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EMS > T5 Behaviour of tumours/ovarian tumours/carcinogenesis > Flashcards

T5 Behaviour of tumours/ovarian tumours/carcinogenesis Flashcards

1
Q

main difference between invasion & metastasis

A

invasion: local
metastasis: systemic

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2
Q

in what way do epithelial cells become similar mesenchymal during cancer?

A

ability to migrate & invade

epithelial-mesenchyma transition

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3
Q

a mutation in what molecule decreases the cell-cell adhesion?

A

E-cadherin

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4
Q

changes in the expression of what molecule leads to decreased cell-matrix adhesion?

A

intigrins

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5
Q

what are the most important proteolytic enzymes in neoplastic invasion? what are they secreted by and what is their function?

A
  • matrix metalloproteinases
  • malignant neoplastic cells
  • digest surrounding connective tissue
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6
Q

which molecules do interstitial collagenases (metalloproteinases) degrade?

A
  • types 1, 2, 3 collagen
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7
Q

which molecules do gelatinases (metalloproteinases) degrade?

A
  • type 4 collagen

- gelatin

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8
Q

what molecules do stromelysins (metalloproteinases) degrade?

A
  • type 4 collagen

- proteoglycans

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9
Q

most commonly invaded tissues and why?

A
  • blood vessels/nerves

- least resistance

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10
Q

what is the most common route of metastasis initially for carcinoma?

A

lymphatics

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11
Q

what is the most common route of metastasis for sarcomas?

A

haematogenous

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12
Q

which organs are most commonly involved in harmatogenous metastasis?

A
  • liver
  • lungs
  • bones
  • brain
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13
Q

where do haematogenous bone metastasis most frequently come from?

A
  • lung
  • breast
  • kidney
  • thyroid
  • prostate
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14
Q

which route of metastasis leads to tumour spreading across the peritoneal/pleural cavity?

A

transcoelomic

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15
Q

what does transcoelomic metastasis lead to? give an example

A
  • effusion containing neoplastic cells

- ovarian cancer

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16
Q

give an example of implantation

A
  • spillage of tumour - surgery
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17
Q

what molecule do cancer cells express to promote new vessel sprouting &angiogeneis?

A

vascular endothelial growth factor (VEGF)

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18
Q

staging

A

extent of tumour spread

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19
Q

grading

A

aggressiveness of tumour

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20
Q

what does TNM stand for in TNM grading system?

A

T(0-4)- extent of tumour spread
N(0-3)- extent of nodal spread
M(0-1)- presence/absence of distant metastases

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21
Q

staging of lymphoma

A
  • stage 1-4 (spread of lymphoma)

- A-B (symptoms present or not)

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22
Q

from well to poorly differentiated tumours, how does the grades change?

A
  • low grade –> high grade
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23
Q

what is pleomorphism in cancer?

A

variation in cell size & shape

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24
Q

what are the most common types of ovarian surface epithelial tumours (all glandular epithelia)

A
  • serous (tubal mucosa)
  • mucinous (endocervical)
  • endometrioid (endometrium)
25
Q

where do ovarian germ cell tumours arise from

A

oocyte

26
Q

where do ovarian sex-cord stroma arise from

A

sex cord stroma

27
Q

name a substance that’s used as a marker in ovarian cancer, complex cysts

A

CA125

28
Q

benign glandular fibrous epithelial tumour composed of cysts

A

cystadenofibroma

29
Q

protective factors of ovarian cancer

A
  • having children
  • brestfeeding
  • COCP
30
Q

give an example of teratoma

A

mature cystic teratoma

(3 elements of germ cell layers) `

31
Q

teratoma is an example of which type of ovarian tumours? give other examples with their markers

A 
germ cell tumours:
- yolk sac tumours - a-FP
- embryonal carcinoma 
- dysgerminomas - LDH
- choriiocarcinoma - bHCG
(all malignant)
32
Q

where do teratomas arise from

A

oocyte that’s completed 1st mitotic division

33
Q

two features of sex cord stromal tumours

A
  • rare

- produce steroid

34
Q

which sex cord tumour produce estradiol

A
  • thecomas
  • fibrothecomas
  • granulosa cell tumours
35
Q

rank sex cord tumours from most to least malignant

A

sertoli-leydig –> granulosa –> thecoma/fibrothecoma/fibroma

36
Q

describe Meig’s syndrome in thecoma/fibrothecoma/fibroma?

A

triad: ovarian tumour; right sided pleural effusion; ascites

37
Q

what steroid do sertoli-leydig tumours produce?

A

androgens

38
Q

how do metastatic ovarian tumours spread?

A
  • direct
  • lymphatic
  • haematogenous
39
Q

origins of metastatic ovarian tumour

A
  • colon
  • stomach (krukenberg)
  • breast
  • uterus
  • fallopian
  • pelvic peritoneum
40
Q

description of Krukenberg tumour

A
  • bilateral

- mucin

41
Q

in the tumour’s sustaining proliferative signalling, what cell surface receptors do growth factors bind to

A

intracellular tyrosine kinase

42
Q

which protein do -ve GFs inhibit? what is the function of that protein?

A
  • Rb protein

- regulator of cell cycle - prevents G1–>S phase

43
Q

how do tumours increase the rate of cell division

A
  • inactivating Rb gene

- resistance to -ve growth regulation

44
Q

how do tumour cells avoid immune destruction

A

binding of PD-1 (T cell) & PD-L1 (tumour cell) inhibit T cell activity

45
Q

how do tumour cells enable replicative immortality

A

telomere shortening

46
Q

how can UV cause DNA damage leading to genome instability

A
  • single stranded break

- double stranded break

47
Q

what substances do tumours release to resist cell death

A
  • Bcl2

- BclXL

48
Q

what is the name of deregulated metabolism caused by tumour cells

A

Warburg effect

49
Q

oncogenes

A
  • mutated version/ increased expression of protogenes

- cause uncontrolled activity

50
Q

TSG function and genetic pattern for disease

A
  • control genome stability

- recessive

51
Q

Proto-oncogenes function & genetic pattern for disease

A
  • encode protein involved in control of cell proliferation

- dominant

52
Q

oncogenes vs TSG

A

look up weekly summary notes

53
Q

mechanisms of oncogene activation

A
  • translocation
  • point mutation
  • amplification
  • insertion
54
Q

tumour supressor genes

A
  • APC
  • P53
  • RB
  • BRCA1 BRCA2
  • hMLH1, hMSH2
55
Q

2 categories of TSGs

A
  • anti-oncogenes - gatekeepers: -ve regulators of cell cycle; +ve regulators of apoptosis
  • caretakers: maintain genetic stability
56
Q

how can carcinogens induce molecular abnormalities in TSGs through epigenetic silencing

A
  • shutdown of gene expression

- methylation of CpG sequences in promoter genes

57
Q

TSG & familial cancer syndrome

A

see summary notes

58
Q

serum markers used for diagnosis

A
  • AFP
  • CA125
  • hCG
  • PSA
59
Q

serum markers used for monitoring

A
  • CEA

- thyroglobulin

EMS (10 decks)

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