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Reproductive Biology 3 > L22: Reproductive Cancers > Flashcards

L22: Reproductive Cancers Flashcards

1
Q

What is tumour?

A

formed by an excessive, uncontrolled proliferation of cells as a result of an irreversible genetic change, which is passed from one tumour cell to its progeny

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2
Q

What is neoplasia?

A

new uncontrolled growth of cells in the body

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3
Q

What is the difference between benign and malignant tumours?

A

Benign tumours stay localised at their site of origin (non-cancerous), while malignant tumours are able to invade and spread to different sites (metastasis)

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4
Q

What are malignant tumours features?

A

Infiltrate, fast growth, large plemorphic nuclei, less differentiated

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5
Q

What is the difference between primary and secondary cancers?

A

Primary - tumour arise at the primary site from cells normally present there, secondary - metastatic

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6
Q

What is the development and progression of cancer cell?

A
  • cell with mutation (usually able to fix during cell cycle, repair mechanism)
  • hyperplasia (expansion of cells)
  • dysplasia (morphology starts to change)
  • in situ cancer (confined in local area)
  • invasive cancer
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7
Q

What causes a cancer to develop?

A
  • loss of tumour suppressor gene function
  • gain of oncogene function
  • could be: mutagens, pathogens, inactive repair
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8
Q

Which genetic abberations can cause cancer?

A
  • duplication (genome multiplied)
  • inversion (DNA twists during S phase)
  • deletion
  • insertion (happens a lot in leukaemia)
  • translocation
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9
Q

What are proto-oncogenes?

A

Normal version of genes that code for proteins that are needed for normal cell division

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10
Q

What are oncogenes?

A

Mutated proto-oncogenes, mutations in certain genes promote uncontrolled cell division/proliferation

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11
Q

What are activating mutations?

A
  • Only certain mutations in a proto-oncogene will convert it to the oncogenic form
  • activation of (proto-) oncogenes allows cells to bypass the need for extracellular growth signals
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12
Q

What is ‘dominant acting’ in regard to oncogenes?

A

Only one allele (copy) of a proto-oncogene needs to acquire an activating mutation

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13
Q

How do oncogenes work? What do they code for?

A
  • oncogenes code for:
    i) a hyperactive version of the protein product

or

the normal protein product but
i) in abnormal quantities
ii) at the wrong time
iii) in the wrong cell type

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14
Q

What are tumour suppresor genes? what are their examples?

A
  • tetrameric transcription factor
  • inhibits cell cycle progression (through p21) - allows for DNA repair
  • p53 is inactivated in around 50% of human cancers
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15
Q

What is a dominant negative effect regarding p53?

A

mutant p53 exerts a dominant negative effect by preventing wild-type p53 from binding to the promoter of its target genes

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16
Q

What is Li-Fraumeni syndrome?

A

germline mutation, which predisposes offspring to cancer, p53 mutation

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17
Q

What effect does HPV have on p53?

A

the E6 protein of HPV inactivates p53 in cervical epithelial cells

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18
Q

What are the steps of cancer metastasis?

A
  1. mutation
  2. primary tumour
  3. vascularization (angiogenesis) - vessels bring nutrients, but also give a root out of the tumour
  4. detachment (epithelial-to-mesenchymal transition) - mesenchymal cells have different morphology able to move around the body
  5. intravasation
  6. extravasation
  7. invasion
  8. secondary tumour
  9. vascularization
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19
Q

What are the routes of metastasis?

A
  • local invasion
  • lymphatic spread (important for breast cancer)
  • blood spread
  • transcoelomic (spreads through cavity, such as peritoneal cavity, as in the case of ovarian cancer)
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20
Q

What are the reasons for increasing survival of breast cancer?

A
  • better awareness
  • introduction of screening (thus, incidence is goign up)
  • improvements in treatment (deaths are going down)
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21
Q

What are the risk factors for breast cancer?

