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Oncology > Breast ca > Flashcards

Breast ca Flashcards

1
Q

Risk factors for breast cancer

A

High to low risk

Genetic factors
Chest radiotherapy age <30 e.g. HL
Dense breast tissue
Previous atypical ductal carcinoma in situ (DCIS)/lobular carcinoma in situ (LCIS)
FHx
Hormonal factors - HRT, nulliparity, menarche <12
Obesity, alcohol, smoking

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2
Q

Most common genetic mutation in breast ca

What conditions or demographic is this mutation associated with?

A

BRCA 1 and BRCA 2 mutations

Invasive breast ca <30 years
Invasive breast ca in men
Triple neg breast ca <60 years (BRCA 1)
Ovarian or primary peritoneal ca (BRCA 1) 
Ashkenazi Jewish heritage
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3
Q

Which BRCA mutation is associated with higher risk of ovarian ca?

A

BRCA 1

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4
Q

Does breast ca need genetic testing?

A

Use Manchester scoring system

A score of 15 or greater = >10% risk of carrying BRCA 1 or 2 mutation

(Refer potential patients to familial cancer service –> calculate their pretest probability –> if pre-test probability >10% then they are funded for BRCA testing)

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5
Q

BRCA 1 mutation and hormonal status

A

More likely to be triple negative (ER, PR, HER2 neg)

More aggressive

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6
Q

BRCA 2 mutation and hormonal status

A

Associated with hormone receptive positive breast ca

More similar to the standard population

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7
Q

How to reduce cancer risk in BRCA1/2 mutation carriers?

A
  • Bilateral mastectomy
  • Bilateral salphingo-oophorectomy once childbearing is complete (before age 40 if possible); particularly BRCA1
  • Increase surveillance - breast MRI from age 30
  • Chemoprevention with tamoxifen, anastrazole or exemestane (rarely done)
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8
Q

Screening for breast ca

A

Mammography every 2 years from 50-74 years old

Women aged 40-49 or >74 are not invited but have access to free screening

MRI
- only for those with familial breast ca or radiotherapy for HL

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9
Q

Early stage breast cancer management

Consider HER2 positive, hormone receptor positive, node positive

A

Early = non-metastatic, resectable. Confined to breast +/- local lymph nodes

Large disease = 2cm or more
Small disease = <2cm

HER2 positive
- Neoadjuvant therapy with chemo and HER2 mab (trastuzumab) –> surgery

Large disease
- Neoadjuvant therapy with chemo +/- HER2 mab (depending on HER2 status) –> surgery

Smaller disease
- Surgery + radiotherapy

All the above will be followed adjuvant therapy (HER2 mab if HER2 pos or endocrine therapy if hormonal receptor pos)

Surgery

  • WLE or mastectomy
  • Radiotherapy MUST be performed after WLE
  • If there is poor prognosis then will need radiotherapy post mastectomy - <40yo, >4cm primary, >4 LN, positive surgical margins
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10
Q

Breast ca main 2 histological subtypes

A

Ductal (80%)

Lobular (15%)
- Tend to be lower grade, ER+

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11
Q

Prognostic factors in early stage breast ca

A 
Tumour grade
Nodal status*
HER2 status
Tumour size
ER/PR status
Age at diagnosis
Gene assay (e.g. Oncotype DX)

*Nodal status is most important prognostic factor

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12
Q

Chemotherapy used in early stage breast ca

A

AC-T (doxorubicin, cyclophosphamide, paclitaxel)

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13
Q

Immunotherapy used in early stage breast ca

A

new evidence in the triple negative (ER, PR, HER2) setting

Pembrolizumab (PD1 inhibitor) with chemotherapy

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14
Q

Endocrine therapy used in early stage breast ca

A

80% are ER+ or PR+

Aromatase inhibitor (post menopausal women only)

SERM (all women and men)

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15
Q

How do aromastase inhibitors work?

When is it used?

