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Foundations 2 > Cancer immune/tumor bio > Flashcards

Cancer immune/tumor bio Flashcards

Know it, ya know

1
Q

HTLV-1 can cause

A

T-cell leukemia/ lymphoma

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2
Q

Epstein Barr Virus can cause

A

Burkitt’s lymphoma

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3
Q

Hepatitis B virus can cause

A

Liver Cancer

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4
Q

Papillomavirus can cause

A

uterine cervix carcinoma

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5
Q

antigen expressed on tumor cells but not on normal cells

A

tumor-specific antigen

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6
Q

antigen expressed on tumor cells but also on normal cells

A

tumor-associated antigen

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7
Q

How do you generate tumor antigen?

A

gp 100 are cut out and spliced together in the protesosome and expressed in HLA-A32

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8
Q

How do NK cells and gamma-delta T cell work?

A

MICs are expressed and NK cells (NKG2D receptor) and GD T cells

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9
Q

How do tumor cells circumvent MIC detection?

A

Tumor cells secrete protease that cleave MIC, which bind to NKG2D receptor, so NK cells do not detect.

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10
Q

What does Tred do? especially in cancer?

A

Express TGF-Beta and IL-10, anti-inflam, controls adaptive system; favors tumor by suppressing T-Cell response

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11
Q

what does gemtuzumab do?

A

AML, Ab is endocytosed by the tumor cell and cleavage of the toxin, toxin breaks DNA, tumor specific response

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12
Q

What does anti-CD20 do?

A

After binding to B-cells, conjuagted to I131 and Indium 111, local radiation–damage the cells’s DNA–cell dead

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13
Q

What does limitless replicative potenial depend on?

A

Evading senecence, evade mitotic crisis, capacity for self-renewal.

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14
Q

Warburg effect?

A

using aerobic glycosis by upregulating GLUT1, intermediates are used for biosynthesis; Glucose hogging and (hypoxic condition) tumors glutamine hog (Krebs cycle)

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15
Q

What is Desmoplasia?

A

growth of stromal component of ECM, prominent in leading edge carcinoma

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16
Q

What cancer associated fibroblasts do?

A

initiation of tumor, EMT–metasis, angiogensis, sustain proliferation

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17
Q

What do cancer asscoiated adipocytes?

A

Release MMPs–migration and inflitration; use as energy source; pro-inflammatory cytokines

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18
Q

What do endothelial cells do in cancer?

A

angiogenic cells: leukocyte recuitment, tumor growth and metastasis; evade immunosurvailance and enhance chemoresistance

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19
Q

What is M1 macrophage associated with?

A

Differeniates by IFN gamma and LPS, and secretes Il-1, il-6, TNF-alpha)–important in immune defense, they are proinflammatory antimicrobial and tumoricidal; ROS tissue damage

20
Q

What is M2 macrophage associated with?

A

differentiated by il-4, il-10, il-13; anti-inflammatory, wound healing, promote tumor growth

21
Q

How to switch between M1 and M2?

A

Normoxia-M1 behavior then, hypoxia–M2 behavior

22
Q

Which one more in tumor promotion, M1 Or M2?

A

M2 as promotes angiogensis, invasion/metastasis

23
Q

Bottom line for macrophages in role cancer?

A

paracrine and autocrine signaling that enhance tumor properties

24
Q

What is ECM role in cancer?

A

tumor cell bind to ECM via integrins–motility, synthesis, and ECM releases factors that are needed for induction and proliferation of neoplastic cells and angiogenesis

25
Q

How does MMPs do in tumor cells?

A

proteolysis of substrates generate fragments that regulate pathways for invasion, angiogenesis, immune regulation, and metastasis

26
Q

How does telomerase activity affect cancer cells?

A

Increase telomerase size –replicative immortality

27
Q

What are MMPs?

A

Zinc and Ca dependent endopeptidases

28
Q

1 step of tumor cell invasion

A

Loosen cancer cell-cell interact. and basement membrane interact. E-cadherins are low/lost (colon, breast, stomach)

29
Q

2 step of tumor cell invasion

A

degrades ECM and BM (due to MMPs, Cathepsin D, plasminogen)

30
Q

3 step of tumor cell invasion

A

Attachment to new ECM components: no integrins that bind to BM , and MMPs give new sites for the tumor to attach

31
Q

4 step of tumor cell invasion

A

Invasion, propel themselves through degraded basement membrane and deeper ECM

32
Q

How does a cancer cell move?

A

produce and release automotilty–bind to collagen and ECM to move, proteolytic fragments are chemotactic–cell moves forward

33
Q

Well diff and mod diff cells move in:

A

collection as cell-cell interactions are maintained

34
Q

poor diff and anaplastic cells move in

A

single cells

35
Q

How does active intravasation of tumor cells

A

factors from tumor associated macro (TNF-alpha and chemokines), tumor cell follows

36
Q

How does passive intravasation of tumor cells

A

increased vaso permeability, increased tumor interstitial pressure push tumor cells

37
Q

How do tumor cells survive intravascularly?

A

cancer cells aggregate into clumps with RBC and platelets–enhance survival and enhance implantion to destination

38
Q

What facilitates extravasation of tumor cells?

A

tumor releases TGF b and TNF-A, increase MMPs–so selectins on cancer cells and endothelial cells

39
Q

What affects metastasis?

A

Anatomic, vascular drainage of primary tumor site, tropism of particular cancer for specific tissues

40
Q

What metastaise to brain

A

lung, breast, melanoma, renal, colorectal

41
Q

What metastaise to lung

A

renal, colorectal, melanoma, breast, sarcoma

42
Q

What metastaise to liver

A

colorectal, pancreatic, breast (ER-), lung, stomach

43
Q

What metastaise to bone

A

breast (ER+), lung, prostate, renal, colorectal

44
Q

When does EMT occur normally

A

Embryonic morphogensis, wound healing

45
Q

In Mesenchymal cells, which adhesive molecule is lost? What genes lead to this loss?

A

E-cadherins (Can also be cleaved by MMP3), SNAIL and TWIST

46
Q

What protein is increased in mesenchymal phenotype?decreased?

A

intermediate filaments (vimentin) and smooth muscle actin increases; keratin decreases

47
Q

What promotes EMT?

A

cross talk in tumor microenvrionment

Foundations 2 (15 decks)

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