A
  • age (>50)
  • positive family history
  • earlier menarche (<12)
  • later menopause (>55)
  • being older at first pregnancy
  • oral contraception use
  • hormone replacement therapy
  • estrogen exposure
  • radiation exposure
  • obesity
  • alcohol
22
Q

What are breast cancer genetic syndromes?

A
  • BRCA1/BRCA2
  • p53 (Li-Fraumeni syndrome)
23
Q

What are BRCA genes responsible for?

A

Tumour suppressor genes that produce proteins that are used by the cell in an enzymatic pathway that makes very precise, perfectly matched repairs to DNA molecules that have double-stranded breaks.
approx. 50 to 65% of women born with a deleterious mutation in BRCA1 will develop breast cancer by age 70

24
Q

what are the symptoms of breast cancer?

A
  • a new lump or thickening in breast or axilla
  • altered shape, size or feel of the breast; pain
  • skin changes: puckering dimpling, skin oedema, rash, redness, feels different
  • nipple changes: tethering/inversion, discharge, eczema-like changes in Paget’s disease
  • rarely, widespread inflammation, redness, pain in inflammatory cancer can simulate infection
25
Q

What is the diagnosis of breast cancer?

A

Triple assessment:
1. clinical (age, examination)
2. imaging (ultrasound, mammography (younger than 45 cannot see because breast is dense)
3. pathology (fine needle aspiration cytology, core-cut biopsy)

26
Q

What are the cancer grades?

A
  • grade 1 - high homology to normal breast
  • grade 2 - structure lost
  • grade 3 - completely lost structure, many nuclei in a cell
27
Q

How is cancer stage and grade different?

A
  • Stage defines development of disease
  • grade is how tissue looks under the microscope
28
Q

How is immunohistochemistry used for determination of breast cancer?

A

Markers produced in cancer:
- ER (oestrogen receptor, key)
- PR (progesterone receptor)
- HER2

for example ER in cancer is stained brown, if seen in the stained tissue, means that it uses oestrogen as fuel for growth

29
Q

Describe oestrogen signalling in breast cancer

A
  1. testosterone in converted to oestradiol by aromatase
  2. oestrogen binds to oestrogen receptor
  3. bound receptor dimerises
  4. the dimer then binds to oestrogen response elements, which switches on cell cycle proteins, for example cyclin D –> cell grows faster
30
Q

How can oestrogen signalling be manipulated?

A
  • aromatase inhibitors stop conversion of testosterone to oestradiol (letrozole, anastrozole, exemestane)
  • tamoxifen competes with oestrogen, so the receptor does not dimerise, partial agonist
31
Q

What is HER2 gene?

A

human epidermal growth factor 2, involved in normal cell growth

32
Q

What is HER2+ breast cancer? What is the possible treatment?

A
  • gene amplification results in increased protein levels
  • HER2 amplification activates cell cycle much more and accelerates cell growth
  • worst cancer to treat, can be treated with monoclonal antibody Trastuzumab (Herceptin) and other Her2-targeted therapies
  • monoclonal antibodies inhibit ligand-independent / ligand-dependent signalling
33
Q

How is breast cancer staged?

A

early stages of breast cancer:
- stage 0 - abnormal/cancer cells present in lining of breast lobule or duct, also called lobular carcinoma in situ (LCIS) or ductal carcinoma in situ (DCIS)
- stage 1 - cancer spread from lobules or ducts to nearby tissue, invasive, tumor is 2 cm or less in diameter
- stage 2 - 2 - 5 cm
- stage 3A - tumor grows extensively into acillary (underarm) lymph nodes

advanced stages of breast cancer:
- stage 3B/3C - locally advanced cancer, spread into the skin of the breast, tissue of the chest wall or lymph nodes
- stage 4 - metastatic cancer

34
Q

How is breast cancer managed?

A
  • surgery
  • radiotherapy
  • chemotherapy
  • immunotherapy
  • targeted therapy
  • hormone therapy
35
Q

What virus is cervical cancer ussually associated with?