A

Stops testosterone –> oestradiol (in peripheral tissues e.g. fat, liver cells, myocytes)

Must be post-menopausal (if not the ovaries are still making oestrogen so this drug has no effect)

1st choice for postmenopausal women with ER+ or PR+ early breast cancer 
5 years (can consider 10 years if high risk disease e.g. large tumour, node positive)

Better than tamoxifen. If they’re perimenopausal, can have 2 years of tamoxifen then switch to aromatase inhibitor

If used in pre-menopausal women must add ovarian function suppression with GnRH analogue. If not can cause paradoxical increase in estrogen levels.

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16
Q

AE aromatase inhibitor

A 
Vasomotor symptoms
Osteoporosis***
Myalgia, arthralgia
weight gain
Vaginal atrophy
mood changes
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17
Q

How do SERMs work?

A

ER blocker in breast
ER agonist in bone thus osteoprotective (can be used in OP)

Tamoxifen

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18
Q

SERM AEs

A

Vasomotor symptoms
DVT
Endometrial cancer

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19
Q

How long to take tamoxifen for?

A

10 years better than 5 years

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20
Q

Management of in situ disease (has not crossed basement membrane, low potential for metastasis)

A

Surgery then adjuvant low dose SERM for 3 years reduces 4 year development of invasive breast ca

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21
Q

How do ovarian suppression work?

A

High dose GnRH agonists –> downregulate GnRH receptors in pituitary –> decreased FSH and LH release –> decreased estradiol production by ovary

22
Q

When do you use ovarian suppresion?

A

Pre menopausal
Young
If no high risk disease

In conjunction with tamoxifen

Also in fertility preservation - reduces ovarian failure rate when used with chemotherapy

However only reduces the likelihood and is not the same as other methods such as embryo cryopreservation, oocyte cryopreservation etc

23
Q

Early stage HER2 positive disease Rx

A

Trastuzumab (Herceptin)
1 year duration

Can also be given neoadjuvantly (pre-op) and the remainder of the 52 week regimen post operatively

In the event of residual disease being detected in the surgical specimen after neoadjuvant trastuzumab, switch to a drug-ab conjugate trastuzumab emtansine (ab drug conjugate) for the remainder of treatment

24
Q

AE Trastuzumab

A

Very well tolerated
Mild like flu like symptoms

Cardiotoxicity

  • Rare
  • Asymptomatic LVEF decline in 13%. Reversible mostly
  • Risk factor: prior anthracycline use, LVEF <55%, HTN, age >50, BMI >25
  • 3 monthly ECHO
  • Cease if LVEF has declined >15%. or <45% or symptomatic HF
  • Add on ACEI +/- b blocker if drop in EF
25
Q

Pertuzumab MOA

A

Also HER2 ab
$$$
Always added to trastuzumab not instead of

Slight improvement in recurrence by 1.5%

26
Q

Olaparib - when is it used?

A

PARPi

Early stage
BRCA1/BRCA2
Used after surgery (adjuvant)

27
Q

What’s oncotype Dx?

A 
Prognostication biomarker (gene expression assay)
$5000

In someone who is borderline suitable for chemotherapy, this can be done to determine recurrence score.
If low recurrence score, can get away with endocrine therapy alone.
If high recurrence score, benefit with chemotherapy.

28
Q

Fulvestrant when is it used and MOA?

A

Selective estrogen receptor down regulator

In HR+ postmenopausal women with metastatic disease, 1st line is fulvestrant + aromatase inhibitor (much better than aromatase inhibitor alone)

29
Q

CDK 4/6 inhibitors - MOA?

A

Palbociclib, ribociclib, ademaciclib

Inhibit a pathway (inhibits the binding of CDK4/6 to cyclin D and stops phosphorylation of Rb) that stops transition in cellular mitosis (G1 phase to S phase)

= stops cell proliferation/growth

30
Q

When is CDK4/6 inhibitor used?

