Ch. 19 Cancer and the Immune System

Question 1

benign

Answer 1

unable to invade healthy surrounding tissue

Question 2

malignant

Answer 2

becomes progressively more invasive

Question 3

metastasis

Answer 3

invasion of other distant tissues

Question 4

Carcinomas arise from

Answer 4

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

Question 5

Sarcomas arise from

Answer 5

mesodermal connective tissues; bone, fat, cartilage

Question 5

Sarcomas arise from

Answer 5

mesodermal connective tissues; bone, fat, cartilage

Question 6

Myelomas arise from

Answer 6

plasma cells

Question 7

Leukemia’s arise from

Answer 7

WBCs in blood

Question 8

Lymphomas arise from

Answer 8

WBCs in lymphatic tissues

Question 9

3 carcinogens that can promote development of cancer

Answer 9

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

Question 10

What agency is responsible for tracking possible links to cancer?

Answer 10

International Agency for Research on Cancer (IARC)

Question 11

What did Dr. Rous discover?

Answer 11

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

Question 12

What did Dr. Temin discover?

Answer 12

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

Question 13

Proto-oncogenes

Answer 13

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

Oncogenes

Answer 16

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

Question 17

Tumor-suppressor genes

Answer 17

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

Question 18

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

Answer 18

tumor suppressor gene

Question 19

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

Answer 19

oncogene

Question 20

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

Answer 20

• 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

Question 21

growth factors/ growth factor receptors

Answer 21

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

Question 22

ex. of growth factor cancer-promoting activity

Answer 22

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

Question 23

products for signal transduction pathways and transcription factors

Answer 23

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

Question 24

chromosomal translocations

Answer 24

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

Question 25

mutations in proto-oncogenes

Answer 25

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

Question 26

ex. of mutation in proto-oncogenes leading to cancer

Answer 26

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

Question 27

viral integration into host cell genome

Answer 27

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

Question 28

p53 is a tumor suppressor protein that

Answer 28

promotes apoptosis

Question 29

pRB regulates

Answer 29

cell cycle

Question 30

retinoblastoma (Rb) gene

Answer 30

encodes a cell cycle regulator that inhibits progression through G1

Question 31

TP53 gene coding for p53

Answer 31

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

Question 32

BCl-2 gene

Answer 32

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

Question 33

Two phases of malignant transformation

Answer 33

initiation and promotion

Question 34

What causes XP to lead to cancer?

Answer 34

- defects in nucleotide excision repair (NER) | - unable to repair UV induced mutations, so build in skin cells over time

Question 35

XP can often lead to early onset of

Answer 35

malignant melanoma or squamous cell carcinoma

Question 36

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

Answer 36

APC, DCC, TP53

Question 37

human colon cancer can occur due to the activation of:

Answer 37

k-ras

Question 38

neoplastic cells

Answer 38

self cells; most Ags are subject to tolerance processes

Question 39

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

Answer 39

TSAs

Question 40

Tumor specific antigens

Answer 40

unique to tumor cells

Question 41

tumor associated antigens

Answer 41

normal cellular proteins with unique expression patterns

Question 42

What intrinsic mechanisms do we have to prevent cancer?

Answer 42

- DNA repair mechanisms | - apoptosis

Question 43

What are the three phases of immunoediting?

Answer 43

- elimination - equilibrium - escape

Question 44

elimination phase

Answer 44

attacking cells that can be targeted

Question 45

equilibrium phase

Answer 45

state of balance between destruction/survival of toughest cells

Question 46

escape phase

Answer 46

most aggressive/least immunogenic cells thrive and spread

Question 47

What is the role of NK cells in cancer prevention?

Answer 47

target neoplasmic cells

Question 48

What causes Chediak-Higashi syndrome?

Answer 48

mutations resulting in loss of NK cells

Question 49

effects of Chediak-Higashi syndrome

Answer 49

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