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Cameron Breast > Breast CA Molecular Profiling > Flashcards

Breast CA Molecular Profiling Flashcards

1
Q

What are the 5 intrinsic breast cancer subtypes?

A

Liminal A, luminal B, Her2, normal-like and basal-like

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2
Q

What are luminal breast tumors?

A

They show expression patterns similar to normall luminal breast epithelial cells, including expression of low molecular wt cytokeratin 8/18, ER, and genes associated w/ an active ER signaling pathway.

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3
Q

What is the prognosis for luminal A tumors?

A

Excellent prognosis

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4
Q

Luminal A tumors usually have what histologic characteristics?

A

low grade, high amount of ER

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5
Q

Luminal A tumors have high or low ER expression?

A

High ER expression

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6
Q

What is the prognosis for luminal B tumors?

A

Poor prognonsis than luminal A

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7
Q

Luminal B tumors usually have what histologic characteristics?

A

Associated with a higher histologic grade and lower ER expression compared to luminal A

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8
Q

HER2 stands for

A

Human epidermal growth factor receptor-2

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9
Q

HER2 tumors are usually ER positive or negative?

A

Negative

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10
Q

HER2 tumors are associated with overexpression of the HER2 amplicon on what chromosome?

A

17q12

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11
Q

What breast cancer subtype does a HER2+ and ER+ cancer fall into?

A

Luminal B

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12
Q

What molecular profile do basal-like breast cancers have?

A

High molecular wt cytokeratins 5/6, 14 and 17; Her1; and smooth muscle actin

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13
Q

Basal-like cancers have what histologic characteristics?

A

High grade and poorly differentiated

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14
Q

Basal-like cancers have what prognosis?

A

Poor

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15
Q

What is the most common receptor status for basal-like breast cancers?

A

ER-/PR-/HER2-

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16
Q

What % of triple negative breast cancers display basal-like expression patterns?

A

70%

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17
Q

What % of basal-like breast cancers are triple negative?

A

77%

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18
Q

Basal-like tumors are more common in what demographic?

A

Younger women, women of African descent and typically in carriers of BRCA1

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19
Q

Luminal A accounts for what % of all breast cancers?

A

50%

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20
Q

Luminal B accounts for what % of all breast cancers?

A

10%

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21
Q

HER2 subtype accounts for what % of all breast cancers?

A

5-10%

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22
Q

Basal-like subtype accounts for what % of all breast cancers?

A

30%

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23
Q

What is the usual receptor status for Luminal A breast tumors?

A

ER+, PR+, HER2-, CK8+, CK18+

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24
Q

What is the usual receptor status for Luminal B breast turmors?

A

ER+, PR+/-, HER2 +/-

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25
Q

What is the usual receptor status for HER2 breast tumors?

A

ER-, PR-, HER2+

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26
Q

What is the Amsterdam signature?

A

A 70-gene expression profile described by Van de Vijver that were classified patients into a good or poor prognosis group. Currently being validated.

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27
Q

What is the Amsterdam signature 10-year disease-free survival in women with a good or poor prognosis.

A

Good 94.5%. Poor 50.6%.

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28
Q

What is Oncotype Dx?

A

A 21-gene assay using RT-PCR to estimate a recurrence score to predict risk of recurrence.

29
Q

What is the Oncotype Dx 10 year disease-free survival in women with a high or low risk designation?

A

High 69%. Low risk 98%.

30
Q

What is the TAILORx trial?

A

Trial dedicated to testing what therapy is best (hormonal or chemo/hormonal therapy) in Oncotype Dx intermediate-risk women.

31
Q

What ER subunit is used in assays for clinical practice?

A

ER alpha subunit. Not beta. Not much is known about the beta subunit.

32
Q

Is PR expressed as a result of ER activation?

A

Yes.

33
Q

What is a SERM?

A

Selective ER modulator.

34
Q

What are two commonly used SERMs?

A

Tamoxifen and raloxifene.

35
Q

How does tamoxifen and raloxifene work?

A

They interact directly with the ER, binding to inhibit estrogen-dependent transcription in the breast but maintaining agonist activity at other sites.

36
Q

How does fulvestrant work?

A

It is an ER antagonist, binds to ER, induces degradation of ER protein. No agonist activity.

37
Q

Adjuvant tamoxifen reduces the odds of breast cancer recurrrence and death by

A

40-50% reduction in recurrence. 30% odds reduction in death.

38
Q

What kind of receptors are EGFRs or the erbB family?

A

Epidermal growth factor receptors are transmembrane type 1 tyrosine kinase receptors

39
Q

What are the erbB subtypes?

