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Immunology -- Jones > Final- Cancers > Flashcards

Final- Cancers Flashcards

1
Q

What are classifications of Cancer?

A
  1. Non-blood cell (solid tumors
  2. Blood cell cancers

OR

  1. Spontaneous
  2. Virus-associated
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2
Q

What are two types of non blood cell cancers? What are they made up of? Which is MC?

A
  1. Carcinomas– MC; epithelial origins

2. Sarcomas– least common; bone, fat, cartilage

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3
Q

What are three types of Blood Cell Cancers? What do they arise from?

A
  1. Leukemias– arise from early lymphoid or myeloid cells
  2. Lymphomas – spread to lymphatic system, swollen nodes
  3. Myelomas– arise from B cells
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4
Q

Are spontaneous cancers or virus-assoc. cancers MC?

A

spontaneous cancers

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5
Q

What do Spontaneous cancers result from?

A

results from exposure over time

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6
Q

What are some environmental links to cancer?

A
  • chimney sweeps– nasal cavity and skin
  • chemicals
  • radiation- UV and ionizing
  • Diet
  • normal metabolism
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7
Q

What are some examples of DNA and RNA tumor viruses?

A
  • HPV
  • Hep. B
  • Epstein-Barr
  • Herpes virus
  • HTLV
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8
Q

What are the following DNA and RNA tumor viruses assoc. with developing what kind of cancer?

  1. HPV
  2. Hepatitis B
  3. Epstein-Barr
  4. Herpes virus
  5. HTLV
A
  1. HPV–> STI
  2. Hepatitis B–> liver CA
  3. Epstein-Barr–> Burkitt’s lymphoma
  4. Herpes virus–> Kaposi’s sarcoma
  5. HTLV–> leukemia
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9
Q

What is the impact of smoking on cancer? what happens if one stops smoking?

A
  • younger you start smokine–> greater risk of CA
  • amount of cigarettes a day has increase risk

If quit–> w/in about 10 years have same risk of CA as someone who didn’t ever smoke

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10
Q

Is cancer generally an inherited disease?

A

no

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11
Q

Is cancer usually due to one thing or multiple events?

A

due to accumulation of multiple events (progression)

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12
Q

In general, what are some characteristics of CA?

A
  1. generally not inherited
  2. genetic or epigentic changes over lifetime
  3. progression
  4. invasion
  5. metastatses
  6. CA rare at cellular level
  7. loss of balance of cell division and death
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13
Q

T/F. Cancer is common at the cellular level.

A

False– CA is extremely RARE at the cellular level

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14
Q

Does cancer spread?

A

yes, metastases–> spread to other areas of body and establish secondary tumors

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15
Q

Does cancer invade?

A

yes, cancer cells proliferate and produce malignant tumors that invade healthy tissue

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16
Q

What are properties of cancer cells?

A
  1. do NOT respond to inhibitory influences
  2. loss of cell signaling and cell cycle
  3. anchorage independent growth
  4. grow in absence of stimulatory growth signals

~cancer cells seem immortal

17
Q

Can cancer develop due to changes in DNA of a cell during lifetime?

A

Yes– call is genetic or epigenetic

18
Q

What type of genes encode proteins that restrain cell growth? Do they act dominantly or recessively?

A

Tumor Suppressor Genes (p53)

act recessively

19
Q

What type of genes encode proteins that promote the loss of growth control and the conversion of a cell to the malignant state? Do they act dominantly or recessively?

A

Oncogenes (Ras)

act dominantly

20
Q

What type of genes encode proteins that have various functions in the cell’s normal activities? Are these normal? What happens if they mutate?

A

Proto-oncogenes

normal; necessary for cell growth and division–>problem is when it MUTATES–> it turns into oncogenes = BAD

21
Q

How do some solid tumor evade CTLs?

A
  • tumor cells produce proteins that activate CTLA-4 and PD-1 (which tell Tcell to die)
  • mutate rapidly and CTLs may not recognize it
  • tumors increase production of Tregs–> TGF-beta, IL-10 (which turn DOWN immune response)
22
Q

Are CTL’s better at providing protection in blood or tissues, where the solid tumors are?

A

better in blood

CTLs may not provide best protection against solid tumors

23
Q

Why may CTLs be more effective to fight blood cancers?

A

Naive CTLs traffic through blood and lymph coming into DIRECT contact with blood cancers

  • blood cancers often express high levels of B7
24
Q

How can highly active macrophages provide protection?

A
  • direct injection of BCG into tumor causes inflammation and macrophages “attack” tumor
  • expression of “unusual” proteins on tumor cells may direct macrophages
25
Q

Where are NK cells located? What do they attack?

A

located in blood and must be “called in”

attack cells expressing low levels of MHC and abnormal proteins

26
Q

How can cancers avoid bring macrophages and NK cell sin?

A

well if no inflammation–> then they don’t get called in to come and attack

27
Q

How can Antibodies be effective against cancer?

A
  • naturally produced IgM against tumors
  • recognize new antigens and modified “normal” antigens
  • complement activation is possible
28
Q

What are “traditional” treatments for CA?

A
  1. Radiation (focus on particular area)
  2. Chemotherapy (goes in whole body)
  3. Surgery (least destructive)
29
Q

What are the CA screenign options out there for CA detection?

A
  1. Cell morphology–> Pap smear
  2. Clinical manifestations– CAUTION
  3. Biochemical tests – PSA test
  4. Imaging– mammogram
  5. Microarray gene expression– screen global gene expression
30
Q

What is CAUTION?

A 
some clinical manifestations of CA
C- change in bowel or bladder habits
A - a sore that does not heal
U - unusual bleeding or discharge
T - thickening or lump in breast or testes
I - indigestion or difficulty swallowing
O - obvious change in a growth or mole
N - nagging cough or hoarsness
31
Q

What cells play a major role in CAR T cells immunotherapy?

A

T cells–> play a major role in tumor protection

32
Q

How can antibodies be used for immunotherapy?

A

produced by specialized B cells, very specific for their target

33
Q

What is the differences b/w “cancer” vaccine and a therapeutic cancer vaccine?

A

“cancer” vaccine–> are ones to help prevent it (Ex: Hep B vaccine to minimize inf.; HPV connected to cervical CA

therapeutic cancer vaccine–> designed to Tx CA

Immunology -- Jones (14 decks)

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