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EMS > Theme 5: Neoplasia - Part 4 > Flashcards

Theme 5: Neoplasia - Part 4 Flashcards

1
Q

What are the three steps in the way malignant tumours behave?

A
  1. invasion
  2. metastasis
  3. angiogenesis
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2
Q

What does invasion mean?

A

-invades adjacent normal tissue

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3
Q

How do epithelial cells change in cancer to help the spread?

A
  • in health, epithelial cells are tightly connected, polarised and tethered to each other
  • mesenchymal cells are loosely connected, able to migrate
  • in cancer, epithelial cells gain mesenchymal properties and can invade and migrate
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4
Q

How do epithelial cells invade and migrate in cancer?

A
  • increased motility
  • decreased adhesion
  • production of proteolytic enzymes
  • mechanical pressure
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5
Q

What are cadherins?

A

cell to cell adhesion molecule - attaches epithelial cells to EACH OTHER
-a mutation in this will reduce cell-cell adhesion

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6
Q

What are integrins?

A

cell to matrix adhesion molecule and receptor

changes in integrin expression leads to decreased cell-matrix adhesion

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7
Q

What is the most important proteolytic enzyme in neoplastic invasion?

A

matrix metalloproteinases

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8
Q

Which cells are matrix metalloproteinases secreted by?

A

malignant neoplastic cells

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9
Q

What are the three major types of matrix metalloproteinases?

A
  1. Interstitial collagenases —> degrade type I, II, III collagen
  2. Gelatinases —> degrades type IV collagen and gelatin
  3. Stromelysins —> degrades type IV collagen and proteoglycans
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10
Q

In normal tissue regulation, how are proteolytic enzymes balanced and how does this change in cancer?

A

tissue inhibitors of metalloproteinases balance matrix metalloproteinases
In cancer, cancer favours ECM breakdown so there are more matrix metalloproteinases

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11
Q

What are the clinical effects of invasion?

A
  • uncontrolled proliferation and invasion –> mass
  • mass can occlude/put pressure on vessels
  • malignant neoplasms invade along “path of least resistance” -usually blood vessels or nerves. cartilage and bone are extremely resistant to neoplastic invasion
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12
Q

What is metastasis?

A

tumour spreads from site of origin (primary) to a distant site to establish tumour there (secondary)
-often secondary tumour exceeds primary lesion

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13
Q

What might be presenting clinical features of metastasis?

A

bone lesions and palpable lymph nodes

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14
Q

What are the 6 steps in the metastatic sequence?

A
  1. detachment invasion
  2. intravasation (invasion of cancer cells through basement membrane into blood vessel)
  3. survival against host defences
  4. adherence extravasation - bind to blood vessel and exit
  5. growth
  6. angiogenesis
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15
Q

How do neoplastic cells become motile?

A

loss of surface adhesion molecules and imbalance of proteolytic enzymes that mean the ECM is broken down

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16
Q

What are 3 routes of metastasis?

A
  1. Lymphatics
    - form secondary tumours in lymph nodes
    - most common route initially for carcinomas
  2. Haematogenous (blood)
    - commenest route for sarcomas
    - organs involved are lungs, liver, bone and brain
  3. transcoelomic
    - spread across the peritoneal/ pleural cavity
    - will lead to effusion containing neoplastic cells
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17
Q

What is the difference between carcinomas and sarcomas?

A

carcinomas - cancers that develop in epithelial cells and sarcomas develop in mesenchymal tissue

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18
Q

What is angiogenesis?

A

growth of blood vessels on existing vasculature

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19
Q

How do tumour cells promote angiogenesis?

A

they express vascular endothelial growth factor (VEGF)

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20
Q

What does stage mean?

A

The extent of tumour spread - has the tumour metastasised?

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21
Q

What does grade mean?

A

how aggressive is the tumour? how different does it look from tissue of origin?

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22
Q

Explain the TNM Tumour staging system?

A

T - extent of tumour spread:

  • T0: no evidence of primary tumour
  • T1-T4: increasing size/ invasion of tumour

N- extent of nodal spread

  • N0: no regional node metastases
  • N1-N3: increasing involvement of nodes

M- presence or absence of distant metastases
-M0: no distant metastases
-M1: distant metastases present
Mx - unable to comment

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23
Q

Explain the Dukes staging system?