A

erbB1, erbB2 (HER2/neu), erbB3 (HER3), and erbB4 (HER4)

40
Q

What are the 3 basic features of the erbB receptors?

A
  1. N-terminus extracellular ligand-binding region
  2. Transmembrane domain
  3. Intracellular region containing the tyrosine kinase domain
41
Q

Do all of the erbBs have an endogenous ligand?

A

No. HER2 does not. All the others (erbB1, erbB3, erbB4) do not.

42
Q

Of the erbBs which one has the strongest kinase activity?

A

HER2

43
Q

What are the best described HER-induced signaling pathways?

A

PI3k/AKT, Ras/MAPk and PLC/PKC

44
Q

Where is the HER2 gene located?

A

Chromosome 17q

45
Q

What kind of gene is HER2?

A

Proto-oncogene

46
Q

What is lapatinib?

A

An oral reversible small-molecule dual inhibitor of both HER1 and HER2 kinases.

47
Q

Is HER2 dependent on its HER family partners (the other erbBs) for tumorignesis?

A

Yes. Particularly HER3.

48
Q

What is the primary oncogenic signaling pathway activated by the HER2-HER3 heterodimer?

A

PI3K/AKT pathway, mediated through the tyrosine phosphorylation of HER3.

49
Q

What cell functions are regulated by the PI3K/AKT pathway?

A

Proliferation, growth, apoptosis, angiogenesis and invasion of cancers

50
Q

Other than HER2/HER3 activation, the PI3K/AKT pathway can also be activated by loss of what tumor suppressor gene?

A

PTEN

51
Q

EGFR is also known as which of the erbBs?

A

erbB1 or HER1

52
Q

What heterodimer has been proposed as the master regulator of the signaling network that drives breast CA epithelial cell proliferation?

A

HER2/EGFR

53
Q

Trastuzumab inhibits what signaling pathway?

A

PI3K/AKT, NOT Ras/MAPK (the latter also activated by EGFR/HER2 heterodimer)

54
Q

The EGFR/HER2 heterodimer activates which signaling pathways?

A

PI3K/AKT and Ras/MAPK

55
Q

How are tumoral microvessels are different from normal vessels?

A

Tumoral microvessels frequently lack complete endothelial linings, and basement membranes, are irregular, tortuous, more permeable

56
Q

What is bevacizumab?

A

Recombinant humanized monoclonal antibody that recognizes all isoforms of VEGF-A

57
Q

What kind of breast cancer demonstrates high-expression levels of VEGF-A and VEGFR-2 (receptor-2)?

A

Inflammatory breast cancer

58
Q

Mutations in BRCA1 and BRCA2 cause what cell deficits?

A

Inability of cells to properly sense DNA damage, transmit the damage response signal or repair DNA by homologous recombination.

59
Q

What kind of DNA repair must cells with BRCA mutations use?

A

Single-strand annealing and nonhomologous end-joining mechanisms, which are particularly error-prone and lead to genomic instability

60
Q

What is PARP1?

A

Poly-ADP-ribose polymerase-1: An enzyme that functions as a DNA damage sensor for both single- and double-strand breaks.

61
Q

What is PARP2?

A

Poly-ADP-ribose polymerase-2: Plays a role in base excision repair by homodimerization and heterodimerization with PARP1.

62
Q

What roles do PARP1 and PARP2 play with DNA maintenance?

A

Maintenance of genomic stability by regulating DNA repair mechanisms

63
Q

What role do PARP1 inhibitors play with BRCA1 and BRCA2 tumors?

A

PARP1 inhibitors reduce repair of both single- and double-strand breaks, resulting in increased DNA damaging agents like cisplatin.

64
Q

What are topoisomerases?

A

Enzymes that catalyze the transiet breaking and rejoining of DNA strands thereby regulating transcription

65
Q

Where is the TOP2A chromosome location?

A

Topoisomerase II is located at 17q12-21 near the HER2/neu gene

66
Q

How is TOP2A a target for chemotherapeutic agents?

A

TOP2A is inhibited by trapping DNA strand break intermediates, leading to peristent DNA cleavage. Thus TOP2A cannot regulate transcription.

67
Q

What are microRNAs?

A

Non-protein-coding RNAs, 18-25 nucleotides in length, that modulate gene expression by targeting mRNAs for translational suppression or mRNA cleavage.

68
Q

T/F: MicroRNAs may play a role in breast tumorignesis?

A

True. They may act as oncogenes or tumor suppressors.

Cameron Breast (9 decks)

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