metastatic site
Deposition of fibronectin indicate potential cancer cells incoming

26
Q

Stroma cells

A

Provide CT framework of the tumour
Important in health and pathology
Genetic mutations in epithelial cells result in activated stroma
Tumour and trona evolve together

27
Q

Mutations in _____________________ that specifically regulate paracrine growth factor expression initiate epithelial cancers

A

Stromal cells

28
Q

Mutations in _____________ that specifically regulate paracrine growth factor depression initiate epithelial cancers

A

Stromal cells

29
Q

Stroma cells secrete (2)

A

Signal proteins that stimulate cancer cell growth and division
Proteases for further remodelling of ECM

30
Q

Origin of carcinoma associated fibroblasts

A

Trasndifferentiation of cancerous epithelium through EMT
Mesothelium, pericytes
Endothelial cell via endoMT
Activation of local fibroblasts
Bone marrow MSC recruitment
CAF stem cell? Self-renewal

31
Q

CAFs function

A

Interaction with cancer cells
Tumour immunology - CAFs are capable of sampling, processing, and presenting tumor antigens via major histocompatibility complex 1 (MHC-I).
Angiogenesis
ECM remodelling

32
Q

Track generation in cancer

A

Tracks are made in ECM by fibroblasts
Squamous cell carcinoma cells use these tracks to invade ECM

33
Q

Anoikis

A

Normal response in cells that lose contact with surrounding ECM an neighbouring cells

34
Q

Avoiding Anoikis

A

Survival signals derived from their junctional signalling networks
Normal matrix attachment

35
Q

Anoikis pathway

A

Integrin signalling initiates BH3-only pro-apoptotic genes
Inhibition of anti-apoptotic proteins
- BH123 protein aggregation
- opening pores in outer mitochondrial membrane
Activates caspase cascade especially from cytochrome C
Cell death

36
Q

Anoikis pathway autocrine mechanisms

A

Production of TrkB protein
Activates Akt/PkB pathway

37
Q

Paracrine mechanisms of Anoikis

A

Involves interactions with external components e.g. immune cells

38
Q

4x pathways of Anoikis avoidance

A

EGFR
Glucose transporters
IGF1R
FAK

39
Q

Give the EGFR resistance pathway

A

EGFR -> SRC -> P13K -> mTOR

40
Q

Give the glucose transporter resistance to Anoikis pathway

A

Glucose transporters -> NADPH -> AMPk -> ATP production and survival

41
Q

IGF1R resistance pathway to Anoikis

A

IGF1R -> P13k -> mTOR

42
Q

FAK structure

A

125 kDa protein
N-terminal FERM domain
Central kinase domain
C-terminal FA targeting domain

43
Q

FAK function

A

Mediates integrin and RTK signalling

44
Q

Explain nuclear and FAK promotion of cell proliferation and survival

A

Autophosphorylation and Src recruitment => activation of FAK
Triggers P13K pathway
Phospholipid production
Akt kinase activation
Inhibition of cell death machinery

45
Q

FAK interaction with P53

A

Loss of cell adhesion -> increased FAK
FERM domain of FAK can interact with p53 suppressing its transcriptional activity
FAK promotes ubiquitin proteasome mediated p53 degradation by mdm2

46
Q

FAK interaction with RIP death domain

A

FAK can directly inhibit Anoikis by sequestering and inhibiting death domain of RIP protein
This protein can either induce apoptosis or lead to pro-survival signalling
FAK binding shifts towards pro-surviving signalling

Tissue Pathology (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions