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BIMM 134 - Cancer > Week 10 > Flashcards

Week 10 Flashcards

1
Q

Metastatic cascade: step 1

3 points

A

Cell detachment

Decrease in cell-cell interaction

E-Cadherin is lost

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2
Q

Metastasis cascade: step 1 - Normal role of e-cadherin

A

To attach normal cells

“Molecular glue”

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3
Q

Metastasis cascade: step 1 - what else happens?

A

B - catenin translocates into the nucleus and acts as a TF

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4
Q

Metastasis cascade: step 1 - what else happens? Pt. 2

A

Increase in pro-tumor molecules via b - cat

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5
Q

Metastasis cascade: step 2 - basement membrane detachment

Explain what happens here

3 points

A

Decrease in normal cell-BM (basement membrane) interactions

Increase in protease production that degrade BM leading to loss of laminin

Upreg of integrins (AvB3 + AvB5)

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6
Q

Step 2/3 - integrin signaling

Outside-in

Inside-out

A

Integrin binds to ECM, initiates intracellular signaling, causes cell proliferation + cytoskeletal changes

Intracellular signals on the inside leads to reduced integrin-ECM binding

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7
Q

Step 3: MATRIX DEGRADATION + CELL MIGRATION

3 points

A

Cancer cells outside blood vessels in ECM

MATRIX degraded via increase in MMPs + uPAs

cancer cells can go through the lining

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8
Q

Step 3: MATRIX DEGRADATION + CELL MIGRATION

What increases?

A

MMPs + uPAs (proteases)

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9
Q

What’s MMP? Where is it upregulated?

A

Matrix Metalloproteinase
upregulated in CAFs, TAMs, tumor cells

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10
Q

What is uPAs?

what converts into what

A

urokinase plasminogen activator
when bound to its receptor, it converts plasminogen to plasmin
which degrades matrix

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11
Q

Step 4 : INTRAVASATION

3 points

A

Entry into circulatory system

EMC has been degraded

Endothelial cell lining is degraded which was connected by VE- cadherin

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12
Q

What happens when the VE-cadherin degraded?

A

Endothelial cells separate in a way where cancer cells go get through

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13
Q

How is VE-cadherin degraded? How are endothelial cells separated?

4 points

A

1) MMPs bind to PAR (protease activated receptor) on EC

2) Notch receptor on cancer cell binds to Notch ligand on EC

3) Activation if ADAM12

4) EC retraction by TNF-a (from TAMs) and TGF-b (from cancer cells)

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14
Q

What’s TMEM?

3 points

A

TMEM: tumor microenvironment of metastasis

combination of tumor cells, endothelial cells, and macrophages
negatively correlated with survival

Degrades VE-cadherin and separates endothelial cells

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15
Q

Step 5: TRANSPORT/SURVIVAL in blood steam

3 points

A

ATP, cancer cells gphave entered the bloodstream

To survive, Cancer cells surround themselves in platelets to form emboli for mechanical and immune protection

Can metastasis

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16
Q

Step 6: capillary bed arrest

What are the 2 ways in which cancer cells will adhere to capillary bed?

A

Way 1) Homing/receptor-mediated arrest = cells bind to receptors to attach themselves to capillary bed

Way 2) Mechanical/physical arrest = cells get trapped in the capillary bed because they’re too big to fit through

17
Q

Step 7: EXTRAVASATION - getting out of the bloodstream

5 points

A

Cancer cells must make it out of the
bloodstream to the underlying tissue to proliferate and metastasis

Process: cancer cells attach to endothelial lining via platelets already attached to cancer cells

Attachment results in increase of inflammatory response + attract macrophages

Results in changes of endothelial cell receptors which increases VEGF

VEGF triggers endothelial cellular connection + retraction

18
Q

Step 8: creating a suitable environment in order for secondary growth to occur

A

Cancer cannot grow w/o correct environment

19
Q

Way 1 for cancer to grow suitable environment

A

Optimal tumor environment already exists

Seed and soil theory vs mechanical theory

20
Q

Seed and soil theory

A

seed = cancer cells w/ correct receptors
Soil = the matrix w/ the correct GF present at the secondary site

Theory argues that seed can be planted anywhere but it will not grow unless it has the right soil

21
Q

Mechanical theory

A

Cancer cells metastasis to where they do based on distance given CC are bigger so they get stuck in an earlier capillary bed

22
Q

way 2 for cancer to grow sutible environment

A

Environmental change to optimize environment - systemic signals that will change the makeup of the soil

Injury, inflammation, infection, long term exposure to carcinogens, removal of primary tumors

23
Q

What are micromets?

A

Cancer cells that have broken away from primary tumor

Are dormant until systematic signals. Secondary tumor grows

24
Q

way 3 for cancer to grow sutible environment

A

CANCER CELLS CREATE
SUITABLE ENVIRONMENT AFTER
ARRIVING by….

(1) THE CANCER CELLS DIRECT NORMAL CELLS WITHIN THE NEW ENVIRONMENT TO PRODUCE GROWTH FACTORS

(2) rELEASE GROWTH FACTORS NTO THE EXTR2ACELLULAr MATRIX

25
Q

OSTEOLYTIC CASCADE

A

In breast tissue
Cancer cells in og tumor Release PTHRP

Activate osteoclasts which breaks down the bone

TGFbeta is released

Helps cancer growth

26
Q

OSTEOBLAST CASCADE

A

In prostrate tissue
Cancer cells in og tumor stimulated osteoblasts which increase bone production

BMP is released

GF are released

Helps cancer grow

27
Q

OSTEOLYTIC CASCADE VS. OSTEOBLAST CASCADE

A

Both help cancer bc of INCREASE in GF

28
Q

Way 4 for cancer to grow sutible environment

A

CANCER CELLS SEND OUT SIGNALS TO
CREATE THE PERFECT ENVIRONMENT &
ARRIVE LATER

29
Q

Emphasizing way 4 of cancer making its perfect environment

A

Remodel kitchen before you arrive

Primary tumor @ first site can send signals to secondary site to release tumor derived factors (TD) + exosomes

——> also sends signals to the bone marrow which sends signals to secondary site ???

Tumor derived factors are able to modify + activate secondary site

Modified stroma can recruit bone marrow cells to further activate and prepare tissue

Cancer cells arrive @ optimal environment

30
Q

What are exsosomes

A

Micro vessicles containing RNA + proteins

31
Q

animal models: Syngeneic

A

Inject mouse tumor cells under skin

32
Q

animal models: Orthotopic

A

Inject cells in tissue of origin (i.e. breast)

33
Q

animal models: Immunocompromised mice

A

Allows human cancer cell growth in
mouse model

34
Q

types of immunodeficient mice

A

Non-Obese Diabetic (NOD)/SCID

Lack B and T cells and depleted NK

NOG/NSG: these also lack dendritic
cells/cytokines and lack NK cells

35
Q

what doe nude mice lack?

A

T cells

36
Q

humanized BLT mice

A

generates a human-like immune system

better at mirroring human cancer + immune response

37
Q

GEMM is good for…

A

long term studies given TET operon promoter

38
Q

Patient-specific humanized mice

A

Tumor biopsy transplanted into mouse creating similar tumor microenvironment

BIMM 134 - Cancer (4 decks)

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