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GSSE Pathology > Neoplasia > Flashcards

Neoplasia Flashcards

1
Q

What are the relative risks of neoplasia and managemnet suggestions for the following

  • Non-proliferative breast changes (fibrocystic changes)
  • Proliferatives breast disease without atypia
  • Proliferative breast disease with atypia
A

NON proliferative

  • 1.0 x risk

PROLIFERATIVE with NO hyperplasia

  • 1.5-2 x risk
  • excisional biopsy

PROLIFERATIVE WITH hyperplasia

  • 4-5 x risk
  • excisional biopsy
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2
Q

What are some examples of non-proliferative breast change? (7)

A 
Duct ectasia
Cysts
Fibrosis
Apocrine change
Mild hyperplasia
Adenosis
Fibroadenoma without complex features
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3
Q

What are some examples of proliferative breast disease without atypia? (5)

A 
Moderate or florid hyperplasia 
Sclerosing adenosis
Papilloma
Complex sclerosing lesion (radial scar) 
Fibroadenoma with complex features
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4
Q

What are some examples of proliferative breast disease with atypia?

A

Atypical ductal hyperplasia

Atypical lobular hyperplasia

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5
Q

Where are the common sites for metastatic breast carcinoma?

A 
Liver
Lungs
Bone
Brain
Meninges
Skin
Adrenals
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6
Q

What is the function of the BRCA1 and BRCA2 genes and what cancers are they linked to (other than breast)?

A

Tumour suppressor genes, promote DNA repair

BRCA1: prostate, colon, pancreas
BRCA2: prostate, pancreas, stomach, melanomas

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7
Q

What is the definition of carcinoma in situ?

A

CIS = neoplastic population of cells limited by the basement membrane

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8
Q

What is the recommended treatment for DCIS?

A

WLE + RTx

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9
Q

What is the presentation, pathogenesis and management of paget’s disease?

A

PRESENTATION: unilateral erythematous eruption of scale crust
PATHOGENESIS:
- paget cells extend from DCIS into nipple skin, do not cross basement membrane
MANAGEMENT: as DCIS, WLE and RTx

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10
Q

What are some key morphological differences between benign and malignant histologies?

A
  • pleomorphism: variation in size and shape
  • abnormal nuclear morphology: high nuclear:cytoplasm ratio
  • mitoses: frequent or bizarre tableaus
  • loss of polarity
  • ischaemic necrosis when outgrowing vascular supply
  • lack of differentiation
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11
Q

Break down the metastatic cascade into its ECM invasion and vascular dissemination phases.

A

ECM INVASION

  • Loosening of tumour cells: e-cadherin lost
  • Degradation of the basement membrane and interstitial connective tissue: usually due to MMPs
  • Changes in attachment of tumour cells to ECM proteins
  • Locomotion/migration using chemoattractants

VASCULAR DISSEMINATION

  • adhering to circulating WCCs and platelets
  • circulate as single cells
  • come to rest in the first capillary bed
  • cells secrete cytokines, GFs and proteases that act on the resident stromal cells to make a home for itself
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12
Q

What are the 4 phases of neoplasia?

A
  1. Transformation: differentiation and anaplasia
  2. Growth of the transformed cells
  3. Invasion locally: involves breaching of ECM
  4. Metastasis: systemic invasion via blood, lymphatics or body cavities
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13
Q

What are the 7 fundamental changes for carcinogenesis?

A
  • self sufficiency to growth signals(oncogene activation)
  • insensitivity to growth inhibiting signals
  • evade apoptosis
  • defects in DNA repair
  • limitless replicative potential (maintenance of telomere length)
  • sustained angiogenesis
  • ability to invade and metastasise
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14
Q

What is a growth fraction and how does it relate to a tumors susceptibility to chemotherapy?

A

Growth fraction = proportion of tumour cells that are in the proliferative pool
 Low GF = slow growing = not good for chemo
 High GF = fast growing = susceptible to chemo
 Anti-cancer agents act on cells that are in cycle, hence they are better for those with high GFs

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15
Q

What are proto-oncogenes?

How can they be converted into oncogenes?

A

Normal cellular genes that affect growth and differentiation -> thus in normal cell, are active and regulate physiological
actions

  • transduction into retroviruses (v-onc)
  • changes in situ that affect their expression, function, or both
  • destruction of adjacent controller genes, which normally suppress their action
  • translocation
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16
Q

What are some examples of tumor suppressor genes?

What is their physiological role?

A

Rb gene, p53, HNPCC, BRCA I & II

Suppress growth

17
Q

Describe the mechanism of INITIATION of chemical carcinogenesis.

A

PERMANENT DNA damage

  • may be direct or indirect
  • highly reactive electrophiles (non-enzymatic)
  • carcinogen produes change in DNA and does not always lead to initiation because of repair by cellular enzymes
  • carcinogen-altered cell must undergo at least one cycle of proliferation to make the change permanent
18
Q

Describe the mechanism of PROMOTION in chemical carcinogenesis.

A

change in DNA due to EXISTING pathways, not new ones

  • apply promotors to proliferate initiated cells
  • often proliferate pre-neoplastic cells that then convert to malignancy and progress into tumour
19
Q

What are oncoproteins?

A

Oncoproteins resemble the normal products of proto-oncogenes but bear mutations that are often inactivate internal regulatory elements

20
Q

What is the normal function of p53?

A
  • p53 = tumor suppresso gene
  • it is a DNA-binding protein localized to the nucleus
  • Major function = cell-cyle arrest and initiation of apoptosis in response to DNA damage
  • p53-induced cell-cycle arrest occurs late in the G1 phase

o If the DNA is successfully repaired, p53 activates MDM2 whose product binds to and DEGRADES p53
o If DNA damage cannot be repaired, p53 induces the activation of APOPTOSIS-inducing genes eg. BAX

21
Q

What is the normal function of the Retinoblastoma protein (from the RB gene)

A

nuclear phosphoprotein that regulates the cell cycle

  • In quiescent cells, RB exists in an active hypophosphorylated state
  • In G1/S cell cyles, RB exists in an inactive hyperphosphorylated state

If RB is absent, the brakes on the cell cycle are released, and the cell moves into the S-phase

22
Q

What are 5 key characteristics of hodgkin’s lymphoma that are not present with NON hodgkin’s lymphoma

A

o Clinically HD may present similar to infection (with fever) B Sx
o Spread is contiguous to adjacent nodes in Hodgkin
o Classification is based on inflammatory response, not on malignant cell
o No leukaemic state
o Extranodal spread uncommon

23
Q

What are some of the histological features of thyroid papillary carcinoma? What proportion of malignant thyroid tumors do they make up?

A
  • papillary pattern
  • occasional psammoma bodies
  • clear “Orphan Annie eye” nuclei
  • nuclear grooves

80%

24
Q

What is thrombophlebitis migrans and what cancers are commonly associated?

A

Migratory thrombophlebitis (Trousseau syndrome) due to hypercoagulability due to the elaboration of platelet-aggregating factors and procoagulants from the tumour or its necrotic products

  • adenoCa of the pancreas
  • colon
  • kidney
  • lung

GSSE Pathology (6 decks)

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