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Cancer - Vicki > Breast Cancer > Flashcards

Breast Cancer Flashcards

1
Q

What is the most common cancer in UK women?

A

BC.
1/9 women will develop at some point.
Incidence increases with age, doubles every 10yrs until menopause.

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2
Q

Incidence of BC _____ every ten years until _______.

A

Doubles every ten years.

Until menopause.

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3
Q

Can breast cancer occur in men?

A

Yes.

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4
Q

What are the main risk factors for breast cancer other than the usual?

A 
Age of menopause. 
Age of first pregnancy. 
Length of lactation. 
Oral contraceptives
HRT
Family history: BRCA1 & BRCA2 genes.
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5
Q

How useful is mammography in diagnosing breast cancer?

A

Does not show 10-15% of breast cancers.

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6
Q

How is BC screened for?

A

3 yearly mammogram = can reduce mortality by 20-30% in certain groups of women.

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7
Q

What does non-invasive BC describe?

A

When the cancer is confined to the ducts and lobules in the breast.

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8
Q

What does invasive BC describe?

A

THe cancer has spread into the basement membrane and the surrounding breast tissue.

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9
Q

What % of BC are invasive at presentation?

A

80%

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10
Q

Using TNM, what does M1 refer to?

A

Presence of metastases

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11
Q

What is the prognosis of early breast cancer (T1, N0, M0)?

A

85% chance of 15yr survival.

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12
Q

What is the prognosis for metastatic breast cancer?

A

<5% survival at 15 years.

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13
Q

What are some adverse prognostic factors for BC?

A
  1. High TNM stage
  2. Poorly differentiated tumours
  3. Lymph or vascular invasion.
  4. ER or PR -ve
  5. HER+ve
  6. Young age at diagnosis.
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14
Q

Oestrogen receptor (ER) concentration predicts response to hormonal therapy with drugs such as what?

A

Tamoxifen and anastrozole.
ER+ve = better prognosis to treatment.

Progesterone receptor (PR) also +ve -> better prognosis.

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15
Q

The presence of what receptors in breast cancer indicate a better prognosis for treatment with hormonal therapy such as tamoxifen and anastrozole?

A

Er +VE

PR +VE

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16
Q

Why does being ER+VE/PR+VE indicate a better response to hormonal treatment using tamoxifen/anastrozole?

A

The drugs will bind to the receptors preventing normal binding of ligands and preventing cell growth?

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17
Q

What does the surgical option of treatment for BC entail?

A

Removal of entire breast including axillary lymph nodes, skin, nipple and areola.

Adjuvant therapy post surgery: radiotherapy, chemotherapy, hormonal therapy, trastuzumab or combination of these.

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18
Q

Why is radiotherapy given post surgery?

A

All pts who have had lumpectomy or full mastectomy are at high risk of recurrence.

Radiotherapy decreases this risk of relapse and improves overall survival due to eradicating micro deposits of cancer cells.

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19
Q

Hormonal therapy is given to

A

All women with ER/PR+Ve breast cancer.

Given for 5 years post surgery.

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20
Q

How long post surgery is hormonal therapy given to patients?

A

5 yrs post surgery.
Sensitive cancer cells need oestrogen to stay alive, removal or oestrogen is very effective at controlling or killing hormone-sensitive cancer cells.

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21
Q

What does it mean to say that hormonal therapy is often used as neo-adjuvant therapy?

A

Used before surgery to shrink large tumours and facilitate breast-conserving surgery.

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22
Q

What is tamoxifen?

A

Oestrogen receptor antagonist.

Can cause hot flushes, weight gain, sweats and increased risk of endometrial cancer.

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23
Q

What is the MOA of tamoxifen?

A

Like oestrogen, the anti-oestrogen tamoxifen enters the cell by passive diffusion, after which it binds the estrogen receptor (ER). The receptor can still bind the DNA but adapts a conformation that prevents the recruitment of cofactors, thereby inhibiting ER dependent gene transcription.