A

For Colorectal cancer:
A- Invades into but not through the bowel wall
B- Invades through the bowel wall, but no LN metastases
C- Local lymph nodes involved
D- distant metastases

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24
Q

How do we stage lymphoma?

A

Stage I: Lymphoma in one group of lymph nodes
Stage II: lymphoma in 2 or more groups of lymph nodes
Stage III: lymphoma on both sides of diaphragm
Stage IV: lymphoma in other organs/bone marrow/ liver or lung

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25
Q

How is lymphoma further classified?

A

A - symptoms absent

B- symptoms present e.g fever, weight loss

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26
Q

What factors do we consider when determining the grade of cancer?

A
  1. differentiation = how much cancer cells resemble normal tissue
  2. pleomorphism = the variation in size and shape of cancer cells
  3. proliferation = mitotic figure, how many cells are actively dividing
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27
Q

What is a poorly differentiated, high grade tumour?

A

cells hardly resemble those of normal tissue

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28
Q

What are the 6 hallmarks of cancer?

A
  1. self sufficiency in growth signals
  2. insensitivity to anti-growth signals
  3. tissue invasion & metastasis
  4. limitless replicative potential
  5. sustained angiogenesis
  6. evading apoptosis
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29
Q

Explain the most fundamental trait of cancer cells

A

ability to sustain chronic proliferation

-intracellular signalling pathways regulate progress and cell growth through the cell cycle

30
Q

How do cancer cells evade growth suppressors?

A
  • Rb protein prevents progression from G1 to S phase
  • inactivating of Rb gene results in resistance to -ve growth regulation
  • this causes loss of gatekeeper between G1 and S phase
  • so there is continuous growth of the cell
31
Q

how do cancer cells avoid immune destruction?

A

blocking of proteins that allow T cell to kill tumour cell

32
Q

how do cancer cells enable replicative immortality?

A

in health, telomeres shorten so the cell dies

in cancer, the telomeres are not shortened so the cells replicate and don’t die

33
Q

Give an example of a factor that interacts and promotes tumour growth?

A

interleukins

34
Q

How do tumours metastasise?

A
  • cells in epithelium break through basal lamina
  • cells enter bloodstream
  • cells divide to form tumour
  • cells adhere to and penetrate the capillary wall
35
Q

How do tumours induce angiogenesis?

A

angiogenic factors cause capillaries to sprout and build new blood vessels that supply the tumour with nutrients and oxygen

36
Q

How are normal cells removed? e.g after DNA damage

A

apoptosis

37
Q

What are proto-oncogenes and oncogenes?

A

Proto-oncogenes - normal cells that promote cell proliferation, survival and angiogenesis
Oncogenes - mutated versions/ increased expression of photo-oncogenes, causing increased/uncontrolled activity of expressed proteins

38
Q

Are TSGs and proto-oncogenes dominant or recessive?

A

Proto-oncogenes - dominant
TSGs - recessive (so if there is a mutation in one allele, there is still normal cell division as there is still another functioning allele to compensate)

39
Q

What are the differences between oncogenes and TSGs?

A
  • In oncogenes, mutations in one of the two alleles is significant
  • In TSGs, both alleles must be affected
  • In oncogenes, gain of function of a protein that signals cell division
  • In TSGs, loss of function of a protein
  • oncogene mutations arise in somatic cells (are not inherited) whereas TSG mutations can be present in germ cells therefore inherited
40
Q

What are some examples of oncogenes?

A

RAS, RAF, HER2, EGFR

41
Q

What are 4 types of mechanisms of oncogene activation?

A
  1. translocation of an oncogene from a low to active transcription type
  2. point mutation - substitution of single base produces a hyperactive oncoprotein
  3. amplification - increased expression by insertion of multiple copies of an oncogene
  4. insertion - of a promotor near an oncogene
42
Q

give examples of TSGs

A

APC, P53, RB, BRCA1, BRCA2, hMLH1, hMSH2

43
Q

What are the two categories of TSGs?

A
  1. gate keepers/ anti-oncogenes - negative regulators of the cell cycle and proliferation and positive regulators of apoptosis
  2. caretakers - maintain genetic stability
44
Q

a mutation in which TSG results in Li-Fraumeni syndrome?