A

In HR+, HER2- women with metastatic breast cancer

Postmenopausal HR+ women with metastatic disease
When added to fulvestrant or aromatase inhibitor, improves OS and PFS

Premenopausal HR+ women with metastatic disease
When added to gosrelin (GnRH agonist) and aromatase inhibitor or tamoxifen, improves OS and PFS

31
Q

PI3K inhibitor - when is it used?

A

Alpelisib
Use with fulvestrant
HR+ HER2- mBrCa after failure of CDK4/6i in those with activating PIK3CA mutations

32
Q

Pertuzumab when is it used?

A

HER2+ metastatic breast ca

Pertuzumab + trastuzumab + docetaxel is standard of care now

33
Q

Tucatinib when is it used?

A

Small molecules
Inhibit intracellular domain of HER2
3rd line setting in metastatic HER2+ disease

34
Q

Sacituzumab govitecan when is it used?

A

Novel chemotherapy-ab conjugate
Metastatic
3rd line
Triple negative breast ca

35
Q

Immunotherapy when is it used in breast ca?

A

Metastatic triple negative breast ca

Pembrolizumab/atezolizumab + chemo is first line

36
Q

Breast cancer in men hormone status

A

Exclusively ER+
Less HER2+

Rx: tamoxifen is the only therapy used in the adjuvant setting

37
Q

Ideal Duration of HRT in postmenopausal women

A

Attempt taper at 3-5 years

38
Q

How does BRCA1/2 mutations increase your susceptibility to breast ca?

A

These genes are important for repair of double stranded DNA breaks via homologous recombination (error free repair).

If this is not working, you become over-reliant on non-homologous end joining (error prone repair) –> predispose to cancer

39
Q

When do you use PARP inhibitors in breast ca?

A

BRCA1/2 mutations

40
Q

How do PARP inhibitors work in breast ca?

A

BRCA mutation –> impaired homologous recombination (error free repair) –> become reliant on basic excision repair regulated by PARP –> by inhibiting PARP, you stop this kind of repair and overload the tumour with mutations –> genome becomes unstable and the cell becomes non-viable

41
Q

Which type of breast ca is most likely to have late recurrence?
A) Hormone receptor positive, HER2 negative
B) HER2 positive
C) Triple negative

A

Hormone receptor positive, HER2 negative

42
Q

Which type of breast ca has good prognosis?
A) Hormone receptor positive, HER2 negative
B) HER2 positive
C) Triple negative

A

Hormone receptor positive, HER2 negative has good prognosis but late recurrence (>5 years) can occur

HER2 positive has good prognosis due to effective targeted therapies

43
Q

What’s Ki67?

A

Special stain

Indicates high turnover

44
Q

What is trastuzumab-emtansine?

A

Ab-drug conjugate
Trastuzumab linked to a cytotoxic agent

On binding to HER2 on the cell surface, the cytotoxic agent is internalised

45
Q

What type to breast ca are brain metastases common?

A

Triple negative

HER2 positive

46
Q

Treatment of brain metastasis in breast cancer

A

Surgery or sterotactic radiotherapy preferred

If not possible, then whole brain radiotherapy

47
Q

Treatment of HR+, HER2- metastatic breast cancer

A

Aromatase inhibitor/tamoxifen (depending on menopausal status)

PLUS

CDK4/6 inhibitor ribociclib

48
Q

Treatment of HER2+ metastatic breast cancer

1st line
2nd line

A

Dual HER2 mab trastuzumab + perzutumab PLUS chemotherapy

2nd line: Trastuzumab-emtansine (ab-drug conjugate)

49
Q

Treatment of triple negative metastatic breast cancer

A

Intense chemotherapy regimen (Nab-paclitaxel)

PLUS

PDL1 inhibitor pembrolizumab or atezolizumab

50
Q

Treatment of BRCA1/2 early stage disease

A

Surgery + adjuvant PARPi (olaparib)

51
Q

How often should we do MRI/mammogram after breast cancer treatment?

A

Every year

52
Q

Does PR status influence treatment?

A

No - does not influence treatment

PR is just associated with better prognosis.

Oncology (7 decks)

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