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Reproductive Biology 3 > 22. Reproductive cancers > Flashcards

22. Reproductive cancers Flashcards

(52 cards)

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1
Q

What are the types of reproductive cancers?

A

Reproductive cancers:
- breast
- cervical
- ovarian
- endometrial
- prostate
- vulval
- vaginal
- penile
- testicular

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2
Q

What is a tumour?

A

Tumour - a tissue formed from excessive, uncontrolled proliferation of cells of irreversible genetic change - passed from one tumour cell to its progeny -> can be benign / malignant (cancer)

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3
Q

What is neoplasia?

A

Neoplasia - new growth

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4
Q

What are neoplasms?

A

Neoplasms - newly grown tissues - tumours - benign or malignant (cancer)

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5
Q

How are tumours classified?

A

Tumours can be:
- benign - stay localised at their site of origin
- malignant - able to invade and spread to different sites = cancer

  • primary - tumours arise at primary site from cells normally present there
  • secondary - metastatic tumours
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6
Q

What is the sequence of events in cancer development?

A

Development events:
1) mutation
2) hyperplasia (abnormal change in number)
3) dysplasia (abnormal change in cell morphology, organisation)
4) in situ cancer
5) invasive cancer (neoplasia - new growth)

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7
Q

What causes cancer to develop?

A

Mutation -> inactives tumour supressor mechanism -> cells overproliferate -> mutation inactivates DNA repair -> mutation of a proto-oncogene - oncogene -> mutation inactivates more other tumour supressor mechanisms => cancer

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8
Q

What are the main origins of cancer?

A

Genetics + epigenetics

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9
Q

What are the types of genetics aberrations which can cause mutations which cause cancer?

A

Genetic aberrations which cause mutations usually occur in S phase:
- duplication
- inversion
- deletion
- insertion
- translocation

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10
Q

Why are oncogenes usually called dominant acting?

A

Only one allele of oncogene needed to cause cancer - dominant acting oncogene

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10
Q

What are oncogenes?

A

Oncogenes - converted mutated proto-oncogenes - undergo activating mutations - cause cancer

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11
Q

What are proto-oncogenes?

A

Proto-oncogenes - normal oncogene version which does not cause cancer - but if aqcuires specific activating mutation - convert into cancer-causing

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12
Q

What genes cause cancer?

A

Cancer caused by:
- mutated proto-oncogenes
- mutated tumous supressor genes - ex: p53

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13
Q

What do oncogenes code for?

A

Oncogenes code for:
- a hyperactive version of a protein
or
normal protein but:
- in abnormal quantities
- at the wrong time
- in wrong cell type

Depends on the mutation and where it happens in the gene

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14
Q

Explain how does p53 work?

A

p53 - tumour supressor gene - inhibits cell cycle progression - arrests for DNA repair - depending on the damage -> apoptosis / metabolic homeostasis / DNA repair / growth arrest

Mutant p53 - dominant negative effect - prevents WT p53 from binding to target genes

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15
Q

Explain Li-Fraumeni syndrome

A

Li-Fraumeni syndrome:
- p53 mutation in the germline - predisposes the child to many cancers

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16
Q

What processes do cancer cells perform?

A

Cancer cells:
- proliferate - limitless replicative potential
- matastate
- invade tissues
- create inflammatory microenvironment
- insensitive to growth inhibitors - self-sufficient in growth signals
- sustain angiogenesis
- evade apoptosis
=> form tumours

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17
Q

What is angiogenesis?

A

Angiogenesis - growth of blood vessels from the existing vasculature

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18
Q

Explain how cancer performs metastasis

A

1) mutation
2) primary tumour formation
3) vascularization (angiogenesis)
4) detachment
5) EMT
6) intrainvasion
7) extrainvasion
8) invasion
9) secondary tumour
10) vascularization (angiogenesis)
repeat cycle

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19
Q

What are the routes of metastasis?

A

Metastasis can take several routes to spread:
- local invasion
- lymphatic spread (breast cancer)
- blood spread
- transcoelomic - spread in peritoneal cavity - lined by peritoneum membrane

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20
Q

Why is metastatic cancer not curable?

Study These Flashcards
A

Metastatic cancer not curable because has spread - multiple locations + acquired different mutations - same therapy might not work for all cancer cells in the body

21
Q

What is the most common female cancer?

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A

Breast cancer - but survival increasing because of routine scans - can catch in early stages and prevent spread - usually in mid 60s

22
Q

What are the most prominent breast cancer risk factors?

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A

Most prominent breast cancer factors:
- age >50
- positive family history
- earlier menarche <12
- later menopause >55
- obesity
- alcohol

23
Q

What are the genetic syndrome associated with breast cancer risk?

