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Oncology Flashcards

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1
Q

Breast cancer risk factors

A

Female
Oestrogen exposure
Older age at first birth
Age
1st deg relative
BRCA1/2 - inc. risk if multiple relatives with breast/ovarian ca
Alcohol

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2
Q

BRCA1/2

A

DNA repair genes
Inherited in Autosomal dominant fashion
50-60% lifetime breast ca risk
Consider tamoxifen pre or post menopausal or raloxifene if post menopausal (40% RR)

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3
Q

Luminal A

A

ER+, HER2 low, low Ki67
Good prognosis
Treat with endocrine therapy

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4
Q

Luminal B

A

ER+ but weaker, HER 2 + or -, high Ki67
High recurrence
Benefit from chemo and trastuzumab if HER2 +

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5
Q

HER 2 enriched

A

ER - HER2 +
Chemo + trastuzumab

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6
Q

TNBC

A

Chemo

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7
Q

Adjuvant endocrine therapy in breast cancer

A

All with ER+ve cancer
SERM pre-menopausal
AI post-menopausal (slightly more effective than SERM at reducing recurrence)
5-10yrs of therapy

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8
Q

SERM

A

Tamoxifen
Antagonists on ER in breast tissue or cancer
Agonist on bone, uterus, liver
Risks: VTE, uterine cancer

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9
Q

Aromatase inhibitors

A

Anastrozole, letrozole
Block DHEA –> testosterone
Slightly more effective at reducing recurrence compared to SERM
Only use in post-menopausal women
Risks: Decreased BMD, arthralgia
No increase in VTE or uterine Ca risk

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10
Q

Trastuzumab in breast cancer

A

Monoclonal Ab to HER2
12 months therapy
Risks: reversible cardiomyopathy
No CNS penetration

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11
Q

Pertuzumab in breast cancer

A

Monoclonal Ab to HER2
Given as neoadvjuvant therapy with pertuzumab in early disease
Or as dual therapy with trastuzumab in metastatic disease

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12
Q

Anthracyclines

A

Doxorubicin most common
Work by inhibiting topoisomerase (which usually helps to form double stranded DNA complex)
Risks: Irreversible cardio toxicity

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13
Q

Adjuvant radiotherapy in early disease breast cancer

A

Give if post-breast conserving therapy - recurrence rates similar to mastectomy
Post mastectomy chest wall RTx if >5cm breast cancer or LN +ve

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14
Q

Metastastic ER+ HER2 -

A

CDK4/6 inhibitor combined with AI or fulvestrant

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15
Q

CDK4/6 inhibitors

A

Ribociclib/abemaciclib/palbociclib
Block transition from the G1 to the S phase by binding to CDK 4/6 to inhibit Rb protein phosphorylation
Risks: cytopenias, hepatotoxicity

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16
Q

Breast cancer subtypes

A

Invasive ductal carcinoma (80%)
Invasive lobular carcinoma
Mixed ductal/lobular

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17
Q

Recurrence based on ER status

A

If ER negative tumours recur - they will recur in first 5 years
ER positive tumours may recur in first 5 years (50%) but can also recur up to 25 years later

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18
Q

Rationale for neoadjuvant therapy in breast cancer

A

Outcomes are equivalent for neo adjuvant vs adjuvant therapy
Neo-adjuvant can downstage a tumour prior to surgery –> less extensive surgery –> better cosmetic outcome

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19
Q

Everolimus in breast cancer

A

mTOR inhibitor
Can be used 2nd line in conjunction with AI/fulvestrant in ER + metastatic breast cancer
Risks: stomatitis, pneumonitis

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20
Q

Tumour markers in breast cancer

A

Tumour markers in breast cancer:
- CA15-3 and CA27-29
- Can aid in assessment of response to systemic therapy
- Not used alone as a reason to change systemic therapy
- May also be elevated in liver failure, B12 deficiency, haemoglobinopathies

