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cancer Flashcards

1
Q

HPV types and associations

A

6, 11 ➡️ genital warts

16, 18, 31, etc. ➡️ cervical cancer

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2
Q

stages of prostate regulation throughout lifetime (4)

A
  1. Development → puberty: paracrine effects; androgens act on stromal AR → growth factor production → epithelial cell proliferation
    Epithelial cells also secrete factors that maintain stromal cells in differentiated state
  2. Adult: AR in epithelial cells important at this stage
  3. Second growth spurt: due to breakdown of regulation w ↑age
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3
Q

investigations for prostate cancer (3)

A
  1. DRE
  2. PSA (can have temporary increases e.g. from DRE, also false positives)
  3. USS: tumours outside prostate capsule
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4
Q

prostate cancer Tx options (4)

A

Low grade tumour, older patients → active surveillance (periodic PSA tests)
Confined to prostate gland (stage T1, T2) → radical prostatectomy
(nerves nearby control erection & urination ∴ risk of incontinence & impotence)
Confined or local spread (T1 to T3) → radical radiotherapy (external or implants)
Metastatic cancer → hormone therapy

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5
Q

possible mechanisms behind castration-resistance prostate cancer (4)

A

Amplified response to low levels of residual/administered hormones due to:

  1. Overexpression/amplification of AR
  2. Overexpression/amplification of coactivator genes
  3. Reduced expression/deletion of corepressor genes
  4. Mutation or alternative splicing of AR (can drive AR target gene expression and growth in absence of ligand)
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6
Q

treatment for breast cancer (4)

A
  1. SERMs e.g. tamoxifen, bind competitively to ER
  2. ovarian ablation (prevention of oestrogen production by ovaries): surgery/hormone therapy e.g. goserelin (LHRH analogue)
  3. SERDs e.g. fulvestrant, bind competitively to ER and induce receptor degradation
  4. aromatase inhibitors: prevent conversion of androstenedione to estrone and testosterone to estradiol
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7
Q

mechanisms of resistance to hormone therapy in breast cancer

A
  1. de novo endocrine resistance: tumour independent of estrogen, despite being ERα-positive
  2. acquired endocrine resistance: growth promotion of initially estrogen-dependent tumours, by other mitogenic pathways
  3. transcription coactivators/repressors
  4. ER mutations
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8
Q

what type of virus is HPV

A

dsDNA

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9
Q

HPV screening

  1. methods
  2. schedule
A
  1. Smear test: taken from SCJ
    25-50: 3 yearly, 50-65: 5 yearly (1/4 false negatives)
  2. HPV DNA test will replace smear test (more sensitive; detected in 99.7%)
  3. CIN 2/3 → colposcopy and loop excision
    Remove affected tissue + assess extent of neoplasia
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10
Q

presentation of cervical cancer

A

Early disease asymptomatic
Irregular bleeding: after intercourse, in between periods
Advanced disease → offensive discharge, backache, leg pain/oedema, haematuria, bowel changes, malaise, weight loss, anaemia

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11
Q

endometrial cancer: types + mutations

A

oestrogen dependent: PTEN mutation
more common, younger women, better prognosis
non-oestrogen dependent: p53 mutation

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12
Q

mainstay treatment of endometrial cancer

A

TAH + BSO

radiotherapy (after surgery; pre-op makes surgery more difficult)

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13
Q

HPV interaction w host genome

A

integrates into host genome -> overexpression of E6 and E7 genes -> proteins degrade tumour suppressors e.g. p53, pRb -> aneuploidy, increased cell cycling and survival

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14
Q

composition of HPV vaccine

A

virus like particle: L1 protein of HPV capsid

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15
Q

breast cancer biomarkers (3)

A

ER: nuclear transcription factor
PR: nuclear transcription factor
- ER and PR -> better response to endocrine therapy
Her-2-neu: growth factor receptor
important in deciding on management (also prognostic factors)

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16
Q

breast cancer risk factors (3)

