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3921 > 9 - Molecular targeted cancer drugs ‐ breast cancer and prostate cancer > Flashcards

9 - Molecular targeted cancer drugs ‐ breast cancer and prostate cancer Flashcards

1
Q

Why is breast cancer a heterogeneous disease

A

Encompasses multiple subgroups with differing molecular signatures, prognoses and responses to therapies

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2
Q

What are three major subtypes of breast cancer

A

1) Hormone receptor positive tumours that express estrogen or progesterone receptors
2) HER2 - amplified breast cancer
3) Triple negative breast cancers that lack ER, PR and HER2 expression

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3
Q

Where is estrogen produced in premenopausal vs postmenopausal women

A

Ovaries

Peripheral aromatase

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4
Q

What do estrogens activate

A

ERa and ERb

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5
Q

What is an ER antagonist

A

Tamoxifen

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6
Q

What does partial agonism of ER in the uterus and vascular system cause

A

Increased risk of endometrial cancer and thromboembolism

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7
Q

What is a steroidal PR antagonist

A

Onapristone

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8
Q

What does tamoxifen require for activation

A

CYP2D6

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9
Q

What are some mechanisms of tamoxifen resistance (3)

A

ERa mutations
Overactivity of ER-independent proliferative pathways
Overactivity of PI3K/Akt survival cascade

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10
Q

What do inhibitors of aromatase do

A

Block conversion of testosterone to estradiol

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11
Q

What are AIs in clinical use

A

Anastrozole
Letrozole
Exemestane

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12
Q

What is HER2 a subtype of

A

EGF

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13
Q

What does trastuzumab (herceptin) do

A

Prevent HER2 dimerisation

Monoclonal antibody

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14
Q

2 Mechanisms of resistance to trastuzumab

A

1) Alternate proliferative pathways used by tumours
2) Increased survival signalling e.g. presence of activating PI3-kinase mutations or loss of function of the phosphatase PTEN
3) HER2 overexpression in tumours

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15
Q

Why is TNBC an aggressive disease

A

No clear therapeutic target

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16
Q

Do women with TNBC benefit from either endocrine therapy or trastuzumab

A

No

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17
Q

What is the breast cancer susceptibility gene

A

BRCA1

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18
Q

What does BRCA1 usually do

A

Co-regulate ERa-regulated gene

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19
Q

What does BRCA1 inhibit

A

1) Proliferation by the ER

2) DNA repair and genome stability rebulation

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20
Q

Are BRCA-1 positive tumours likely to be ER and HER-2 negative

A

Yes

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21
Q

What is the current mainstay of TNBC treatment

A

Combination chemotherapy

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22
Q

What is effective against TNBC

A

Anthracycline

Newer cytototxic agents ixabepilone

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23
Q

What is an emerging treatment for TNBC

A

DNA repair enzyme PARP

PARP inhibitors as PARP is higher in TNBC

24
Q

What is a PARP inhibitor

A

olaparib

25
Q

What occurs in patients with advanced prostate cancer

A

Bone metastases that form osteoblastic lesions

26
Q

Are there subtypes of prostate cancer

A

No

27
Q

How is localised prostate cancer treated

A

Surgically or with radiation

Or monitored if low risk

28
Q

How is recurrent prostate cancer treated

A

Androgen deprivation therapy

Bilateral orchietomy

29
Q

How does luteinising hormone releasing hormone work

A

Act on pituitary to release LH which activates steridogenesis

30
Q

What is an LHRH agonist

A

Leuprolide

31
Q

What is a LHRH antagonist

A

Degarelix

32
Q

What is an AR antagonist

A

Bicalutamide

33
Q

WHat is a CYP17 inhibitor

A

Abiraterone

34
Q

What is a 5a-reductase inhibitor

A

Finasterise

35
Q

What are adverse effects of ADT

A

Osteoporosis and fractures
Obesity and insulin resistance
Increased serum cholesterol and triglycerides
Increased diabetes and CV disease risk

36
Q

What are mechanisms of CRPC

A

1) AR overexpression
2) Ligand-independent AR activation
3) Androgens produced within the tumour, stimulating AR
4) Loss of signalling control

37
Q

How do cytokines and chemokines affect prostate cancer

A

Enhanced proliferation of progenitor cells

38
Q

What can IL-4 do to prostate cancer cells

A

Render them resistant to apoptosis and activate AR in absence of androgen

39
Q

What is treatment for CRPC

A

Chemo
Biological therapies
Radiopharmaceuticals
Anti-hormonal agents

40
Q

What are some biological therapies in CRPC (3)

A

Bevacizumab
Aflibercept
Sipuleucel-T

41
Q

What is bevacizumab

A

Humanised anti-VEGF receptor antibody

42
Q

What is aflibercept

A

Soluble fusion protein corresponding to the VEGF-receptor extracellular domain

43
Q

What is sipuleucel-T

A

A vaccine derived from dendritic cells activated by antigen prostatic acid phosphatase

44
Q

Where are breast metastases found

A

Bones
Brain
Lungs
Liver

45
Q

Where are prostate metastases found

A

Bone

Lungs

46
Q

Which receptor is overexpressed in prostate cancers that have metastasised to bone

A

MET receptor (KI)

47
Q

How is MET activated

A

Hepatocyte growth factor

48
Q

What is MET involved in

A

Proliferation
Differentiation
Migration of osteoblasts and osteoclasts

49
Q

What is a MET receptor inhibitor

A

Cabozantinib

50
Q

Which tyrosine kinase has a central role in growth, invasion and metastasis of prostate carcinomas

A

SRC

51
Q

What is a SRC inhibitor

A

Dasatinib

52
Q

What is a biological therapy in metastatic breast and prostate cancer

A

RANK-ligand

53
Q

What is an anti-RANK-ligand monoclonal antibody

A

Denosumab

54
Q

What does denosumab do

A

Supress bone resorption by RANK

55
Q

What does zoledronic acid do

A

1) Reduce number of skeletal events in patients with bone metastases
2) Increase bone mineral density
3) Inhibit osteoclast-mediated bone resorption

3921 (22 decks)

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