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21
Q

Pembrolizumab in breast cancer

A

PD-L1 inhibitor
In combination with chemo in TNBC metastatic if PD-L1 positive

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22
Q

Olaparib in breast cancer

A

PARP inhibitor
Used 2nd line or later in metastatic TNBC that is BRCA positive
Risks: decreased Hb, pneumonitis, MDS/leukaemia, Nausea and diarrhoea

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23
Q

Radiotherapy indications in metastatic breast cancer

A

Bone pain
Spinal cord compression
Cerebral mets
Ulcerating skin/primary lesion

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24
Q

Screening in BRCA + patients

A

BSE, 6/12 clinical breast examination
Annual mammogram from 40 (or 5 yrs younger than relative)

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25
BRCA genetic testing
All women <70 years old with epithelial ovarian cancer
26
Melanoma risk factors
> 10 dysplastic naevi > 100 common naevi Fair skin, red hair High intermittent sun exposure (e.g. blistering sunburn as a child)
27
Melanoma subtypes
Superficial spreading - most common 70% Lentigo maligna - high cumulative UV exposure Acral lentiginous - not caused by UV light. Occurs on palms, soles, under nails. Asians and Black people Nodular - vertical growth, 50% of melanoma deaths, rapidly growing
28
Melanoma immunohistochemistry
Positive for S100 and Melan A
29
Ulceration in melanoma
Upstages diagnosis Increases risk for metastasis a lot
30
Stage 1 melanoma
No imaging required
31
Stage 2 melanoma
WLE and SNB MRI brain, CT CAP, PET scan Tx: Nivolumab or pembrolizumab
32
Stage 3 melanoma
No longer get full LN dissection - completion dissection if disease progression Pembrolizumab/nivo in all patients BRAF mutant: Dabrafenib + trametinib (BRAF + MEK inhibitor) Give vemurafenib if BRAFV600E mutation present
33
Stage 4 melanoma
10 yr survival 50-60% Surgical resection of mets if possible3 1st line: ipi + nivo regardless of mutational status (single agent nivo if old or poor ECOG) 2nd line: BRAF mutant: encorafenib + binimetinib. BRAF wildtype: Nivo/relatimab or clinical trial
34
Predictor of response to immunotherapy
High mutational burden Melanoma has highest mutational burden
35
Sunitinib
TKI with anti-VEGF activity Give in renal cell carcinoma Hypertension is a predictive marker - treat with ACE-I Other side effects: ON of jaw, hand-foot skin reaction, hypothyroidism
36
Pancoast tumour
Apical lung tumour Usually NSCLC Can present with shoulder pain or neuropathic arm pain Horners syndrome via sympathetic ganglion (stellate ganglion) compression
37
Lung cancer risk factors
Cigarette smoking Radiation Environmental toxins: smoking, asbestos, inhaled metals Pulmonary fibrosis Genetic factors
38
Lung cancer subtypes/histology
Adenocarcinoma 40% Squamous cell 20% Small cell 13% Large cell 7% Other 20%
39
Small cell lung cancer
Early to metastasise, high mitotic rate Classically bulky lymphadenopathy Very chemo/radiosensitive Almost always non-smokers Don't cause clubbing Can present with paraneoplastic syndromes and/or SIADH
40
Small cell lung cancer treatment limited stage
Surgery Chemoradiotherapy Prophylactic cranial irradiation (brain is sanctuary for micro metastatic disease)
41
Small cell lung cancer extensive stage treatment
1st line: chemoimmunotherapy and PDL1 Atezolizumab + carboplastin + etoposide 2nd line: topotecan/irinotecan or cyclophosphamide/dox/vincristine
42
Mesothelioma