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24
Q

What do anastrozole, letrozole and exemestane all have in common?

A

They are all aromatase inhibitors.
They block the conversion of androgens from adrenal cortex into oestrogens in the peripheral tissues.

They are only effective in postmenopausal women.

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25
Q

What are the side effects of aromatase inhibitors and what is the agent of choice?

A

Agent of choice in postmenopausal women is Anastrozole.

Decreased bone mineral density: all patients have bone density scan when treatment is started.

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26
Q

Hormonal therapy for BC that causes hot flushes, weight gain, sweats and increased risk of endometrial cancer.

A

Tamoxifen.

Oestrogen receptor antagonist.

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27
Q

MOA of aromatase inhibitors

A

Block conversion of androgens from adrenal cortex into oestrogens in peripheral tissues.

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28
Q

Examples of aromatase inhibitors

A

Anastrozole, letrozole, exemestane

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29
Q

Why do all patients have a bone scan before starting treatment with aromatase inhibitors?

A

A side effect is a decrease in bone mineral density.

30
Q

Chemotherapy is used as adjuvant treatment for pts at _______/_______ risk of recurrence.

A

intermediate/high risk.

Anthracycline-based regimens are the most effective.

31
Q

According to systematic review, what chemotherapy regimens are most effective?

A

Anthracycline based regimens.

32
Q

Chemotherapy for BC is most effective in what type of patient?

A

Pre-menopausal, node +ve pts.

25% increase in overall survival

33
Q

The adjuvant chemotherapy regimen composed of Fluorouracil, Epirubicin and Cyclophosphamide is known as

A

FEC100

34
Q

How often and for how long is FEC100 given for?

A

Fluorouracil 500mg/m2 IV day 1
Epirubicin 100mg/m2 IV day 1
Cyclophosphamide
500mg/m2 IV day 1

Given every 21 days for 6 cycles

35
Q

All patients have a bone mineral density scan before starting what treatment?

A

Hormonal treatment with aromatase inhibitors.

They block the conversion of androgens from adrenal cortex into oestrogens in the peripheral tissues.

No use in post menopausal women.

36
Q

FEC100 is given every __ days for _ cycles.

A

Fluorouracil 500mg/m2 IV day 1
Epirubicin 100mg/m2 IV day 1
Cyclophosphamide 500mg/m2 IV day 1

Given every 21 days for 6 cycles

37
Q

What are the main side effects (other than the usual N/V, alopecia etc) of FEC100? [2]

A

Mucositis

Cardiac arrhythmias/cardiomyopathy.

38
Q

What are the pharmaceutical care issues with FEC?

A
  1. Doses/BSA must be checked against FEC100 protocol.
  2. Check FBC (Neuts >1.0, plts >100)
  3. Renal function
  4. LFTs; may need to decrease both epirubicin and fluorouracil doses if LFTs are impaired.
  5. Prescribe antiemetics
  6. Monitor cumulative dose of epirubicin.
  7. Older pts – may need ECHO prior to chemo. Caution in pts with cardiac disease
  8. Ensure patient understands how to take antiemetics (start day before chemotherapy)
  9. Ensure patient is vigilant for signs & symptoms of infection as there is a risk of neutropenic sepsis.
39
Q

WRT FEC100 treatment, what must the FBC show before starting treatment/each dose?

A

Neuts >1.0

Plts >100

40
Q

We may need to decrease the dose of what components of FEC if LFTs indicate decreased function?

A

Epirubican

Fluorouracil

41
Q

We should monitor the cumulative dose of _______ component of FEC

A

Epirubicin

42
Q

Why do some older pts need to have an ECHO prior to FEC treatment?

A

It can cause cardiac arrhythmia/cardaic myopathy

43
Q

When should patients take the anti emetic prescribed in conjunction with FEC treatment?

A

Start the day before each chemo session.

FEC: every 21 days for 6 cycles.

44
Q

Why should patients taking FEC be advised to look out for signs of infection?

