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Hormones and Cancer Flashcards

1
Q

What is the incidence of breast cancer?

A

55 per 100000

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2
Q

What is the incidence of lung cancer?

A

23 per 100,000

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3
Q

What is the incidence of colorectal cancer?

A

19 per 100,000

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4
Q

What is the death rate for lung cancer?

A

16 per 100,000

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5
Q

What is the death rate for breast cancer?

A

11.5 per 100,000

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6
Q

What is the death rate for colorectal cancer?

A

7.5 per 100,000

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7
Q

What is the difference in survival between lung cancer and breast cancer?

A

If you get lung cancer, you are likely to die from it; if you get breast cancer, you are more likely to survive.

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8
Q

What is a modifiable risk factor for breast cancer?

A

High socio-economic group factors include obesity, alcohol, high fat diet, smoking, fewer pregnancies, and less likely to breastfeed.

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9
Q

Are there any modifiable breast cancer stats in men?

A

Yes, they are also present in men (1% of cases).

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10
Q

What is the strongest non-modifiable risk factor for breast cancer?

A

Age, with peak chance of getting it between 50-70 years.

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11
Q

What are other non-modifiable risk factors for breast cancer?

A

Previous breast disease, family history (BRCA and others), and hormone-related factors.

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12
Q

What did Beatson demonstrate about oestrogen exposure and cancer?

A

He showed an association between oestrogen levels and breast cancer, and that bilateral ovariectomy could cause remission.

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13
Q

What is the link between oestrogen exposure and breast cancer risk?

A

Longer exposure to oestrogens increases risk, such as early menarche, late menopause, and higher BMI post-menopause.

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14
Q

How much does breastfeeding reduce breast cancer risk?

A

4% per 12 months.

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15
Q

How would you test for estrogen receptor positivity (ER+)?

A

By immunohistochemistry (IHC) on biopsied or surgically removed tumors.

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16
Q

What indicates a positive ER test?

A

At least 1% of cells expressing ER.

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17
Q

Why do people die from breast cancer?

A

Due to metastatic spread to other organs such as bones, liver, lung, brain, skin, ovaries, and GI system.

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18
Q

What are the methods of adjuvant systemic therapy for breast cancer?

A

Hormone therapy and chemotherapy.

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19
Q

What is Luminal A type cancer?

A

ER and PgR positive, HER2 negative, low proliferation, responsive to endocrine therapy.

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20
Q

What is the oestrogen receptor?

A

A protein found in the nucleus, part of the nuclear hormone superfamily.

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21
Q

What does the oestrogen receptor bind to?

A

It specifically binds to oestrogen (17β-oestradiol).

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22
Q

What happens when oestrogen binds to its receptor?

A

The receptor undergoes a conformational change, exposing a DNA binding domain.

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23
Q

How many domains does the oestrogen receptor have?

A

Five domains.

24
Q

What is E2?

A

A steroid that passes through the membrane and binds to the oestrogen receptor.