Study These Flashcards
A

Breast cancer risk:
- BRCA1/BRCA2 mutation
- p53 mutation (ex Li-Fraumeni syndrome)

24
Explain how BRCA1/BRCA2 cause breast cancer
**BRCA1/BRCA2** - **tumour supressor genes** - produce **proteins** involved **in dsDNA repair** -> in mutated BRCA1/BRCA2 - **DNA not repaired efficiently** -> **increase in p53**, cell cycle arrest, apopotosis or proliferation of cells - **cancer**
25
What are the symptoms of breast cancer?
Breats cancer symptoms: - new **lump** - **altered shape, size, pain** - **skin** changes - **nipple** changes - spread **inflammation** (rare)
26
What is the typical diagnosis routine for breast cancer?
27
Explain between cancer stage vs grade
**Stage** = **how advanced cancer is** - stage I (local) - stage IV (metastatic) **Grade** = **how tissue looks** under a microscope (histology) - higher grade - poorer prognosis
28
What is a further diagnosis approach for classifying cancer?
Performing **immunohistochemistry** - ex: in **breast cancer Abs for ERs** / **PRs** / human epidermal growth factor (**HER2**) receptors
29
Why is immunohistochemistry performed in cancer diagnosis?
To figure out **which receptors in cancer cells** are present which could be **'feeding'** them - ex: in breast cancer Abs for ER / PR / HER2 receptors
30
Explain how steroid can be driving cancer?
**Estrogen** in pre-menopausal women - from ovaries, in **post-menopausal** - from **fat** cells - **in breasts** -> **higher estrogen levels** **signal for growth**: binds ER - 2 bound ERs **dimerize** - move into the nucleus => **gene activation**
30
Explain how endocrine therapy can be used to treat breast cancer?
**Endocrine therapy** - **affecting estrogen**: - **aromatase inhibitors** (AIs) - inhibit testosterone conversion into estrogen - no ER binding - **tamoxifen** - synthetic estrogen analogue - **prevents ER from dimerizing**, moving into the nucleus and **activating genes** cells no longer 'fed' - can't survive
31
Why is adjuvant tamoxifen beneficial?
**Adjuvant tamoxifen** taken **10 years after sugery** - for **all estrogen driven cancer cells to die off** => lower rates of recurrence
32
Explain HER2 driven breast cancer
**HER2 gene amplification** - abnormal cancer cells with **overexpressed HER2** levels - **respond more to growth factor** signals - initiate **overproliferation** Treatment - **Her2-targeted monoclonal Ab** Trastuzumab
33
What is the test for exact HER2+ diagnosis in breast cancer?
1) **Immunohistochemistry** - **Ab for HER2** - see if stained 2) **FISH** - if inconclusive (some stained) - perform FISH - see **# gene copies of HER2 gene** in cells
34
What are the therapies used to treat HER2 cancers?
**Monoclonal Ab therapies** which **inhibit** **signaling**: - ligand-indep signaling - ligand-dep signaling - ligand dep+indep signaling
35
What are the stages of breast cancer?
36
What are the approaches for breast cancer management?
Approaches for breast cancer management: - **surgery** - **radiotherapy** - **chemotherapy** - **immunotherapy** - **targeted therapy** - **hormone** (endocrine) **therapy**
37
Explain cervical cancer
**Cervical cancer** - 4th most common maliganncy in women - mainly **caused by HPV** infection - from **skin-to-skin sexual contact** - if **infection resolves - no cancer** - return to baseline - but if **not resolved => cancer**
38
Explain cervical cancer physiopathology
**HPV infection** -> usally **cleared in 3 years** - **if not** -> persistance - **genomic integration** - latency incubation - invasion = **carcinoma**
39
What are the risk factors for cervical cancer?
**Cervical cancer risk factors**: - **45-49** age - **HPV** infection - **multipel sexual partners** - **non-barrier contraception** - **immunosuppression** - **smoking** - reduces viral clearance
40
What are the approaches for diagnosing cervical cancer?
Diagnosing cervical cancer: - **vaginal and bi-manual examination** - **pap smear** - HPV testing - **colposcopy** - observing **cervical surface using a microscope** loooking for **neoplastic cells** - **punch biopsy** / large loop excision - -> **excised out transformation zone** from the cervix
41
Explain pap smear
Taking **tissue swab** - looking for **abnormal cells** which could **indicate HPV**
42
Explain colposcopy
**Colposcopy** - **observing cervical surface** using a **microscope** loooking for **neoplastic cells**
43
What is CIN and how is it assessed?
**Cervical intra-epithelial neoplasia (CIN)** - use **histology to observe abnormal changes** to squamous cells **in cervix**
44
Explain what is punch biopsy / large loop excision
Cervical cancer management strategies
45
Explain ovarian cancer
**Ovarian cancer** - 2nd most common gynaecological cancer after uterine - **increased chance with age** - **silent killer** because **no** specific, apparent **symptoms** - **only when spread can be identified**
46
What are the two origins of ovarian cancer?
**Ovarian cancer** can **arise from**: - **high grade serous** - debated if arises from ovarian or oviduct cells - **p53 mutation** - **ovarian surface epithelium (OSE)** and **mullerian inclusion cysts**
47
What are the spread routes for ovarian cancer?
Ovarian cancer spreads thorugh: - **direct extensions** exfoliation into **peritoneal cavity** - transcoelomic - **lymphatic** invasion
48
What are the risk factors for ovarian cancer?
**Ovarian cancer risk factors**: - **age** - **lifestyle** factors - **oral contraceptives** - **early menarche** - **late menopause**
49
What are the screening options for ovarian cancer?
**No screenings** - but **diagnosis via**: - measuring **US / CA125 levels** - elevated in malignancies - **CT scan**
50
What are the treatment options for ovarian cancer?
**No specific treatment**, usually **not curative because of late diagnosis** - surgery, chemotherapy, radiotherapy

Reproductive Biology 3 (22 decks)

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