A
  1. oestrogen exposure
  2. family history
  3. genetic syndromes e.g. BRCA1 and 2
17
Q

breast cancer investigations (3)

A

triple assessment

  1. clinical: palpation
  2. imaging: mammography / USS (young pts)
  3. biopsy: fine needle aspiration / core-cut biopsy
18
Q

breast cancer presentation (7)

A

Breast lumps/thickening (w or w/o pain)
Nipple discharge, reaction, excoriated rash
Lumps in armpits
Pain in breast/armpits
Change in how breast feels/looks
Rarely, metastasis related symptoms: bone pain, pathological fracture, convulsions, jaundice
Asymptomatic → mammographic abnormalities upon screening

19
Q

endometrial cancer risk factors (6)

A 
Obesity
Diabetes mellitus
Nulliparity 
PCOS 
Oestrogen only HRT 
Prolonged tamoxifen use
20
Q

prostate cancer symptoms

A 
Urinary symptoms: 
Polyuria, nocturia 
Poor urinary stream
Urgent need to urinate 
Hesitancy whilst urinating
Lower back pain 
Blood in the urine (rare) 
Can also be asymptomatic and go undetected
21
Q

hormone therapy for prostate cancer + MOAs (5)

A
  1. GnRH analogues e.g. gosrelin: overstimulate GnRHR → downregulation
    Takes 2 weeks; initial rise in LH and testosterone
  2. GnRH antagonists: block GnRHR activation ∴ more rapid effects
  3. AR antagonists (anti-androgens) e.g. flutamide
    a. Compete w ligand for AR binding
    b. Sequester AR in cytoplasm
    c. Prevent dimerisation
    d. Prevention formation of active transcription complex
  4. 5α-reductase inhibitors: inhibit testosterone → DHT
  5. Abiraterone: inhibits CYP17
    Affects synthesis of other steroids; ↑11-deoxycorticosterone + corticosterone (glucocorticoids + mineralocorticoids) → secondary mineralocorticoid syndrome (hypertension etc.)
22
Q

how is blood vessel integrity maintained (3)

A
  1. angiopoietin 1 binds to tie 2 receptor
  2. contact w ECM
  3. physical contact between endothelial and mesenchymal cellst
23
Q

regulation of ECM remodelling (MMPs and TIMPs)

A

MMP-TIMP complex requires both dissociation of TIMP and cleavage of MMP N-terminus to expose active site

24
Q

actions of angiopoietins

A

angiopoietin 1: agonist for tie2
angiopoietin 2: antagonist for tie2 (produced by tumours)
multiple signalling pathways -> endothelial cell assembly and survival, ECM interactions -> blood vessel formation and maintenance

25
Q

process of angiogenesis

A
  1. loss of contact between endothelial cells
  2. proliferation, invasion of ECM
  3. contact w pre-existing blood vessel
  4. formation of new junction between vessels
26
Q

hallmarks of cancer (10)

A
  1. sustained proliferative signalling:
  2. evasion of tumour suppressors e.g. pRb, CKIs
  3. resisting cell death
  4. replicative immortality e.g. uregulation of telomerase
  5. induction of angiogenesis e.g. increased HIF, VEGF
  6. invasion and metastasis
    emerging hallmarks:
  7. deregulation of cell energetics
  8. evasion of immune response
    enabling hallmarks:
  9. DNA instability and mutations
  10. inflammation
27
Q

imatinib:

  1. moa
  2. development of resistance
A
  1. ATP analogue which binds to BCR-ABL (fusion protein found in CML)
    also targets some receptor tyrosine kinases e.g. PDGF-receptor and c-Kit (gastrointestinal stromal tumours)
  2. threonine mutation to larger amino acid -> loss of imatinib binding
28
Q

type 1 vs type 2 kinase inhibitors

A

type 1 targets active receptor e.g. dasatinib

type 2 targets inactive receptor (juxtamembrane region blocks active site) e.g. imatinib