Related to Asbestos and tobacco Asbestos also increases NSCLC risk Long latency 30-40 years Incurable Dual ipi/nivo
43
NSCLC
Complete full workup including MRI brain, CT CAP, PET
44
NSCLC stage 1 treatment
Resection if fit Stereotactic RTx if not fit
45
NSCLC stage 2 treatment
Resection if fit/amenable Adjuvant chemotherapy: 4 months cisplatin + cinorelbine Adjuvant immunotherapy: Atezolizumab if PDL1 >50% Adjuvant osimertinib
46
NSCLC stage 3 treatment
Neoadjuvant chemo or immunotherapy to try and downstage to allow resection Combined chemoradiotherapy Durvalamab (PD-L1) post chemoRTx improves survival to 50% - no benefit if PDL1 0% or EGFR +
47
NSCLC stage 4 treatment
Incurable - 6 months survival without treatment Check for driver mutation and if present treat with specified agent first line (more effective than chemo) No driver mutation and PDL1 <50% - give platinum doublet + PDL1 No driver mutation and PDL1 >50% - single agent PDL1
48
EGFR driver mutation
15% Osimertinib 3rd gen EGFR inhibitor Good CNS activity Side effects: Acne-like rash, diarrhoea, pulmonary fibrosis NO cytopenias
49
EGFR inhibitor resistance
NSCLC driver mutation present in 15% Occurs with 1st and 2nd gen EGFR inhibitors after 6-24 months therapy. Due to T790M mutation Osimertinib effective against T790M
50
ALK gene rearrangement driver mutation
NSCLC driver mutation present in 5% NSCLC associated with EML4-ALK fusion gene Treat with Alectinib - 62% 5 year survival Prolonged QT
51
ROS1 fusion gene driver mutation
NSCLC driver mutation present in 2% Respond to Crizotinib/lorlatinib/entrectinib
52
KRAS driver mutation
NSCLC driver mutation present in 25% More common in smokers (other driver mutations more common in non-smokers) 50% of KRAS mutations are KRAS G12C Treat with Sotorasib as 2nd line after chemo
53
ALK inhibitors
Alectinib, crizotinib, ceritinib
54
KRAS mutation inhibitor
Sotorasib
55
EGFR inhibitors
Osimertinib, afatinib, gefitinib, erlotinib
56
MEN1
Autosomal dominant Tumours of: -Parathyroid -Anterior pituitary -Pancreatic islet cells 90% penetrance by age 50-70
57
MEN2A
Autosomal dominant with very high penetrance RET proto-oncogene on chromosome 10 Tumours of: -Medullary thyroid cancer -Phaeochromocytoma -Parathyroid hyperplasia
58
MEN2B
Autosomal dominant with very high penetrance RET proto-oncogene on chromosome 10 Tumours of: -Medullary thyroid cancer -Phaeochromocytoma -NOT PARATHYROID Associated with mucosal neuromas on lips or tongue - not see in 2A Tumours at an earlier age and more aggressive than 2A
59
Prostate Cancer screening
PSA 2 yearly from 50-69 and further investigation if PSA >95th percentile for that age group
60
Prostate cancer localised disease management
Prostatectomy Radiotherapy If intermediate risk add on ADT
61
Prostate cancer advanced disease management
ADT (hormonal therapy or bilateral orchidectomy) combined with novel anti-androgen Chemotherapy if high volume disease (visceral mets and >4 bone mets)
62
ADT
Hormonal or bilateral orchidectomy Hormonal -GnRH agonists: goserelin, leuprolide -GnRH antagonists: dagarelix Need to give androgen receptor blocker for 2 weeks prior to starting GnRH agonist due to flare effect
63
Novel anti-androgens
CYP17 blockers: Abiraterone (inhibits 17a-hydroxylase) -Reduced testosterone AND cortisol - give with steroid. Increased mineralocorticoid - hypokalaemia, hypertension, CCF Androgen receptor blockers: Bicalutamide, enzalutamide
64
Side effects of ADT
Vasomotor symptoms Decreased libido Decreased BMD Decreased muscle mass Increased cardiovascular risk factors