A

Risk of severe neutropenic sepsis.

45
Q

What is Herceptin/Trastuzumab?

A

Recomb humanised monoclonal antibody which targets HER2 protein.

20% BC pts have overexpressed HER2 - poor prognosis.

Pts with HER2 overexpression of 3+ or greater benefit the most from trastuzumab.

46
Q

How does Trastuzumab work?

A

Herceptin blocks the HER2 receptor antagonistically preventing its activation by EGF.

Recomb humanised monoclonal antibody which targets HER2 protein.

20% BC pts have overexpressed HER2 - poor prognosis.

Pts with HER2 overexpression of 3+ or greater benefit the most from trastuzumab.

47
Q

What percentage of patients with BC have HER2 over expression?

A

Recomb humanised monoclonal antibody which targets HER2 protein.

20% BC pts have overexpressed HER2 - poor prognosis.

Pts with HER2 overexpression of 3+ or greater benefit the most from trastuzumab.

48
Q

What impact does HER2 overexpression have on Bc prognosis?

A

Recomb humanised monoclonal antibody which targets HER2 protein.

20% BC pts have overexpressed HER2 - poor prognosis.

Pts with HER2 overexpression of 3+ or greater benefit the most from trastuzumab.

49
Q

Patients with HER2 overexpression of greater than or equal to what, benefit most from trastuzumab?

A

Recomb humanised monoclonal antibody which targets HER2 protein.

20% BC pts have overexpressed HER2 - poor prognosis.

Pts with HER2 overexpression of 3+ or greater benefit the most from trastuzumab.

50
Q

What was the PERSEPHONE trial?

A

Looked into if 6 months treatment was just as effective as the current 1 year treatment length (every 3/52) of early BC with trastuzumab.

51
Q

What is the HER2 receptor?

A

Human Epidermal Growth Factor Receptor 2.
Overexpressed in 20% of BCs.

Leads to cell growth and spread.

52
Q

How exactly does herceptin work?

A

Herceptin blocks the HER2 receptor antagonistically preventing its activation by EGF.

53
Q 
Some BC patients now receive:
Surgery.
Chemo (~\_\_ months)
Radiotherapy (\_\_ weeks)
Trastuzumab (\_\_ year)
Hormonal therapy (\_\_ years)
A 
Some patients now receive:
surgery
chemotherapy (~ 5 months)      
radiotherapy (4 wks)               
trastuzumab (1 yr)                    hormonal therapy (5 yrs)
54
Q

What are the main side effects of trastuzumab?

A

Cardiotoxicity in ~4% patients.
rash
myalgia/arthralgia.

55
Q

Hormonal therapy for BC consists of:

A 
Oestrogen antagonists: Tamoxifen (increased risk of endometrial cancer)
Aromatase inhibitors (block conversion of androgens into oestrogens in periphery - not useful in pre-menopause: anastrazole.)
56
Q

Chemotherapy for BC consists of:

A

FEC100

57
Q

Targeted therapy consists of

A

HER2 antagonists HERceptin/trastuzumab.

58
Q

A new therapy for BC is everolimus. It is a selective mTOR inhibitor. What is mTOR?

A

Mammalian target of rapamycin.

mTOR is a key serine-threonine kinase, activity is known to be upregulated in breast cancer

59
Q

Everolimus is licensed for the treatment of ER/PR +ve, HER2 neu/-ve advanced breast cancer, in combination with exemestane, in _______ women after progression following hormonal treatment.

A

Everolimus is licensed for the treatment of ER/PR +ve, HER2 neu/-ve advanced breast cancer, in combination with exemestane, in postmenopausal women after progression following hormonal treatment.

60
Q

Everolimus is licensed for the treatment of _____, ______ advanced breast cancer, in combination with exemestane, in postmenopausal women after progression following hormonal treatment.

A

Everolimus is licensed for the treatment of ER/PR +ve, HER2 neu/-ve advanced breast cancer, in combination with exemestane, in postmenopausal women after progression following hormonal treatment.

