13- Metastasis Flashcards Preview

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Flashcards in 13- Metastasis Deck (60)
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1
Q

What is metastasis?

A

spreading to other tissues

2
Q

Which type of tumor (primary or secondary) that is responsible for the death of patients?

A

secondary

3
Q

What do cancer patients die of?

A

organ failure

4
Q

What (freeway) systems do tumor cells use to travel throughout the body?

A

lymphatic | circulatory

5
Q

What are metastatic cells called?

A

mets

6
Q

What is parenchyma?

A

tissue area of an organ that is functional (inner part)

7
Q

What is stroma?

A

tissue part of an organ that is structural (outer part)

8
Q

Which, stroma or parenchyma, do tumor cells originate from?

A

can be from both

9
Q

Is the method that tumor cells spread random or systematic (there is a pattern)?

A

there is a pattern

10
Q

What are nude mice?

A

mice with no immune system = allows us to study carcinogenesis

11
Q

What is intravasation? When does this happen?

A

tumor cells push through endothelial cells to get into the vessels | after angiogenesis

12
Q

What is extravasation?

A

tumor exits vessels &raquo_space;> replicates and grows secondary tumor on another organ

13
Q

What is Stage I of cancer?

A

local | no invasion

14
Q

What is Stage II of cancer?

A

some invasion | tumor cells not yet seen in lymph nodes (via biopsy)

15
Q

What is Stage III of cancer?

A

more invasion | begin to see tumor cells in lymph nodes = may need to resect lymph nodes

16
Q

What is Stage IV of cancer?

A

metastasized tumor cells = have invaded other tissues

17
Q

How do we know it’s metastasis versus a primary tumor?

A

primary tumor = a lot of disruption of tissue (due to invasion) | mets = more defined orders

18
Q

Why do tumor cells have a preference? Why do they go to certain areas?

A

tumors have cell-surface receptors &raquo_space;> when traveling throughout body = areas secreting chemicals that stimulate its receptors = will stay there

19
Q

What is “metastasis homing”?

A

dictated by the relative abundance of chemokines and receptors on the tumor cell = the more of both = will stay at that area

20
Q

What does “SCP” stand for?

A

single clonal population

21
Q

What does metastasis homing help explain in oncology?

A

explains the patterns of secondary tumor formation certain cancers associate with

22
Q

What are the 3 types of homing mechanisms?

A

selective growth | selective adhesion | selective chemotaxis

23
Q

What is the homing mechanism of selective growth?

A

selectively grow only in organs with appropriate growth environments, but travel aimlessly | no chemokines involved

24
Q

What is the homing mechanism of selective adhesion?

A

stick only to endothelial cells at site of organ that it calls home

25
Q

What is the homing mechanism of selective chemotaxis?

A

tumor cells only travel to where its chemokine is being secreted

26
Q

Where do these tumor cells get the receptor from that is involved with homing?

A

from the cells they used to be prior to de-differentiation

27
Q

Do tumor cells look for and go towards the circulatory system because they need more O2/nutrients or are they sensing chemokines?

A

they are sensing nutrients

28
Q

Where do tumor cells get the tools to cut through basal lamina?

A

tumor cells have access to every gene in the genome = turn on genes that can allow them to do this

29
Q

What does the ECM consist of?

A

fibronectin, collagen, many other proteins

30
Q

What are matrix degradation enzymes?

A

tools that the tumor cells use to get through ECM

31
Q

What are matrix metalloproteases?

A

matrix degradation enzyme | takes shape of chainsaw | can be secreted, mostly is a cell surface molecule

32
Q

What is the most dangerous thing about a tumor cell?

A

when it gains the ability to spread

33
Q

Why is surgery out as an option if the tumor has metastasized? What is the recommended treatment?

A

because tumor has spread = surgery will be more risky as opposed to taking out one tumor, now it is many tumors | depend on chemotherapeutic drug targeting metalloproteases

34
Q

What is TIMP2?

A

protein that inhibits metalloprotease from cutting their target = makes it harder for tumor cells to walk/invade

35
Q

Do all tumor cells need to have the ability to cut through the ECM?

A

no | tumor cells work as a team = some can break through ECM , others will follow | can also stimulate normal cells to produce metalloprotases

36
Q

Where do metalloproteases come from?

A

cells that need to replace connective tissue

37
Q

Why would connective tissue need to be replaced?

A

anti-aging | due to injuries

38
Q

What proteins are used to move through the ECM?

A

matrix metalloproteases | ADAM proteins | integrins | cadherins | CAMs | Selectins

39
Q

What are ADAM proteins?

A

disintegrin and metalloprotease | cuts certain adhesion molecules and other types of cell-surface molecules

40
Q

Which cells use the walking mechanism?

A

macrophages

41
Q

What are the 5 functions of cytoskeleton?

A

dynamic scaffolding providing structure | positioning organelles | provide tracks for movement of materials and organelles | cell movement | transduce signals

42
Q

How does a cell move towards a nutrient signal?

A

actin polymerization via actin filaments

43
Q

Explain the mechanism of actin polymerization and treadmilling.

A

whatever direction the actin is being added = direction cell is moving | actin is recycled | ARP allows for #D direction of polymerization

44
Q

What is the purpose of cell membrane protrusion and movement?

A

pushes cell membrane towards direction desired

45
Q

What does treadmilling allow the cell to do?

A

change shape and move

46
Q

What is Presenilin 1?

A

allows cell to know which direction it is going | in the focal points (“feet of cells”) | involved in Alzheimer’s

47
Q

What is the function of focal points in a cell?

A

allows cell to know where it is or what it is touching

48
Q

What are the hands that tumor cells use?

A

integrins

49
Q

What are integrins?

A

heterodimer | disulfide-alpha subunit = flexible “elbow” that can move and grab onto ECM proteins (connective fibers)

50
Q

How does a tumor cell know if integrin has grabbed onto something?

A

signal transduction pathway connected to integrin will tell the tumor cell

51
Q

Why would tumors need to change the kind of “hands” they are using?

A

depending on the environment they are in = helps with survival

52
Q

What do selectins bind to?

A

sugar molecules

53
Q

What are CAMs?

A

cell adhesion proteins

54
Q

What cells is basement membrane made out of?

A

endothelial cells

55
Q

How do selectins make tumor cells move? And on what?

A

tumor cells roll on the endothelial cells | tumor cells that are able to express glycoproteins which latch onto selectins

56
Q

What “hands” do the tumor cells use for extravasation?

A

CAMs – cell adhesion molecules

57
Q

What is vinblastin?

A

interferes with cytoskeleton = can’t put actin subunits together to make it work

58
Q

What affects does vinblastin have on tumor cell activity?

A

no treadmilling | inhibits actin polymerization | no cytokinesis

59
Q

What is taxol?

A

can’t break actin-filament apart

60
Q

What affects does taxol have on tumor cell activity?

A

inhibits depolymerization of actin filaments