65
Chemotherapy for prostate cancer
Taxane based Give with ADT if visceral mets or >4 bone mets
66
Taxanes
Docetaxel, cabazitaxel Interfere with microtubule growth --> cell cycle arrest in G2/M phase Also inactivate BCL-2 --> apoptosis SE: Hair loss, pancytopenia, mucositis/diarrhoea, peripheral neuropathy
67
Seminoma
AFP not elevated
68
Testicular cancer markers
AFP and bHCG Marker of disease severity Should normalise post radical inguinal orchidectomy Used for surveillance/follow-up
69
Adjuvant chemo in localised testicular cancer
Seminoma - carboplatin NSGCT - BEP
70
Chemo for metastatic/advanced testicular cancer
BEP (Bleomycin, etoposide, cisplatin)
71
Bleomycin
Causes DNA strand scission leading to inhibition of DNA synthesis G phase, M phase and S phase Skin side effects most common, pneumonitis in 10%
72
Etoposide
Topoisomerase II inhibitor Myelosuppression, alopecia, N/V/D
73
Cisplatin
Platinum based agent Binds to DNA and disrupts DNA function SE: Ototoxicity (30%), tinnitus, myelosuppression, neurotoxicity (peripheral neuropathy), nephrotoxic
74
Colorectal cancer risk factors
Increased body weight, decreased activity High consumption of processed meat and alcohol Low fibre diet Cigarette smoking IBD HNPCC/FAP
75
HNPCC
AD inheritance, high penetrance Defect in DNA mismatch repair genes MLH1, MSH2, MSH6, PMS2 DNA mismatches often occur in areas of micro satellites Screening for HNPCC: Amsterdam 3:2:1 criteria Screening with HNPCC: 1-2 yearly colonoscopies from age 25 or 5 years younger than earliest affected relative Give aspirin in HNPCC - decreases risk of developing CRC
76
Microsatellite instability
Expansion or contraction of microsatellites seen in tumours compared to normal tissue Not specific for HNPCC Can have epigenetic silencing of MLH1 associated with BRAF V600E - generally rules out HNPCC
77
FAP
1% of CRC Germline mutation in APC gene on Chromosome 5 Location of mutation associated with severity of polyposis Screening: sigmoidoscopy from age 10-15. When first adenoma detected do yearly colonoscopies until colectomy
78
Colectomy indications in FAP
Documented/supsected CRC Adenoma with high grade dysplasia Significant symptoms related to polyps e.g. bleeding Marked increase in number of polyps from one exam to another Inability to survey colon due to polyposis
79
Stage 1 CRC management
Surgery
80
Stage 2 CRC management
Surgery Consider adjuvant chemo if high risk features
81
Stage 3 CRC management
Surgery Adjuvant chemo definitely (CAPOX or FOLFOX) -Fluoropyrmidine + oxaliplatin
82
Stage 4 CRC managemenet
Chemotherapy backbone +/- targeted therapy -VEGF regardless of RAS/RAF status) -EGFR only in RAS wild-type and left-sided
83
VEGF inhibitors
Bevacizumab Inhibits angiogenesis SE: Hypertension, delayed wound healing
84
EGFR inhibitors
Cetuximab/Panatumumab Mechanism of resistance is downstream KRAS/BRAF mutations Hence only use in wild-type KRAS SE: Acneform rash, hypomag
85
Fluoropyrmidines
5-FU (IV) or capecitabine (oral pro-drug converted to fluorouracil in tumour) SE: Hand foot syndrome (Cape > 5FU) Myelosuppression (5FU > Cape)
86
Oxaliplatin
Platinum derivative Used in combo with fluoropyrmidines for CRC SE: Cumulative peripheral neuropathy Cold sensitivity/dysthaesias
87
CRC poor prognostic factors
Right sided tumours BRAF mutant (more common in right sided tumours) Number of LN involved --> higher risk of recurrence
88
Stage 4 CRC with MMR or high MSI
Can use PDL1

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