61
Q

Everolimus is licensed for the treatment of ER/PR +ve, HER2 neu/-ve advanced breast cancer, in combination with ________, in postmenopausal women after progression following hormonal treatment.

A

Everolimus is licensed for the treatment of ER/PR +ve, HER2 neu/-ve advanced breast cancer, in combination with exemestane, in postmenopausal women after progression following hormonal treatment.

62
Q

Everolimus is a new therapy targeting which key serine-threonine kinase, the activity of which is known to be upregulated in breast cancer?

A

mTOR is a key serine-threonine kinase, activity is known to be upregulated in breast cancer.

Mammalian target of rapamycin.

63
Q

Other than usual S/E, what can Everolimus cause?

A 
Decreased appetite. 
Stomatitis. 
Rash
Fatigue
Diarrhoea
Infections
Nausea
64
Q

What route is Everolimus given via?

A

Oral

65
Q

Why might Pertuzumab be classed differently to Trastuzumab despite them both targeting the HER2 receptor?

A

Pertuzumab targets a specific domain of the HER2 protein.

Licensed for neoadjuvant treatment of early BC and in metastatic disease.

66
Q

Perjeta is

A

Pertuzumab

67
Q

_______ is a humanised IgG1 monoclonal antibody produced in mammalian (Chinese hamster ovary) cells by recombinant DNA technology.

A

Pertuzumab is a humanised IgG1 monoclonal antibody produced in mammalian (Chinese hamster ovary) cells by recombinant DNA technology.

68
Q

Perjeta is indicated for use in combination with trastuzumab and docetaxel in adult patients with HER2-positive metastatic or locally recurrent unresectable breast cancer, who ______ received previous anti-HER2 therapy or chemotherapy for their metastatic disease.

A

Perjeta is indicated for use in combination with trastuzumab and docetaxel in adult patients with HER2-positive metastatic or locally recurrent unresectable breast cancer, who have not received previous anti-HER2 therapy or chemotherapy for their metastatic disease.

69
Q

What are the most important side effects patients on Perjeta/pertuzumab should be aware of?

A

Infections are very common.

Can cause insomnia.

70
Q

How does Perjeta/Pertuzumab work?

A

Perjeta is a recombinant humanised monoclonal antibody that specifically targets the extracellular dimerization domain (subdomain II) of the human epidermal growth factor receptor 2 protein (HER2), and thereby, blocks ligand-dependent heterodimerisation of HER2 with other HER family members, including EGFR, HER3 and HER4. As a result, Perjeta inhibits ligand-initiated intracellular signalling through two major signal pathways, mitogen-activated protein (MAP) kinase and phosphoinositide 3-kinase (PI3K). Inhibition of these signalling pathways can result in cell growth arrest and apoptosis, respectively. In addition, Perjeta mediates antibody-dependent cell-mediated cytotoxicity (ADCC).

71
Q

Perjeta is a recombinant humanised monoclonal antibody that specifically targets the extracellular dimerization domain (_________) of the human epidermal growth factor receptor 2 protein (HER2), and thereby, blocks ligand-dependent heterodimerisation of HER2 with other HER family members, including EGFR, HER3 and HER4.

A

Perjeta is a recombinant humanised monoclonal antibody that specifically targets the extracellular dimerization domain (subdomain II) of the human epidermal growth factor receptor 2 protein (HER2), and thereby, blocks ligand-dependent heterodimerisation of HER2 with other HER family members, including EGFR, HER3 and HER4. As a result, Perjeta inhibits ligand-initiated intracellular signalling through two major signal pathways, mitogen-activated protein (MAP) kinase and phosphoinositide 3-kinase (PI3K). Inhibition of these signalling pathways can result in cell growth arrest and apoptosis, respectively. In addition, Perjeta mediates antibody-dependent cell-mediated cytotoxicity (ADCC).

Cancer - Vicki (12 decks)

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