Oncology Flashcards

1
Q

What cancers are associated with HNPCC (Lynch Syndrome)?

A

Colon cancer Endometrial cancer Gastric cancer Small bowel cancers CNS cancers eg glioblastoma Urinary tract cancers

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2
Q

At what stages is chemotherapy used for lung cancer? What is the drug basis?

A

Defined role for adjuvant chemotherapy from stage 2 onwards, controversial in stage 1b

Use a cisplatin containing regimen. Alkylating agents have an adverse effect on survival

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3
Q

What is the role of cetuximab and panitumumab in colorectal cancer?

A

These are EGFR antibodies

Can be used in metastatic colorectal cancer when it is left sided and KRAS, NRAS, BRAF wild type

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4
Q

What are the side effects of FOLFOX?

A

5-FU - hand/foot, diarrhoea, coronary spasm

Irinotecan - anti-cholinergic (give with atropine)

Oxaliplatin - peripheral neuropathy

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5
Q

What mutations are seen in prostate cancer?

A

PTEN mutation - more frequent in metastatic disease

TMPRSS2-ERG fusion gene - 50%

DNA repair abnormalities - 20%

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6
Q

What is biochemical reccurent disease and what is its management in prostate cancer?

A

When PSA rises but no disease recurrence can be seen on imaging

Treat with androgen deprivation therapy

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7
Q

What is the staging work up for prostate cancer?

A

Biospy and PSA
MRI pelvis

Bone scan

Can do PSMA PET scan which is very sensitive but not very specific

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8
Q

What is the mechanism of action of abiraterone? When is it used?

A

It blocks 17a hydroxylase and c17, 20lyrase in teh adrenal to stop androgen production

Used in castrate resistant prostate cancer

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9
Q

What is the mechanism of action of enzalutamide? When is it used?

A

A potent androgen receptor antagonist which blocks testosterone binding, receptor activation and nuclear translocation.

It is used in castrate resistant prostate cancer

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10
Q

What drugs must be given with abiraterone?

A

Continue the baseline antiandrogen eg groselin

Must be paired with steroids to mitagate side effects due to acculmulation of steroid precursors (works on the CYP17 pathway in the adrenal gland)

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11
Q

What are the most common driver mutations in melanoma?

A

BRAF - 40-50%

RAS - 20%

NF-1 - 10-15%

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12
Q

When is chemotherapy used in prostate cancer? What agents are used?

A

Only in metastatic disease

Docetaxel upfront if high risk

As 2nd and 3rd line options

Cabazitaxel is another option for very refractory disease

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13
Q

What is CDKN2A mutation associated with?

A

Familial melanoma

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14
Q

What are the TKIs used in melanoma?

A

Dabrafenib + trametinib

Vemurafenib + gobimetinib

a BRAF and a MEK inhibitor - always paired

Used in BRAF mutated stage 3 and 4 disease

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15
Q

What are the common mutations in clear cell renal cancer?

A

Chromosome 3p deletions

VHL inactivation

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16
Q

What are the side effects of dabrafenib and trametinib?

A

Rash, photosensitivity, fever, fatigue and GI upset

Skin cancer risk reduced by the combination

17
Q

What is the HENG classification?

A

Used to risk stratify metastatic renal cell cancer:

  • <1yr from diagnosis to treatment
  • KPS <80%
  • Anaemia
  • Hypercalcaemia
  • Neurophilia
  • Thrombocytosis

Each give a point. 0 is good prognosis and >3 is poor

18
Q

What is the 1st line treatment for metastatic renal cancer? What are the other options for treatement?

A

If intermediate or high risk then dual check point inhibitors

Single agent PD-1

TKI - sunitinib and pazopanib 1st line then cabozantinib and axilinib

Evrolimus

Bevacizumab

19
Q

What is the most powerful prognostic factor in breast cancer?

A

Nodal status

20
Q

What are luminal A and B breast cancer?

A

Both are ER positive

A is HER2 negative

B is HER2 positive

21
Q

What is the malignancy risk with BRCA1 and 2?

A

BRCA 1:

  • Breast Ca 50-80%
  • Ovarian Ca 25-40%
  • Prostate 30%

BRCA 2:

  • Breast 40-70%
  • Ovarian 15-20%
  • Prostate 40%
22
Q

What type of breast cancer does BRCA1 and 2 get?

A

BRCA1: 70% triple negative

BRCA2: 15% triple negative (same as general population)

23
Q

What is neratinib?

A

A HER2 and EGFR inhibitor

Used in HER2 positive breast cancer in the adjuvant setting after completion of trastuzumab

Risks - diarrhoea and hepatotoxicity

24
Q

How do trastuzumab and pertuzumab differ?

A

Both a HER2 inhibitors used primarily in breast cancer

Pertuzumab binds to subdomain II and inhibits dimerization of HER2 with HER3

Trastuzumab binds to subdivision IV inhibiting cleavage and signalling

25
Q

What are the cyclin D inhibitors?

A

Palbociclib and ribociclib

Tyrosine kinase inhibitors which inhibit CDK4/6 binding to its ATP pocket. CDK normally works with cyclin D for the G1-S transition.

Used in 1st line ER positive metastatic breast cancer with an aromatase inhibitor

Risks are myelosuppresion, prolonged QTc, hepatotoxicity

26
Q

What is the metabolism of tamoxifen?

A

Metabolised by CYP2D6

Altered by genetic variation

Interactions with sertraline, escitalopram, citalopram

27
Q

What are the histological types of breast cancer? Which are more aggressive?

A

Ductal - 75-80%, more aggressive

Lobar - tend to be lower grade and ER pos

Others:

Cribiform, tubular, mucinous - endocrine responsive

Medullary, metaplastic - aggressive

Secretory juvenille, adenoid cystic, apocrine - low risk

28
Q

What is trastuzumab emtansine? What is its use?

A

An antibody drup conguagte

Anti-HER2 paired with a microtubule inhibitor

Used for metastatic HER2 breast cancer as 2nd line

29
Q

What is the order of treatment for castrate resistant prostate cancer?

A

Abiraterone then enzalutamide the chemotherapy

30
Q

What is the downstream pathways of a VHL mutation?

A

Found on short arm of chromosome 3

Mutations in this or loss of 3p causes an accumulation of hypoxia inducible factors which then cause the transcription of factions such as VEGF

31
Q

How is seminoma and non-seminoma differentiated?

A

AFP is always normal in seminoma

32
Q

What type of testicular cancer is radiosensitive?

A

Only seminomas (AFP negative)

33
Q

What is the mechanism of action of PARP inhibitors?

A

Poly-ADP ribose polymerase

Normal action is single strand DNA break repair as well as expression f inflammatory genes and programmed cell death.

PARP inhibitors block PARP on the DNA inhibiting it as well as preventing other DNA damage repair proteins from working. This leads to a double strand break

Double strand breaks are imposible to repair in teh setting of BRCA

34
Q

What are the indications for PARP inhibitors?

A

BRCA positive breast cancer - must be HER2 neg

Metastatic prostate cancer with DNA repair mechanism defects

High grade serous or endometrioid ovarian cancer

35
Q

What is the most important prognostic factor in head and neck cancers?

A

SIgnificantly better prognosis if there is p16 on immunohistochemistry. This is a marker of HPV association

36
Q

What infections are associated with head and neck cancers?

A

Nasopharyngeal - EBV

Other - HPV infection

37
Q

What is the treatment for ALK positive metastatic lung cancer?

A

Crizotinib