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personalised medicine and cancer > cancer Part 5 > Flashcards

cancer Part 5 Flashcards

1
Q

What is the most prevalent cancer in women in the western world?

A

Breast cancer

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2
Q

What is the driver for breast cancer?

A

Oestrogen exposure

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3
Q

TNM system is used in Breast cancer. True/false?

A

True

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4
Q

Describe breast cancer

A

Breast cancers usually are epithelial tumours of ductal or lobular origin

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5
Q

List the various classifications of breast cancer

A

Ductal carcinoma in situ( DCIS)
Lobular carcinoma in situ
Invasive ductal carcinoma (ductal breast cancer)
Invasive lobular carcinoma
medullary carcinoma
Inflammatory BC
Mammary Paget disease
tubular carcinoma
Papillary carcinoma

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6
Q

what is the biggest risk factor in breast cancer?

A

Age

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7
Q

Familial breast cancer is associated with what?

A

altered BRCA1/2 or p53

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8
Q

What is associated with greater than 70% breast cancer ?

A

BRCA1

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9
Q

Greater than 40% of ovarian cancer is associated with —

A

BRCA1

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10
Q

Most breast cancer treatment plans use combined modalities. True/False?

A

True

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11
Q

State what combined modalities in BC comprises of

A

Primary tumour removed by surgery (mastectomy/lumpectomy)
Radiation therapy to remaining breast and/or axilla
Adjuvant chemotherapy
Hormonal therapy to eradicate any micro-neoplastic disease/prophylaxis

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12
Q

State the genetic test used to determine when to treat a patient

A

Oncotype DX test

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13
Q

What does RS score mean in oncotype DX test

A

This suggests the likelihood of cancer coming back

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14
Q

A low RS means what?

A

Cancer is unlikely to come back
RS is less than 18

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15
Q

A high RS using oncotype Dx suggest what ?

A

Suggests the cancer is more likely to come back
RS greater than 31

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16
Q

Describe a chemo brain

A

Chemo brain include disorganized behaviour or thinking, confusion, memory loss, and trouble concentrating, paying attention, learning, and making decisions.

17
Q

What does SERM stand for?

A

Selective estrogen receptor modulator

18
Q

List examples of drugs that are SERMS

A

Tamoxifen
Droloxifene
Toremifene
Raloxifene
Idoxifene

19
Q

SERms are called modulators because?

A

They have both estrogenic and anti-estrogenic property

20
Q

There are two types of estrogen receptors namely?

A

Alpha and beta estrogen receptor

21
Q

State how Tamoxifen work

A

Tamoxifen is a partial antagonist - it has pro-oestrogenic affects
Associated with oestrogen receptor subtype distribution
Increased incidence of endometrial cancer
Tamoxifen consistently reduces the risk of contralateral breast cancer

22
Q

State the mechanism of action of Estradiol as a hormonal therapy used in breast cancer treatment

A

Estradiol binds to the estrogen receptor upon estrogen binding, AFI (ACTIVATION FACTOR), there is dimerization and AF2 is activated, this translocate to the nucleus and binds to the DNA - fully activated transcription

23
Q

State how Nolvadex(tamoxifen) works.

A

Tamoxifen binds to estrogen receptor, AFI is activated but upon dimerization, AF2 is not activated, there’s a partial transcription

24
Q

State how Faslodex works

A

binds to the estrogen receptor, upon dimerisation, neither AF1 nor AF2 is activated- no co-factors hence, no transcription. hence, they are not pro-estrogenic and it is degraded

25
Q

Tamoxifen is a prodrug that requires activation by CYP3A to ……

A

Endoxifen

26
Q

Facts about the metabolism of Tamoxifen

A

Poor metaboliser – decreased production of active metabolite?
Extensive metaboliser – higher levels of active metabolite?

27
Q

What are SERDs?

A

selective estrogen receptor down-regulators

28
Q

State why SERDs are more effective than SERMs (Tamoxifen)

A

they cause less interaction between DNA and estrogen receptor,

29
Q

State when SERDs are used in Cancer treatment

A

In treatment resistant to tamoxifen, they arent first-line treatment options

30
Q

Facts about Selective Estrogen Receptor downregulators

A

Very different structure to tamoxifen
All steroid analogues
Side chain at 7 position

31
Q

Facts about RV-471 - selective protein degrader currently under clinical trail

A

ARV-471 directly binds an E3 ubiquitin ligase and ER to trigger ubiquitination of ER and its subsequent degradation

personalised medicine and cancer (16 decks)

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