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Blood & Lymph > Tumor Immunology > Flashcards

Tumor Immunology Flashcards

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
Q

The effect of retrovirus depends on _____

A

where it integrates into the infected cell (if it is near tumor suppressor genes → tumorigenesis)

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26
Q

Hodgkin’s vs. Non-Hodgkin’s lymphoma

A

Hodgkins: Reed-sternberg cells

Non-Hodgkins: large B cell lymphoma, follicular lymphoma, many B & T cells form non-hodgkins

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27
Q

Tumor Surveillence theory

A

adaptive immune system prevents outgrowth of transformed cells or destroys them

28
Q

What evidence supports tumor surveillance theory (4)?

A
  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
Q

If you transfer T cells (CD8+) from a tumor-bearing mouse to syngeneic recipient (same MHC), what happens?

A

protection is transferred → tumor eradicated

(CD8+ response is what kills tumors)

30
Q

MC form of cancer in solid organ transplant recipients

A

skin cancer

31
Q

Why does immune response fail to prevent tumor growth in some cases (4)?

A
  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
Q

How do you classify tumor antigens (2)?

A
  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
Q

products of mutated oncogenes is specific to which classification of tumor Ag?

A

tumor-specific

(TQ)

34
Q

Over-expressed & abnormally expressed cellular proteins are associated w/which classification of tumor antigens?

A

tumor-associated Ag

(weakly immunogenic bc they are like self)

35
Q

What type of tumor Ag are Oncofetal Ag?

A

tumor-associated

(expressed in cancer cells and during fetal development, but not in adults.)

36
Q

AFP is secreted in fetal life in the yolk sac & liver. If secreted in the adult it could lead to _______ (cancers)

A
  1. hepatocellular carcinoma
  2. germ cell tumors
  3. gastric
  4. pancreatic

(oncofetal Ag)

37
Q

Altered Glycolipid and/or glycoprotein Ag are classified as ______ type tumor Ag?

A

tumor-specific Ag

(good for diagnostic marker; best tx is vaccine-type technique)

38
Q

Targets of therapy for altered glycolipid and/or glycoprotein Ag?

A
  1. Gangliosides in melanoma
  2. mucins in ovarian CA
  3. MUC-1 in breast carcinoma
39
Q

Tissue-specific differentiation antigens on B-cell derived tumors (2)?

A
  1. CD10
  2. CD20

(weakly immunogenic; tumor-associated → change w/transformation)

40
Q

Oncogenic viruses are their own class of tumor Ag, but are still technically ______.

A

tumor-specific

(ex: DNA & RNA viruses & HIV)

41
Q

Almost all lymphomas contain ______.

A

viral proteins

(tumor-specific Ag)

42
Q

What is the immune system’s general response to tumors?

A
  1. cell-mediated: T cell, Ab (opsonization, ADCC), NK cells, MF
  2. humoral
43
Q

Endogenous antigen processing pathways is ______(MHC I/MHC II). Exogenous antigen processing pathways is ______ (MHC I/MHC II).

A
  • MHC I
  • MHC II

(these processes are happening at all times; class I expressed by all nucleated cells. This is surveillance)

44
Q

How are CD8+ T cells activated against tumor cells when there are no virus triggers?

A

Dying tumor cell (some w/viral epitopes) triggers cross-presentation → processed as MHCI & MHCII

(this is important when considering tx)

45
Q

What is the principle immune response to tumors?

A

CD8+ T lymphocytes + CTLs

(NKs are the 2nd line of defense)

46
Q

CD8 + T cell + CTL response is a necessary response to tumors. Additionally, what is needed for a robust response?

A
  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
Q

Why is TNF-a & IFN-g important in immune response to tumors?

A

increases MHC I expression → increases sensitivity to lysis by CTLs

48
Q

How are tumor antigens identified?

A

biopsy & identify T cells & tumor cells

(looking for a way to turn the CTLs on)

49
Q

How does humoral immunity contribute to tumor killing?

A
  1. Complement activation
  2. ADCC: killing by Fc receptor-bearing MF or NK cells
  3. ADCP: MF killing

(Antibody-Dependent cell-mediated cytotoxicity)

50
Q

What is the utility of Mabs in tumor-specific antigens?

A
  1. detection of tumors: before & after tx
  2. treatment
51
Q

What is the role of NK cells in fighting off tumors?

A

they are the 2nd wave of defense when CTLs don’t kill it

(less NK = more tumor development)

52
Q

How are NK cells activated to kill tumor cells?

A

secretion of INFs & ILs (IL-2 & IL-12) increases tumoricidal capacity of NK cells (they target IgG-coated tumor cells)

53
Q

What is the mechanism of NK cells activation?

A

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
Q

IL-2 activated NK cells are called _____

A

Lymphokine-activated killer (LAK) cells

(potential candidate for adoptive immunotherapy; note the 2 different methods of activating NK cells)

55
Q

What is macrophage-mediated anti-tumor activity?

A
  • IFN-g activates MF → releases lysosomes, reactive oxygen intermediates, NO & peroxynitrite & TNF
  • TNF kills tumors by introducing thrombosis into its blood supply
56
Q

What is the MC tactic of immune evasion by tumor cells?

A

inhibition of MHC I expression

(B2-microglobulin or components of Ag processing machinery (TAP or proteasome).

57
Q

What does the survival of MHC-I expressing tumor cell suggest?

A

more than one method of escape by tumor cells

58
Q

Downregulation of MHC-I as a means of tumors evading the immune system is demonstrated experimentally by

A

inducing MHC-I w/exogenously w/ INF-g or gene transfection → decreases tumorigenicity (in vivo) or increases CTL killing (in vitro)

59
Q

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?

A
  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
Q

What can be concluded from the experimental result of serial transplantation of tumors in mice decreasing expression of tumor antigens?

A

high mitotic rate → mutation & deletion of genes encoding tumor Ag → faster growth → metastasis

61
Q

Antigen masking

A

tumors coat cell w/sugar (gycocalyx) to mask/hide antigens & prevent immune cells from getting in

62
Q

What is the result of lack of expression of costimulatory molecules and MHC II on tumor cells?

A

anergy: MHC II activates CTLs (tumor-specific response; cross-priming/presentation)

63
Q

What therapy can address anergy (due to decreased MHC II)?

A
  1. increase co-stimulatory molecules for APC
  2. make tumor cells become APC
  3. induce cross-priming by ensuring viral trigger
64
Q

What mediators can tumor cells product to evade anti-tumor immune responses (2)?

A
  1. TGF-B: inhibits lymphocytes & MF, increases Tregs (which inhibit immune cells)
  2. Fas-L: kill lymphocytes
65
Q

How can tumor cells create tolerance?

A
  • 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
Q

What is MIC and how does it contribute to immune evasion?

A

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

Blood & Lymph (29 decks)

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