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Reproductive Biology > Reproductive Cancers > Flashcards

Reproductive Cancers Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What is a tumour?

A

Excessive, uncontrolled proliferation of cells as a result of an irreversible genetic change

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2
Q

How would you classify tumours?

A

Benign - tumours stay localised at their site of origin
Malignant - able to invade and move = cancer (the features of which are less differentiation, large pleopmorphic nuclei and fast growth).

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3
Q

What is primary tumours?

A

They arise at the site from cells normally present

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3
Q

What are secondary tumours?

A

Metastatic cancer (where it’s moved)

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4
Q

What are the steps of cancer cell development?

A

Mutation
Hyperplasia
Dysplasia
In situ cancer (confined to a local area)
Invasive cancer

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5
Q

What causes cancer to develop?

A
  • A mutation causes proliferation of cells and a mutation inactivates DNA repair gene
  • Loss of tumour suppressor gene function and gain of oncogene function
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6
Q

Steps towards breast cancer?

A

Normal breast epithelium
Atypical breast hyperplasia
Ductal carcinoma in situ (genetic alterations happen here)
Invasive ductul carcinoma
Metastatic disease

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7
Q

What are some genetic aberrations?

A

Duplication
inversion
Deletion
Insertion
Translocation

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8
Q

What is some epigenetic things? E.g their shape/structure etc

A

DNA Methylation packed into Histone code and nucleosomes

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9
Q

What are oncogenes?

A

Mutations in certain genes promote uncontrolled cell division.

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10
Q

What are the normal versions of oncogenes called

A

Proto-oncogenes

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11
Q

What are mutated oncogenes called?

A

Oncogenes

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12
Q

What type of mutations will turn a proto-oncogene into an oncogene?

A

Activating mutations and you only need one of these

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13
Q

What does activating a proto-oncogene mutation do?

A

Allows cells to bypass the need for extracellular growth signals

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14
Q

What does the oncogene mutations do to the proteins?

A

can make it hyperactive or be in an abnormal quantity, at the wrong time or in the wrong cell type.

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15
Q

What are tumour supressor genes?

A

P53 which pauses the cell cycle to help with DNA repair.

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16
Q

What type of mutational effect does mutants of P53 have?

A

Dominant negative

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17
Q

What things drive cancer?

A

Proliferation,
Angiogenesis,
Apoptosis turns of
Tissue invasion
Inflammatory supressors.

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18
Q

How does cancer mestasis?

A

A mutation in a cell grows into a primary tumour which vascularises. This then detaches and a cell intravasation occurs. This goes through blood until it extravasation, invades more cells and causes secondary tumours which also vascularise.

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19
Q

What are the different routes of invasion?

A

Local invasion
Lymphatic spread
Blood spread
Transcoelomic

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20
Q

Why isn’t mestatic cancer curable?

A

There is lots of different mutated genes (they need to be treated in different ways)

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21
Q

Survival and incidence of breast cancer?

A

Incidence is increasing as screening is better

Survival is increasing as screening is better and treatment is better

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22
Q

What are some risk factors to breast cancers?

A

Age (over 50)
Positive family history
Earlier menarche (less than 12)
Later menopause
Older first pregnancy
OC use
HRT
Endogenous estrogen exposure
Increased breast density
Radiation exposure
Obesity
Alcohol

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23
Q

What is BRCA?

A

Tumour supressor genes which commonly mutate in breast cancer (either BRCA1 or 2)

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24
Q

Symptoms of breast cancer?

A

New lump of thickening in breast or axilla

Altered shape, size or feel of breast, pain.

Skin changes - puckering, dimpling, skin oedema, rash, redness, feels different

Nipple changes - tethering/inversion, discharge, eczema- like changes in paget disease

Rarely widespread inflammtion, redness, pain in inflammatory cancer can stimulate infection

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25
Q

How do they diagnose breast cancer?

A

If you go to the doctors with a lump they send you to the breast clinic who do an exam, history, imaging (an ultrasound in younger people), pathology (biopsy)

26
Q

What are the different grades of cancer and what does that mean?

A

Grade 1 - a well-differentiated tumour
Grade 2 - a moderately differentiated tumour
Grade 3 - poorly differentiated

27
Q

Immunohistochemistry - breast cancer

What is the allred score?

A

They check for ER, PR, and HER2

If you see ER - the breast cancer uses oestrogen to fule it.

28
Q

Can breast cancers signal to surrounding fat cells to secrete the oestrogen it needs to grow?

A

Yes

29
Q

How does oestrogen cause breast cancer?

A

Oestrogen binds to ER which dimerizes and bind to the genome at promotor regions (ERE) this drives growth of the cell

30
Q

What are some endocrine treatment of breast cancer

A

Selective Estrogen Receptor Modulators (SERMS) - tamoxifen
Aromatase Inhibitors (AI) - letrozole and anastrozole and Exemestane

31
Q

What is HER2 positive breast cancer?

A

HER2 gene is amplified but the protein is normal although there is now lots of them which will turn on cell cycle through down stream signalling.

32
Q

How do you test for HER2?

