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
where do ovarian germ cell tumours arise from
oocyte
26
where do ovarian sex-cord stroma arise from
sex cord stroma
27
name a substance that's used as a marker in ovarian cancer, complex cysts
CA125
28
benign glandular fibrous epithelial tumour composed of cysts
cystadenofibroma
29
protective factors of ovarian cancer
- having children - brestfeeding - COCP
30
give an example of teratoma
mature cystic teratoma | (3 elements of germ cell layers) `
31
teratoma is an example of which type of ovarian tumours? give other examples with their markers
``` germ cell tumours: - yolk sac tumours - a-FP - embryonal carcinoma - dysgerminomas - LDH - choriiocarcinoma - bHCG (all malignant) ```
32
where do teratomas arise from
oocyte that's completed 1st mitotic division
33
two features of sex cord stromal tumours
- rare | - produce steroid
34
which sex cord tumour produce estradiol
- thecomas - fibrothecomas - granulosa cell tumours
35
rank sex cord tumours from most to least malignant
sertoli-leydig --> granulosa --> thecoma/fibrothecoma/fibroma
36
describe Meig's syndrome in thecoma/fibrothecoma/fibroma?
triad: ovarian tumour; right sided pleural effusion; ascites
37
what steroid do sertoli-leydig tumours produce?
androgens
38
how do metastatic ovarian tumours spread?
- direct - lymphatic - haematogenous
39
origins of metastatic ovarian tumour
- colon - stomach (krukenberg) - breast - uterus - fallopian - pelvic peritoneum
40
description of Krukenberg tumour
- bilateral | - mucin
41
in the tumour's sustaining proliferative signalling, what cell surface receptors do growth factors bind to
intracellular tyrosine kinase
42
which protein do -ve GFs inhibit? what is the function of that protein?
- Rb protein | - regulator of cell cycle - prevents G1-->S phase
43
how do tumours increase the rate of cell division
- inactivating Rb gene | - resistance to -ve growth regulation
44
how do tumour cells avoid immune destruction
binding of PD-1 (T cell) & PD-L1 (tumour cell) inhibit T cell activity
45
how do tumour cells enable replicative immortality
telomere shortening
46
how can UV cause DNA damage leading to genome instability
- single stranded break | - double stranded break
47
what substances do tumours release to resist cell death
- Bcl2 | - BclXL
48
what is the name of deregulated metabolism caused by tumour cells
Warburg effect
49
oncogenes
- mutated version/ increased expression of protogenes | - cause uncontrolled activity
50
TSG function and genetic pattern for disease
- control genome stability | - recessive
51
Proto-oncogenes function & genetic pattern for disease
- encode protein involved in control of cell proliferation | - dominant
52
oncogenes vs TSG
look up weekly summary notes
53
mechanisms of oncogene activation
- translocation - point mutation - amplification - insertion
54
tumour supressor genes
- APC - P53 - RB - BRCA1 BRCA2 - hMLH1, hMSH2
55
2 categories of TSGs
- anti-oncogenes - gatekeepers: -ve regulators of cell cycle; +ve regulators of apoptosis - caretakers: maintain genetic stability
56
how can carcinogens induce molecular abnormalities in TSGs through epigenetic silencing
- shutdown of gene expression | - methylation of CpG sequences in promoter genes
57
TSG & familial cancer syndrome
see summary notes
58
serum markers used for diagnosis
- AFP - CA125 - hCG - PSA
59
serum markers used for monitoring
- CEA | - thyroglobulin