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Immunology > 19: Cancer and the Immune System > Flashcards

19: Cancer and the Immune System Flashcards

1
Q

Name four cancer cell characteristics.

A
  1. Altered self-cells
  2. Have undergone a genetic change
  3. Exhibit uncontrolled cell growth (immortal)
  4. Invade surrounding tissue
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2
Q

Cells that have lost control of the cell cycle will produce what?

A

tumor/neoplasm

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3
Q

Benign

A

Characteristics 1-3, unable to invade healthy surrounding tissue

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4
Q

Malignant

A

Becomes progressively more invasive, characteristics 1-4

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5
Q

Metastasize

A

Invade blood or lymphatic vessels and are carried to other tissues

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6
Q

Name the steps of cancer in order.

A

a. initiation, DNA repair (initially modified tumor cell)
b. promotion (localized, benign tumor)
c. progression (invasive tumor cells)
d. metastasis (tumor cells invade vessels and spread)

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7
Q

DNA alterations induce ________________________.

A

malignant transformation

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8
Q

Transformation can be induced by _____________ (4).

A

-chemical substances
-physical agents
-ionizing radiation
-viruses and other infectious agents

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9
Q

Genes associated with ____________ control cell ________________ and _________________.

A

cancer; proliferation and survival

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10
Q

Proto-oncogenes

A

enhance cell survival when their control mechanisms fail

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11
Q

Tumor-suppressor genes

A

allow cancer cell survival when they fail

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12
Q

Apoptosis

A

gene problems can also lead to abnormal cell survival

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13
Q

Apoptosis

A

gene problems can also lead to abnormal cell survival

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14
Q

Proto-oncogenes are found in _____________ cells.

A

normal

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15
Q

Oncogenes encode what type of factors, and what type of receptors?

A

growth factors, growth factor receptors

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16
Q

Oncogenes lead to cancer if there is loss of control of ________________.

A

expression

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17
Q

Alterations to genes can occur through:

A

-actions of transforming viruses
-exposure to carcinogens or x-irradiation
-genetic predispositions

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18
Q

What type of cancer is associated with the C-neu (HER2 protein) growth factor receptor?

A

breast cancer

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19
Q

Name three examples of overexpression/activity leading to unchecked cell activation. (3 products for signal transduction pathways and transcription)

A
  1. Src
  2. abl
  3. ras
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20
Q

Name and describe two examples of viral integration into the host-cell genome.

A
  1. avian leukosis virus integrates into c-myc gene, transform to B-cell lymphoma
  2. human papillomavirus (HPV) linked to cervical cancer
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21
Q

Normal expression of tumor-suppressor genes inhibits excessive cell ____________________.

A

proliferation

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22
Q

Tumor-suppressor genes require a _____________ disabling sequence (to fail).

A

two-hit

23
Q

The two hit disabling sequence causes failure of tumor-suppressor genes which is akin to “cutting brakes” of the _________________.

A

cell cycle

24
Q

Retinoblastoma (Rb) gene

A

problem in a hereditary rare childhood cancer where one copy is mutated, and the second copy is later somatically inactivated

25
Q

TP53 gene codes for _________.

A

p53

26
Q

Mutation of the TP53 gene is found in ______ percent of all tumors.

A

60%

27
Q

TP53 gene encodes a nuclear _________________ with _______________ roles, including involvement in ____________, _________________, and DNA _______________.

A

phosphoprotein, multiple, growth arrest, apoptosis, repair

28
Q

What is the role of pro-apoptotic genes?

A

-they act as tumor suppressors to inhibit cell survival

29
Q

What is the role of anti-apoptotic genes?

A

-they behave like oncogenes to promote cell survival

30
Q

Failure of _________________ genes or overactivity of ________________ genes can encourage ____________________ of cells.

A

pro-apoptotic, anti-apoptotic, neoplastic transformation

31
Q

Name the 4 steps involved in malignant transformation.

A
  1. initiation
  2. promotion
  3. progression
  4. metastasis
32
Q

Describe initiation.

A

Change or mutation alters cell proliferation that, by itself does not lead to malignant transformation.

33
Q

Describe promotion.

A

Accumulation of preneoplastic cells.

34
Q

Describe progression.

A

Further genetic alterations allow for rampant cell proliferation and acquisition of new mutations to potential cancer-promoting genes.

35
Q

Describe metastasis.

A

Final stage where solid tumors lose adhesion and move outside original site.

36
Q

Human colon cancer (4 steps).

A
  1. small benign tumors (adenomas) in colorectal epithelium
  2. adenomas grow/disorganize and acquire malignant phenotype
  3. inactivation/loss of 3 tumor suppressor genes
  4. activation of one oncogene
37
Q

How does the immune system fight off cancer?

A

-New mutations create new self-Ag
-Difficult if oncogene is just overexpressed and no new Ag is created

38
Q

Neoplastic cells are _________ cells.

A

self

39
Q

Tumor cells may express ________ or __________________________ Ag that can be detected by the immune system.

A

unique, inappropriately expressed

40
Q

Name the four groups of tumor Ag that are recognized by T cells (so far).

A
  1. Ag encoded by genes exclusively expressed by tumors (viral genes)
  2. Ag encoded by variant forms of normal genes altered by mutation
  3. Ag normally expressed only at certain stages of development
  4. Ag overexpressed in particular tumors (harder for the immune system to recognize)
41
Q

Tumor-______________ antigens are unique sequences, and may result from __________ in tumor cells that generate ____________ proteins (new non-self Ag).

A

specific, mutations, altered

42
Q

Virally induced tumors display __________ proteins that ________ can detect and kill.

A

foreign, CTLs

43
Q

These proteins are expressed in ~80% of cervical cancers.

A

HPV E6 and E7

44
Q

Nuclear antigen of what has been observed in some Burkitt’s lymphoma?

A

EBV

45
Q

TAAs are unique to the cancer itself. T or F?

A

F; they are not unique to the cancer itself

46
Q

Tumor-associated antigens (TAAs) are normal cellular proteins with ___________ expression patterns.

A

unique

47
Q

Immunoediting is

A

a newly proposed model which both protects against and promotes tumor growth.

48
Q

Anti-tumor immune responses select for the weakest cells. T or F?

A

F; selects for the toughest cells

49
Q

Three phases of anti-tumor immune responses proposed:

A
  1. elimination
  2. equilibrium
  3. escape
50
Q

Elimination

A

-attacking the cells that can be targeted (Immunosurveillance)
-but, some cells acquire mutations that allow them to resist immune detection

51
Q

Equilibrium

A

-state of balance between destruction/survival of “best” cells
-low level of abnormal cells persist, but adaptive immune system keep in check

52
Q

Escape

A

-most aggressive/least immunogenic cells thrive and spread
-acquire more mutations in surviving tumor cells
-immune system shifts from anti- to pro-tumor responses

53
Q

Name two innate inhibitors of cancer and the mechanism by which they do so.

A
  1. NK cells can target neo-plasmic cells
  2. Activated macrophages bind to Ab-coated tumor cells (ADCC) and secrete TNF-alpha (strong antitumor activity)
54
Q

Name 3 types of adaptive cell types involved in cancer eradication and they mechanism by which they do so.

A
  1. Anti-tumor CTLs; lack of T cells leads to increases in cancer
  2. Tumor-infiltrating lymphocytes (TILs); T cells, NKT cells, NK cells
  3. B cells generate antitumor Ab against tumor-specific Ag; Promotes tumor-cell recognition and lysis; May block CTL access to tumor Ag, so anti-tumor Abs may not always be a good thing

Immunology (14 decks)

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