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Tumor Immunology Flashcards

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1
Q

Cell transformation

A

Changes in physiology, morphology, protein expression, and growth characteristics that take place as a normal cell become malignant

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2
Q

Carcinogenesis

A

Tumor formation

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3
Q

What is the difference between malignant and metastatic tumors?

A
  • Malignant grows & invades other tissues
  • Metastatic disseminates to distant organs → blood → creates new tumors there
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4
Q

What is the difference between a carcinoma and a sarcoma

A
  • Carcinomas effect that the little cells
  • Sarcomas effect organs of mesenchymal cell origin (i.e. bone, lymph, CT, circulatory)
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5
Q

Which cells are affected by Leukemia, Lymphoma and Myeloma?

A
  1. Leukemia: circulating immune cells (B, T, Myeloid)
  2. Lymphoma: lymphoid cells
  3. Myeloma: plasma B-cells
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6
Q

What is the difference between de-differentiation & re-differentitaion

A
  • De-differentiation: cells lose their differentiation as they become malignant
  • Re-differentiation: they lose their ability to respond to signals as they reach their terminal end
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7
Q

Somatic cell mutation Theory

A

Somatic mutation to cells → development of oncogenes and results in protective effects to the cancer cell

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8
Q

What is an example of a somatic cell mutation Theory?

A

Philadelphia chromosome; t(9;22) → ABL/BCR oncogene: activates bcr apoptotic protective protein

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9
Q

Cancer stem cell hypothesis

A

Polyclonal evolution of cells from within a primary tumor; one of which may have capabilities of a stem cell

(self-renewal, proliferation, tumorigenicity, resistance to chemotherapy)

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10
Q

Cancer stem cell hypothesis means what in terms of treatment?

A

must target the stem cell-like cells to stop it

(even w/chemo the CSCs are still present and malignancy can reappear after some time)

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11
Q

What characteristics enhance cancer growth?

A
  1. signal their own growth
  2. ignore apoptosis signal/immune system evasion
  3. angiogenesis
  4. metastasis
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12
Q

Oncogenes are the mutant of ______.

A

proto-oncogenes: stimulate growth & regulate apoptosis

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13
Q

Overall, the development of tumors is a multistep process of ______ → expression of phenotype.

A

clonal evolution (somatic mutation)

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14
Q

What families to the following oncogenic viruses belong to:

  1. Epstein-Barr
  2. Human T Lymphocyte Virus
  3. Kaposi Sarcoma
A
  1. EBV: herpesviridae
  2. HTLV-1: retroviridae
  3. KSHV/HHV-8: herpesviridae
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15
Q

What type of cancer is caused by EBV (4)?

A
  1. Burkitt’s lymphoma
  2. Hodgkin’s lymphoma
  3. Post transplantation lymphoma
  4. Nasopharyngeal carcinoma
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16
Q

What type of cancer is caused by HTLV-1?

A

Adult T-cell leukemia

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17
Q

What type of cancer is caused by KSHV/HHV-8 (3)?

A
  1. Kaposi’s sarcoma
  2. Pleural effusion lymphoma
  3. Multicentric Castleman’s disease
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18
Q

Oncogenes of EBV & HTLV-1?

A
  • EBV: LMP-1
  • HTLV-1: Tax
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19
Q

Oncogenes of KSHV/HHV-8 (8)

A
  1. Kaposin B
  2. LANA
  3. vCyclin
  4. vFlip
  5. vBcl2
  6. vMIPs
  7. vGCPR
  8. vIL-6

(Mn: Kaposin B. LANA is a pro Cycler who Flipped her bike over a Buckle left in the road. Her MIPs helmet saved her brain, but they had to do CPR for 6 minutes)

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20
Q

LMP-1 function

(EBV oncogene)

A
  • molecular signaling dysregulation NF-kB activation
  • lymphoproliferation
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21
Q

Tax function

(HTLV-1 oncogene)

A
  • Molecular signaling dysregulation NF-kB activation
  • Immortalization

(first one is the same as EBV)

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22
Q

Oncogene function of KSHV (5)

(Kaposi B, LANA, vFlip, vCyclin, vBcl2, vMIP, vGCPR, vIL-6)

A
  1. multiple-signaling events
  2. cell cycle dysregulation
  3. Inhibition of apoptosis
  4. Immune evasion
  5. Autocrine & paracrine functions
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23
Q

EBV will infection which cell types?