29
Q

tyrosine kinase inhibitor resistance; mechanisms (5)

A
  1. mutation prevents drug binding
  2. upregulation of alternative kinase
  3. alternative kinases
  4. downregulation of phosphatase
  5. downstream mutation in receptor signalling pathway
30
Q

cancers associated w infection (4)

A

H. pylori → stomach cancer
Hep B → liver cancer
Pancreatitis → pancreatic cancer
HPV → cervical cancer

31
Q

immune responses that can be prognostic in cancer (2)

A

Tumour infiltrating lymphocytes (TILs) → better prognosis

Tregs → worsened prognosis

32
Q

how do tumours evade the immune response (6)

A
  1. Secrete cytokines e.g. IL10, IGFβ → ↓effector T cell response, ↑Treg
  2. ↓MHC class I and II
  3. Expression of ligands e.g. CTLA-4/PDL1 that bind to inhibitory receptors on T cells
  4. Loss of Fas and other death receptors
  5. Upregulation of anti-apoptotis proteins e.g. Bcl2
  6. Continuous shedding of tumour associated antigens → tolerance
33
Q

immunotherapy approaches for cancer Tx (4)

2017 essay

A
  1. Cytokines (e.g. Interferons, IL2)
  2. Monoclonal Antibodies (mAbs)
  3. Cancer vaccines
  4. Adoptive immunotherapy e.g. TILs, haematopoetic stem cells, NK cells, T cells
34
Q

immunotherapy: cytokine therapy examples (2) + issues (2)

2017 essay

A

Examples

  1. IL-2 → activation and expansion of CD4 and CD8 T-cells (metastatic melanoma and renal cell carcinoma)
  2. IFN → expression of MHC class I, maturation of DCs, activation of CTLs (melanoma)

Issues:

  1. Non-specific (cytokines have multiple effects) → toxic side effects
  2. Redundancy; alternative pathways compensate
35
Q

immunotherapy: monoclonal Abs examples and MOA (4)

2017 essay

A
  1. Herceptin → HER2 (breast cancer) internalisation and degradation
  2. Rituximab binds to CD20 (malignant lymphoma) → Fc receptors of NK cells can bind → crosslinking → perforin, granzymes → cell lysis
  3. Ipilimumab blocks co-stimulation needed for T cell activation (melanoma)
  4. Brentuximab targets CD30 Ag of lymphocytes, delivers chemo drug MMAE (Hodgkin’s lymphoma)
36
Q

what is adoptive immunotherapy + one example

2017 essay

A

transfer of lymphocytes to patient

e.g. TILs (tumour infiltrating lymphocytes): retrieve T cells from pt, select, expand and then transfer back

37
Q

how does obesity and insulin resistance increase endometrial cancer risk

2017 SAQ

A
  1. Adipose tissue aromatase: androgens → oestrogens
  2. Fat cells produce adipokines that may stimulate or inhibit cell growth
    a. Leptin promotes cell proliferation
    b. Adiponectin may have anti-proliferative effects
  3. Fat cells have direct & indirect effects on tumour growth regulators, including mammalian target of rapamycin (mTOR) and AMP-activated protein kinase
  4. Obese people often have chronic low-level, or “sub-acute,” inflammation, which has been associated with increased cancer risk
38
Q

side effects of anti-androgens (5)

2015 SAQ

A

Osteoporosis, muscle loss, ↑fat deposition, gynaecomastia, loss of libido

39
Q

management of cervical cancer (4)

A
  1. CIN (cervical intraepithelial neoplasia)/CIS are resected to avoid progression to cancer
  2. Invasive cancer: radical hysterectomy and lymph node dissection OR radical chemoradiation therapy
  3. Radical hysterectomy
    ○ Benefits: ovarian preservation
    ○ Complications: bowel-bladder dysfunction
  4. Radiotherapy:
    ○ Benefits: Good for frail patients with co-morbidities
    ○ Complications: menopause, late sequelae on bladder

rds (13 decks)

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