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pathophysiology > ch10: biology of cancer and tumor spread > Flashcards

ch10: biology of cancer and tumor spread Flashcards

1
Q

mutated cells

A

cells affected by genetic or environmental factors

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2
Q

cancerous cells

A

have the ability to blow past cell cycle checkpoint

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3
Q

tumor

A

mutated cells growing rapidly with no control from checkpoints or neighboring cells

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4
Q

_____ precedes the growth of a neoplasm

A

cellular dysplasia

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5
Q

dysplasia

A

abnormal cell growth in number, shape, size

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6
Q

when cells are dysplastic, they have a higher __________

A

higher mitotic index: higher ability and rate at which cells go through mitosis (therefore get more access to nutrients to fuel growth)

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7
Q

what natural body cells have the highest mitotic index (that are targeted by chemotherapy)

A

hair cells, skin cells, stem cells of bone marrow

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8
Q

neoplasm

A

tumor

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9
Q

in situ

A

neoplasm hasn’t extended to the basement membrane or surrounding tissues (yet)

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10
Q

invasive neoplasm

A

tumor extends past basement membrane and into other types of tissues

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11
Q

benign tumor

A
  • encapsulated (keeps it from metastasizing and extravasating)
  • lower mitotic index
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12
Q

malignant tumor

A
  • not encapsulated
  • metastasize and extravasate
  • higher mitotic index
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13
Q

what are the three places you can commonly find metastasis and why?

A

liver, lungs, lymph

- lots of narrow capillaries and small spaces

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14
Q

carcinoma

A

epitelial tissue derived tumor

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15
Q

carcinoma in situ

A

carcinoma that has not passed basement membrane

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16
Q

adenocarcinoma

clinical manifestation?

A

gland/duct tissue derived

- swings in hormone balance

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17
Q

sarcoma

A

connective tissue derived

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18
Q

lymphoma

A

lymphatic tissue derived

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19
Q

leukemia

do you see tumors forming?

A

blood forming tissue derived

- don’t see tumors forming

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20
Q

teratoma

A

germ cell derived

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21
Q

clinical staging of tumors (4 stages)

A 
0 - no evidence of tumor/cancer
1 - there but confined to organ of origin
2 - locally invasive 
3 - spread to "regional" structures 
4 - spread to distant sites
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22
Q

what is the only way for a tumor to reach stage 4?

A

to metastasize and extravasate

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23
Q

explain the TNM system

A 
T = degree of tumor spread
N = lymph node involvement 
M = presence of distant metastasis
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24
Q

clinical staging of tumors depend on how _____ the tumor is and how ______ it is.

A

obvious, contained

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25
Q

what are tumor markers

A

abnormal concentration of normal molecules indicate possible cancerous growth

26
Q

what can you use tumor markers for?

A
  • screen high risk individuals
  • diagnose tumors
  • follow treatment –> provide prognosis
27
Q

t/f: cancer prevalence increases with age

A

true

28
Q

what is the multi-hit hypothesis

A

older cells = more likely to get mutations bc of time

29
Q

spontaneous mutation

A

DNA polymerase makes a mistake and won’t correct

30
Q

induced mutation

A

outside force came in and caused mutation to happen =MUTAGEN

31
Q

why do cancer cells have a competitive advantage?

A

“clonal expansion/proliferation”

- cancer cells divide more rapidly –> more access to nutrients vs normal tissues

32
Q

why are cancerous tumors “jerks”

A
  • autonomy
  • inappropriate autocrine signaling
  • lose density dependent inhibition
  • lose anchorage dependence
  • disable apoptosis
  • Warburg effect
  • angiogenic factors
  • fibronectin synthesis
  • telomerase enzyme
33
Q

cancer cell autonomy

A

cares only about self disregarding other cells

34
Q

inappropriate autocrine signaling

A

secrete hormones to stimulate themselves

35
Q

loss of density dependent inhibition

A

cancerous tissues don’t stop dividing when a certain density is reached

36
Q

lose anchorage dependence

A

cancer cells do not have to be anchored to another tissue/basement membrane in order to function
- makes metastasis easier

37
Q

disable apoptosis

A

cancerous tumors don’t go through preprogrammed cell suicide

38
Q

warburg effect

A

cancerous cells use pyruvate to make into molecules they can use for growth (building blocks, amino acids) instead of ATP

39
Q

angiogenic factors

A

molecule that encourages development of blood vessels (tumor gets nutrients for itself)

40
Q

down regulate fibronectin synthesis

A

allows cells to stick to each other/other things, if down regulated, EXTRAVASATION happen (squeeze extensions out to other tissues)

41
Q

telomerase enzyme

A

lengthens telomeres and prevents wear down of chormosome = increase lifespan = increase likelihood of mutations

42
Q

oncogene

A

gene that can lead to the development of cancerous tumor proliferation

43
Q

proto-oncogene

A

inactive oncogene

44
Q

what is the theory about oncogenes?

A

used to be genes that we’re used in embryonic development (rapid growth) that are turned off and don’t need anymore, but are turned on again

45
Q

how can oncogenes be activated?

A
  • point mutations
  • chromosomal alterations/amplifications
  • loss of herterozygosity
  • gene silencing (DNA methylation)
  • external pathogens
46
Q

point mutations

A

when a single base pair is added, deleted or changed

47
Q

chromosomal alterations/amplifications

A

one section of a chromosome gets copied and replicated over and over again

48
Q

loss of heterozygosity

A

one copy of good gene and one bad gene –> if something happens to good gene, bad gene dominates

49
Q

gene silencing (dna methylation)

A

turning off genes by adding molecules (wrong gene gets turned off at the wrong time = trouble)

50
Q 
external pathogens 
(what virus is known as a link to cancer)
A

HPV –> can indirectly trigger oncogenes

  • other pathogens trigger chronic inflammation –> trigger dev of cancer
51
Q

what does COX-2 have to do with cancer

A

COX-2 = inflammation promoting chemical that can trigger cancer dev

52
Q

what genes make hereditary risks for cancer?

A

BRCA1, BRCA2 = breast cancer gene

53
Q

what are some of our body’s internal protectors from cancer?

A
  • tumor suppressor genes
  • caretaker genes
  • t-cells
54
Q

tumor suppressor genes

A

antioncogenes that negatively regulate cell growth; help body control several types of cancer when it develops

55
Q

what is an example of a tumor supressor gene

A

retinoblastoma gene

56
Q

caretaker genes

A

function all the time; repair damage to genes/chromosome

57
Q

t-cell

A

able to recognize cancerous cells; can be flagged down when cells present cancerous molecules

58
Q

metastasis

A

spread to distant sites via fragmenting

59
Q

5 parts of metastasis?

A
  1. direct spread to adjacent tissues (down regulation of fibronectin)
  2. penetration into blood/lymph system
  3. fragmentation into blood/lymph
  4. transport to secondary sites (the three Ls)
  5. entry, attachment, and growth in secondary sites
60
Q

organ tropism

A

certain cancers that originate in certain tissues DO have a preference for spreading to certain places for a secondary site

pathophysiology (16 decks)

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