A
  • Epithelial cells
  • B cells

(there will be pools of uninfected & infected cells; some may become latent → lytic replication when favorable)

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24
Q

How do the EBV proteins (EBNAs) lead to immortalization (lymphoma development)?

A
  1. EBNA-1: genome replication; p53 degradation
  2. EBNA-2: upregulates viral (LMP1) & cellular (c-myc) oncogenes
  3. EBNA-3A: reg. notch signaling
  4. EBNA-3B: overcomes cell cycle inhibition
  5. LMP-1: mimics CD40L binding signal → blocks apoptosis & upregulates cell signaling
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25
The effect of retrovirus depends on \_\_\_\_\_
where it integrates into the infected cell (if it is near tumor suppressor genes → tumorigenesis)
26
Hodgkin's vs. Non-Hodgkin's lymphoma
Hodgkins: Reed-sternberg cells Non-Hodgkins: large B cell lymphoma, follicular lymphoma, many B & T cells form non-hodgkins
27
Tumor Surveillence theory
adaptive immune system prevents outgrowth of transformed cells or destroys them
28
What evidence supports tumor surveillance theory (4)?
1. lymphocytic infiltrate around tumors 2. enlargement of draining lymph nodes = better prognosis 3. specificity & memory (transplanted tumors are attacked) 4. Immune deficient patients
29
If you transfer T cells (CD8+) from a tumor-bearing mouse to syngeneic recipient (same MHC), what happens?
protection is transferred → tumor eradicated (CD8+ response is what kills tumors)
30
MC form of cancer in solid organ transplant recipients
skin cancer
31
Why does immune response fail to prevent tumor growth in some cases (4)?
1. tumor cells few non-self Ag 2. tumors can elicit strong immune response 3. rapid growth overwhelms immune system 4. evasion of immune system
32
How do you classify tumor antigens (2)?
1. **tumor-specific Ag** (only found on tumor cell) from infection w/oncogenic virus or mutations 2. **tumor-associated Ag** found on normal & tumor cells (tumor specific = better target for tx)
33
products of mutated oncogenes is specific to which classification of tumor Ag?
tumor-specific ***_(TQ)_***
34
Over-expressed & abnormally expressed cellular proteins are associated w/which classification of tumor antigens?
tumor-associated Ag (weakly immunogenic bc they are like self)
35
What type of tumor Ag are Oncofetal Ag?
tumor-associated (expressed in cancer cells and during fetal development, but not in adults.)
36
AFP is secreted in fetal life in the yolk sac & liver. If secreted in the adult it could lead to _______ (cancers)
1. hepatocellular carcinoma 2. germ cell tumors 3. gastric 4. pancreatic (oncofetal Ag)
37
Altered Glycolipid and/or glycoprotein Ag are classified as ______ type tumor Ag?
tumor-specific Ag (good for diagnostic marker; best tx is vaccine-type technique)
38
Targets of therapy for altered glycolipid and/or glycoprotein Ag?
1. Gangliosides in melanoma 2. mucins in ovarian CA 3. MUC-1 in breast carcinoma
39
Tissue-specific differentiation antigens on B-cell derived tumors (2)?
1. CD10 2. CD20 (weakly immunogenic; tumor-associated → change w/transformation)
40
Oncogenic viruses are their own class of tumor Ag, but are still technically \_\_\_\_\_\_.
tumor-specific (ex: DNA & RNA viruses & HIV)
41
Almost all lymphomas contain \_\_\_\_\_\_.
viral proteins (tumor-specific Ag)
42
What is the immune system's general response to tumors?
1. cell-mediated: T cell, Ab (opsonization, ADCC), NK cells, MF 2. humoral
43
Endogenous antigen processing pathways is \_\_\_\_\_\_(MHC I/MHC II). Exogenous antigen processing pathways is ______ (MHC I/MHC II).
* MHC I * MHC II (these processes are happening at all times; class I expressed by all nucleated cells. This is surveillance)
44
How are CD8+ T cells activated against tumor cells when there are no virus triggers?
Dying tumor cell (some w/viral epitopes) triggers cross-presentation → processed as MHCI & MHCII (this is important when considering tx)
45
What is the principle immune response to tumors?
CD8+ T lymphocytes + CTLs (NKs are the 2nd line of defense)
46