25
What is the genomic action of oestrogen (E2)?
It causes ER to undergo dimerisation and phosphorylation, increasing binding of co-activators.
26
What does IGF do?
Binds to cell surface receptors, activating pathways that increase expression of cyclin D1, stimulating tumor growth.
27
What are SERMs?
Selective oestrogen receptor modulators, e.g., Tamoxifen.
28
How effective are SERMs in breast cancer treatment?
Reduces recurrence by 42% with 5 years treatment and improves survival by 22% in early breast cancer.
29
How is Tamoxifen used?
20 mg per day after testing for ER presence.
30
What are the treatment-related complications of Tamoxifen?
Menopausal symptoms, fatigue, joint pain, nausea, and rare severe side effects.
31
What is the mechanism of acquired tamoxifen resistance?
Upregulation of EGFR signaling pathways and amplification of Cyclin D expression.
32
What controls oestrogen levels in post-menopausal women?
Conversion of testosterone to oestradiol in adipose tissues by aromatase enzymes.
33
How can aromatase inhibitors help in breast cancer treatment?
They inhibit the conversion of androgens to oestrogen, reducing oestrogen levels.
34
What was the ATAC trial?
A study comparing Anastrozole and Tamoxifen in early stage disease, showing Anastrozole is more effective with fewer side effects.
35
Outline the ATAC trial
This study compared Anastrozole, Tamoxifen, Alone or in Combination. Compared tamoxifen with anastrozole adjuvant therapy in early stage disease in 9366 post menopausal women. Showed anastrozole more likely to stop cancer recurrence than tamoxifen with lower side-effects (risk of endometrial cancer and DVT). Conclusion: AIs preferred initial treatment for postmenopausal women with localised hormone receptor positive breast cancer. Published 2005 in Lancet 365 (9453), p60-62
36
What are the side effects of Aromatase inhibitors?
Hot flushes and Vaginal dryness, Nausea, Rashes, Joint stiffness, Raised cholesterol, Osteoporosis, Neurological effects on extremities, Lack benefits of Tamoxifen (lowers cholesterol, maintains bone density)
37
Outline the BIG 1-98 trial
Trial looked at whether there is benefit in giving AIs instead of Tamoxifen, or of sequential treatments (i.e. 5 yr Tam then 5 yr AI with 8,000 patients). This approach allows for longer treatment as patients can become resistant to both treatments. Population: Post-menopausal women with receptor positive early breast cancer. Results: Use of LET (AI) ⇒ disease reoccurrence is lower. AI is better than Tamoxifen then switch to AI. Node negative disease: equal benefit with Tamoxifen first or AI. Node positive disease: need to be on AI straight away.
38
What produces oestrogen if you are a pre menopausal woman?
Oestrogen is produced by your ovaries in response to FSH produced from the pituitary, which is stimulated by LHRH from the hypothalamus.
39
What drug is used to target ER in pre menopausal women?
Goserelin
40
What is goserelin?
Goserelin is a drug that is a LHRH agonist. It has a 10 AA sequence with 9 AA the same as LHRH, one being changed.
41
What does Goserelin do?
The AA sequence allows it to bind strongly to receptors in the pituitary and initially stimulates FSH/LH release. Continuous exposure results in down regulation of receptors, leading to reduced FSH and oestrogen release, causing chemically induced menopause.
42
How is goserelin administered and why is this advantageous?
Goserelin is given in the arm which lasts about a month, making it better for busy women as they do not have to take a daily dose.
43
What happens if you have luminal B BCa cancer cell type?
ER positive, responds to therapies but not as effectively as Luminal A. Luminal B may have mutations (HER2 positive, Ki-67, PR -ve) and is responsive to endocrine therapy and more sensitive to chemo.
44
What is oncotype DX?
A genetic test based on a panel of 21 genes to decide who benefits from chemotherapy. Generates a recurrence score: more altered genes = higher score; high score indicates need for chemotherapy, low score indicates safe to treat with endocrine therapy.
45
What is the incidence of prostate cancer?
Globally, prostate cancer is the sixth most common cancer and the third most frequently diagnosed cancer in men. It is primarily a disease of older men and is the most common form of cancer in men in the UK.
46
What is the aetiology of prostate cancer?
Age is the biggest factor, with increased risk after 70. Family history, high fat and meat diet, and frequency of sexual activity are also factors. Prostate cancer mortality rises sharply with increasing age.
47
What are the signs and symptoms in early prostate cancer?
Symptoms are limited as the tumour is small, mainly urinary: Difficulty passing urine, Nocturia, Pain on urination, Haematuria.
48
What are the signs and symptoms in advanced prostate cancer?
Impotence, Tiredness, General feelings of unwellness, Loss of appetite, Bone metastases causing pain in hips and spine, Increased fractures, Spinal nerve compression leading to paraesthesia or weakness and incontinence.
49
How is prostate cancer diagnosed?
Diagnosis involves Prostate Specific Antigen (PSA), Digital Rectal Examination, and Transrectal biopsy. PSA is effective for monitoring therapy.
50
Describe how the prostate specific antigen is effective or not.
PSA is sensitive (levels increase as prostate enlarges) but not specific for prostate cancer. Up to 2/3rds of men with raised PSA do not have prostate cancer, and 20% of patients with prostate cancer may not have raised PSA.
51
What are some problems with prostate cancer diagnosis methods?
Aging population increases incidence. Increased PSA testing leads to greater diagnostic rates, but despite early detection, mortality rates remain stable, leading to over treatment of indolent disease.
52
What are the treatment options for non-metastatic prostate cancer?
Deferred treatment/active surveillance for low grade tumours, Radical prostatectomy for localized tumours (risks include incontinence and impotence), Radiotherapy for disease in pelvis or higher PSA (External beam and Brachytherapy).
53
When is Hormone Treatment for Prostate cancer carried out?
Hormone treatment is done if patients are too frail for surgery/radiotherapy, have metastatic disease, or as neoadjuvant therapy prior to definitive radiotherapy.
54
How does Goserelin treat prostate cancer?
Goserelin is a GnRH agonist that initially causes a tumour flare, increasing testosterone and oestrogen. Within a couple of months, it reduces testosterone production by testes and adrenal glands.
55
What are some longer term treatments for prostate cancer?
Longer term treatments often include anti-androgen therapies like Abiraterone, which compete with testosterone receptors in the prostate.

Y2S2M2 (22 decks)

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