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Immunology > Ch. 19 Cancer and the Immune System > Flashcards

Ch. 19 Cancer and the Immune System Flashcards

1
Q

benign

A

unable to invade healthy surrounding tissue

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2
Q

malignant

A

becomes progressively more invasive

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3
Q

metastasis

A

invasion of other distant tissues

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4
Q

Carcinomas arise from

A

epithelial cells; skin, gut, glands, lining of internal organs

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5
Q

Sarcomas arise from

A

mesodermal connective tissues; bone, fat, cartilage

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5
Q

Sarcomas arise from

A

mesodermal connective tissues; bone, fat, cartilage

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6
Q

Myelomas arise from

A

plasma cells

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7
Q

Leukemia’s arise from

A

WBCs in blood

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8
Q

Lymphomas arise from

A

WBCs in lymphatic tissues

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9
Q

3 carcinogens that can promote development of cancer

A
  • chemical subs (formaldehyde)
  • physical agents (asbestos)
  • Irradiation (x-rays)
  • viruses
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10
Q

What agency is responsible for tracking possible links to cancer?

A

International Agency for Research on Cancer (IARC)

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11
Q

What did Dr. Rous discover?

A

observed that a cancer-causing retrovirus (Rous sarcoma virus) leads to malignant transformation; malignant sarcomas in chickens could be transferred to another via cell-free filtrate

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12
Q

What did Dr. Temin discover?

A

suggested that oncogenes may be normal in cells and viruses might acquire these growth-promoting genes from previously infected cells (proto-oncogenes)

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13
Q

Proto-oncogenes

A

produce essential growth-controlling proteins; may lead to cancer if altered to lose control of expression or protein function.

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14
Q

What ways can convert a proto-oncogene to a v- or c-oncogene?

A
  1. actions of transforming viruses
  2. exposure to carcinogenes
  3. genetic predispositions
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15
Q

How can malignant transformation be accomplished by a virus like RSV?

A

RNA retroviruses reverse transcribe their genomes into DNA and integrate into the host genome–> viral genome has close contact with neighboring genes –> RSV acquires a copy of src causing infected cells to misregulate their growth because they have an extra copy of the src once infected

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16
Q

Oncogenes

A

enhance cell survival when their control mechanisms fail; become enemy when activity is enhanced

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17
Q

Tumor-suppressor genes

A

allow cancer cell survival when they fail; become the villain when activity is depressed

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18
Q

Which one needs to be underactive to promote cancer (oncogene or tumor suppressor gene)?

A

tumor suppressor gene

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19
Q

Which one needs to be overactive to promote cancer (oncogene or tumor suppressor gene)?

A

oncogene

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20
Q

What are five categories of cancer-promoting activity of oncogenes?

A
  • growth factors/growth factor receptors
  • products for signal transduction pathways and transcription factors
  • chromosomal translocations
  • mutations in proto-oncogenes
  • viral integration into the host cell genoome
21
Q

growth factors/ growth factor receptors

A

-one cell population secretes GF, which binds receptors on another cell population and promotes proliferation (receive more GF and proliferate more often)

22
Q

ex. of growth factor cancer-promoting activity

A

GF sis and GF receptor fms, erbB, neu, and erbA can cause cancer when overexpressed

23
Q

products for signal transduction pathways and transcription factors

A

src, able, and ras overexpression can transform cells; Jun, fos, and myc well known cancer-promoting transcription factors

24
Q

chromosomal translocations

A

translocations involving BCR and TCR loci; movement of c-myc from chom. 8 to chrom. 14= overexpression of myc

25
Q

mutations in proto-oncogenes

A

chemical carcinogens or irradiation converts proto-oncogenes into cancer-inducing oncogenes

26
Q

ex. of mutation in proto-oncogenes leading to cancer

A

single point mutation in c-ras leads to overactive ras= highly active epidermal growth factor (EGF) signaling

27
Q

viral integration into host cell genome

A

2 v-onc gene products (E6 and E7) made by high risk HPVs interfere with cell functions that normally prevent excessive growth –> tsp p53 and prB

28
Q

p53 is a tumor suppressor protein that

A

promotes apoptosis

29
Q

pRB regulates

A

cell cycle

30
Q

retinoblastoma (Rb) gene

A

encodes a cell cycle regulator that inhibits progression through G1

31
Q

TP53 gene coding for p53

A

encodes a nuclear phosphoprotein with multiple roles, including involvement in growth arrest, apoptosis, and DNA repair

32
Q

BCl-2 gene

A

anti-apoptosis gene that is important in the survival of selected B and T cells during maturation

33
Q

Two phases of malignant transformation

A

initiation and promotion

34
Q

What causes XP to lead to cancer?

A
  • defects in nucleotide excision repair (NER)

- unable to repair UV induced mutations, so build in skin cells over time

35
Q

XP can often lead to early onset of

A

malignant melanoma or squamous cell carcinoma

36
Q

human colon cancer can occur due to the inactivation of TSGs:

A

APC, DCC, TP53

37
Q

human colon cancer can occur due to the activation of:

A

k-ras

38
Q

neoplastic cells

A

self cells; most Ags are subject to tolerance processes

39
Q

Which of these is easier for the immune system to handle: TAAs, TSAs, or neoplastic cells?

A

TSAs

40
Q

Tumor specific antigens

A

unique to tumor cells

41
Q

tumor associated antigens

A

normal cellular proteins with unique expression patterns

42
Q

What intrinsic mechanisms do we have to prevent cancer?

A
  • DNA repair mechanisms

- apoptosis

43
Q

What are the three phases of immunoediting?

A
  • elimination
  • equilibrium
  • escape
44
Q

elimination phase

A

attacking cells that can be targeted

45
Q

equilibrium phase

A

state of balance between destruction/survival of toughest cells

46
Q

escape phase

A

most aggressive/least immunogenic cells thrive and spread

47
Q

What is the role of NK cells in cancer prevention?

A

target neoplasmic cells

48
Q

What causes Chediak-Higashi syndrome?

A

mutations resulting in loss of NK cells

49
Q

effects of Chediak-Higashi syndrome

A
  • improper lysosomal trafficking
  • albinism
  • peripheral neuropathy
  • decrease in phagocytosis and impairment of secretory lysosome trafficking, impairing NK fxn

Immunology (17 decks)

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