A

p53

45
Q

a mutation in which TSG results in familial adenomatous polyposis ?

A

APC

46
Q

a mutation in which TSG results in HNPCC?

A

hMLH1, hMSH2

47
Q

What is the minimum number of genetic alterations needed to transform a normal cell into a neoplastic cell?

A

3-6

48
Q

What are the 3 locations that ovarian tumours can arise from?

A
  1. Surface epithelial tumours (90% of cases)
  2. Germ cell tumours - arise from the oocyte
  3. Sex chord stroma
49
Q

What are the most common types of surface epithelial tumours?

A
  • serous (tubal mucosa)
  • mucinous (endocervical)
  • endometroid (endometrium)
50
Q

What does nulliparous mean?

A

Hasn’t given birth

51
Q

What is serum Ca125 used for?

A

a tumour marker in ovarian cancer

52
Q

What is a bilateral sapling-oophrectomy?

A

Removal of both ovaries

53
Q

What are the 3 types of epithelial tumours?

A
  • benign
  • borderline - abnormal architecture but no evidence of invasion
  • malignant - evidence of invasion
54
Q

What prefix is used to describe tumours composed of glandular epithelium?

A

Adeno

55
Q

How are benign ovarian epithelial tumours sub classified?

A

Based on components:

  1. Composed of cysts (cyst adenoma)
  2. Fibrous tissue (adenofibroma)
  3. Cystic and fibrous (cystadenofibroma)
56
Q

Explain the nomenclature of ovarian malignant epithelial tumours

A
  1. cystadenocarcinoma = malignant ovarian epithelial tumour
  2. then classified by type of epithelium i.e serous cystadenocarcinoma
  3. then further classified into:
    - high grade (aggressive), low grade (slower growing, less aggressive, better prognosis)
57
Q

What is FIGO staging?

A

staging for ovarian cancer

58
Q

what are non-specific symptoms of epithelial ovarian cancer?

A
  • weight loss
  • bloating
  • fatigue
  • urinary frequency
  • sometimes PV bleeding
59
Q

What are 3 protective factors of epithelial ovarian cancer?

A
  • having children
  • breast feeding
  • contraceptive pill
60
Q

What structures can a mature cystic teratoma contain?

A

hair, sebaceous material (hair follicles), teeth

61
Q

Give 4 examples of germ cell tumours?

A
  • teratomas (most common)
  • yolk sac tumours
  • embryonal carcinoma
  • dysgerminomas
62
Q

What is an immature teratoma?

A

malignant teratoma (only 1% of teratomas are malignant most are benign)

63
Q

what is a mature cystic teratoma?

A

“tumour that contains elements of all three germ cell layers”:

  1. ectoderm e.g skin and hair
  2. mesoderm e.g muscle, bone, cartilage
  3. endoderm e.g respiratory epithelium, GI epithelium
64
Q

What are dysgerminoma?

A
  • malignant
  • very rare
  • sensitive to chemo
  • LDH used as tumour marker
65
Q

What are yolk sac tumours?

A
  • malignant
  • sensitive to chemo
  • a-FP used as tumour marker
66
Q

What are choriocarcinomas?

A
  • extremely rare
  • usually in placenta
  • malignant
67
Q

How do sex-cord stromal tumours arise?

A

arise from ovarian stroma that was derived from the sex cord of the embryogenic gonad

68
Q

What are the 3 types of sex-cord stromal tumours?

A
  1. Thecoma / fibrothecoma/ fibroma
    - benign
    - thecomas and fibrothecomas produce estradiol
  2. granulosa cell tumours
    - low grade malignant, produces estradiol
  3. Sertoli-leydig cell tumours
    - produce androgens
69
Q

What is meig’s syndrome?

A

triad of ovarian tumour (fibroma), right sided pleural effusion ascites

70
Q

What is the most effective way of evaluating an ovarian mass?

A

pelvic ultrasound

71
Q

Which serum markers do we use in ovarian neoplasms?

A
  • Ca125

- a-FP, LDH, BHCG

72
Q

What is a Krukenberg tumour?

A

metastatic tumour in the ovary that originates in the stomach

EMS (16 decks)

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