A

Immunohistochemistry (you wouold do antibodies or FISH)

33
Q

What is the treatment for HER2 breast cancer?

A

Trastuzumab (herceptin) and Pertuzumab are monoclonal antibodies

34
Q

What are stages in breast cancer diagnosis?

A

How spread the cancer is e.g. stage 1 and stage 4

35
Q

What are breast cancer treatment options?

A

Surgery - cut lump out or remove breasts
Radiotherapy
Chemotherapy
Immunotherapy
Targeted therapy
Hormone therapy

36
Q

Incidence of Cervical cancer

A

Most common malignancy in women worldwide and normally between 34 - 44 years old.

The PAP smear has reduced incidence and mortality

37
Q

What is the aetiology of cervical cancer?

A

Persistant infection with HPV which is spread through skin to skin sexual contact

38
Q

What can HPV form on the skin?

A

Warts

39
Q

What is our main preventative treatment of cervical cancer?

A

The HPV vaccine

40
Q

What is the normal pathophysiology of cervical cancer?

A

The two main oncoproteins involved in HPV are E6 and E7 and the tumour supressor p53 is inactivated by E6.
E7 competes with pRb protein releasing transcription factor E2F which pushes infections through the cell cycle

41
Q

Risk factors for cervical cancer?

A

Age 45 - 49
HPV infection
Multiple Sexual Partners
Non-barrier contraception
Early onset of sexual activity (less than 18),
Immunosuppression - HIV and transplant patients
Smoking - reduces viral clearance

42
Q

What is the presentation of cervical cancer?

A

Cervical Smear
Post-coital bleeding
Abnormal vaginal bleeding
Weight loss
Ureteric obstruction
Bowel disturbance

43
Q

What are the investigations of cervical cancer?

A
  • Vaginal and bi-manual examination
  • HPV testing
  • Colposcopy (irregular cervical surface, abnormal vessels)
  • Punch biopsy or diagnostic loop biopsy
44
Q

Depends on stage and age

How do you manage cervical cancer?

A

Surgery,
Radiotherapy
Chemotherapy
Immunotherapy

45
Q

What is the pap smear - how is it done?

A

Method of cervical screening used to detect potentially precancerous and cancerous processes in the cervix

46
Q

What are the cytology markers of cervical cancer?

A

Increased nuclear to cytoplasmic ration
Abnormally shaped/dense nuclei
Inflammation
Infection
Mitosis

47
Q

What is colposcopy?

A

Magnified visualisation of the transformation zone after application of 5% acetic acid

48
Q

Cervical Cancer

What would you do if the colposcopy was abnormal?

A

Do a punch biopsy

49
Q

What is the histology of cervical cancer?

A

Cervical intra-epithelial neoplasia (CIN)

You can get CIN 1 - 3 and this tells you how it should be treated.

50
Q

This is based on the CIN number

How do you manage cervical cancer?

A

Large loop excision of transformation zone (LLETZ)

CIN1 will spontaneously regress so conservative management and a LLETZ is persistant

CIN3 = LLETZ followed up at 6 months with cytology and HPV test

51
Q

Is a LLETZ safe and can it be done under local?

A

Yes

52
Q

What are complications of a LLETZ?

A

Heamorrhage, infection, cervical stenosis, cervical incompetence

53
Q

What is the incidence of ovarian cancer?

A

Increased incidence with increasing age

54
Q

Ovarian cancer - the silent killer?

A

Over 60% of advanced disease at initial presentation however many women have abdominal issues years before diagnosis

55
Q

What is Epithelial ovarian cancer?

A

Common type of ovarian cnacer which is derived from serosal surface of ovary, arise from single layer of cells that cover the ovary or lines cysts. Increasing evidence of tubal origin in high grade perous tumours

56
Q

What are the 2 types of ovarian cancer?

A

High grade serous - resembles fallopian tube mucosa or p53 mutations

Arise from ovarian surface epithelium and mullerian inclusion cysts - endometriod, clear cell, mucinous, low grade serous

57
Q

How does ovarian cancer spread?

A

Direct extension (transcoelemic)
Exfoliation into the peritoneal cavity
Lymphatic invasion

58
Q

Risk factors of ovarian cancer?

A

Smoking
Low parity
One child is protective
Oral contraceptives
Infertility (but independant on drugs)
Tubal ligation
Early menarche
Late menopause

59
Q

Do we screen for ovarian cancer?

A

No as the two trials are showing no evidence to support screening (even in high risk women)

60
Q

What is the presentation of ovarian cancer?

A

Symptoms are vague and non-specific

Altered bowel habit
Abdominal pain/bloating
Difficulty eating
Feeling full quick
Urinary/pelvic symptoms
Bowel obstruction
SOB

61
Q

How do you investigate ovarian cancer?

A

Ultrasounds
Look into CA125 (glycoprotein elevated in malignancies, and benign things such as menstruation).

CT - used to determine initial treatment and response to treatment

62
Q

Treatment for ovarian cancer?

A

Not usually curative

Surgery - major role, primary debulking surgery, delayed primary surgery

Chemotherapy - Neo-adjuvant, adjuvant

Radiotherapy

Reproductive Biology (21 decks)

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