CD8 + T cell + CTL response is a necessary response to tumors. Additionally, what is needed for a robust response?
1. costimulation → T cell response 2. cross-presentation (sometimes doesn't happen if no viral PRRs) 3. MHC II presentation 4. TH1 CD4+ cytokines: INFg & TNFa 5. Costimulation B7.1 (CD80), B7.2 (CD86)
47
Why is TNF-a & IFN-g important in immune response to tumors?
increases MHC I expression → increases sensitivity to lysis by CTLs
48
How are tumor antigens identified?
biopsy & identify T cells & tumor cells (looking for a way to turn the CTLs on)
49
How does humoral immunity contribute to tumor killing?
1. Complement activation 2. ADCC: killing by Fc receptor-bearing MF or NK cells 3. ADCP: MF killing (Antibody-Dependent cell-mediated cytotoxicity)
50
What is the utility of Mabs in tumor-specific antigens?
1. detection of tumors: before & after tx 2. treatment
51
What is the role of NK cells in fighting off tumors?
they are the 2nd wave of defense when CTLs don't kill it (less NK = more tumor development)
52
How are NK cells activated to kill tumor cells?
secretion of INFs & ILs (IL-2 & IL-12) increases tumoricidal capacity of NK cells (they target IgG-coated tumor cells)
53
What is the mechanism of NK cells activation?
activating receptors check cells for MHC I → kills those who don't have it (viruses & tumor cells downregulate it to escape CTLs. This is why NKs are the second wave of security)
54
IL-2 activated NK cells are called \_\_\_\_\_
Lymphokine-activated killer (LAK) cells (potential candidate for adoptive immunotherapy; note the 2 different methods of activating NK cells)
55
What is macrophage-mediated anti-tumor activity?
* IFN-g activates MF → releases lysosomes, reactive oxygen intermediates, NO & peroxynitrite & TNF * TNF kills tumors by introducing thrombosis into its blood supply
56
What is the MC tactic of immune evasion by tumor cells?
inhibition of MHC I expression (B2-microglobulin or components of Ag processing machinery (TAP or proteasome).
57
What does the survival of MHC-I expressing tumor cell suggest?
more than one method of escape by tumor cells
58
Downregulation of MHC-I as a means of tumors evading the immune system is demonstrated experimentally by
inducing MHC-I w/exogenously w/ INF-g or gene transfection → decreases tumorigenicity (in vivo) or increases CTL killing (in vitro)
59
Experimentally, if you stained a histological section of human prostate cancer with peroxidase-conjugated Ab to HLA class I, what would you expect to see?
1. no staining on the tumor cells 2. only staining on infiltrating lymphocytes & tissue stromal cells (tumor selection: the ones that survive, don't express MHC-I)
60
What can be concluded from the experimental result of serial transplantation of tumors in mice decreasing expression of tumor antigens?
high mitotic rate → mutation & deletion of genes encoding tumor Ag → faster growth → metastasis
61
Antigen masking
tumors coat cell w/sugar (gycocalyx) to mask/hide antigens & prevent immune cells from getting in
62
What is the result of lack of expression of costimulatory molecules and MHC II on tumor cells?
anergy: MHC II activates CTLs (tumor-specific response; cross-priming/presentation)
63
What therapy can address anergy (due to decreased MHC II)?
1. increase co-stimulatory molecules for APC 2. make tumor cells become APC 3. induce cross-priming by ensuring viral trigger
64
What mediators can tumor cells product to evade anti-tumor immune responses (2)?
1. TGF-B: inhibits lymphocytes & MF, increases Tregs (which inhibit immune cells) 2. Fas-L: kill lymphocytes
65
How can tumor cells create tolerance?
* they are self-antigens * present antigen in a tolerogenic form to mature lymphocytes → **anergy** by inhibitory signals (**via CTLA4 & CD28**; instead of C7 & CD28)
66
What is MIC and how does it contribute to immune evasion?
MHC-I related molecules expressed by cancer cells. They also express a protease that clips them off the surface→solubilizing them → they stick to receptors of NK & CD8s → they have their hands full and can't recognize the tumor cells

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