A
  • associated with persistent infection with high-risk HPV subtypes - HPV 16 and 18
  • cervical cancer without HPV infection can occur but is extremely rare
36
Q

How is HPV infection spread?

A

skin-to-skin sexual contact

37
Q

What are the two main oncoproteins associated with cervical cancer?

A
  • two main onco-proteins of high-risk HPV are E6 and E7, which get integrated into the host genome
  • the tumour supressor protein p53 is inactivated by E6
  • E7 competes with the retinoblastoma (pRb) protein releasign the transcription factor E2F, which pushes the infected cell through the cell cycle
  • if you get HPV doesn’t mean you will get cervical cancer
38
Q

What are the risk factors for cervical cancer?

A
  • age 45-49
  • HPV infection
  • multiple sexual partners
  • non-barrier contraception
  • early onset of sexual activity
  • immunosuppression - HIV and transplant patients
  • smoking - reduces viral clearance
39
Q

What is the possible management of cervical cancer?

A

Depends on stage and age:
- surgery
- radiotherapy
- chemotherapy
- immunotherapy

40
Q

What is used for screening of cervical cancer?

A
  • papanicolaou test (Pap smear)
  • method of cervical screening used to detect potentially precancerous and cancerous processes in the cervix
41
Q

What are the cytological markers of cervical cancer?

A
  • increased nuclear to cytoplasmic ratio
  • abnormally shaped nuclei
  • abnormally dense nuclei
  • inflammation
  • infection
  • mitoses
42
Q

What is colposcopy regarding cervical cancer?

A

magnified visualisation of the transformation zone after application of 5% acetic acid (preferential taken up by neoplastic cells). If abnormal - punch biopsy or definitive treatment

43
Q

What is CIN regarding screening of cervical cancer?

A
  • cervical intra-epithelial neoplasia
  • CIN is characterized by loss of differentiation and maturation from the basal layer of the squamous epithelium upwards
  • CIN1, CIN2, CIN3 - check slide 48 for visuals
  • at different CIN level cells are getting more and more round (dysplasia) developing cancer
44
Q

What is the management of cervical cancer?

A
  • depends on grade of CIN
  • Large loop excision of the transformation zone (LLETZ)
  • CIN1 will spontaneously regress
  • CIN3 - LLETZ recommended - follow up at 6 months with cytology and HPV test
  • complications - haemorrhage, infection, cervical stenosis, cervical incompetence
45
Q

What is epithelial ovarian cancer?

A
  • derived from serosal surface of ovary
  • arise from single layer of cells that cover the ovary or lines cysts immediately below surface
  • increasing evidence of tubal origin in high grade serous tumours
46
Q

What are the two types of epithelial ovarian cancer?

A
  1. high grade serous (resembles fallopian tube mucosa; p53 mutations)
  2. arise from ovarian surface epithelium and mullerian inclusion cysts (subgroups: endometriod, clear cell, mucinous, low grade serous)
47
Q

How can ovarian cancer spread?

A
  • direct extension (transcoelemic)
  • exfoliation into the peritoneal cavity
  • lymphatic invasion
48
Q

What are the risk factors for epithelial ovarian cancer?

A
  • smoking
  • low parity
  • one child is protective
  • oral contraceptives
  • early menarche
  • late menopause
49
Q

What is the screening for ovarian epithelial cancer?

A

no screening yet

50
Q

what are the symptoms of ovarian epithelial cancer?

A
  • altered bowel habit
  • abdominal apin / bloating
  • feeling full quickly
  • difficulty eating
  • urinary / pelvic symptoms
51
Q

what is the treatment available for ovarian epithelial cancer?

A
  • not usually curative
  • surgery (major role, primary debulking surgery, delayer primary surgery)
  • chemotherapy (neo-adjuvant (before surgery), adjuvant to consolidate surgery)
  • radiotherapy

Reproductive Biology 3 (21 decks)

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