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Lung Cancer + Basic Sciences Flashcards

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1
Q

Risk factors for lung cancer

A

• Smoking
○ Increases risk of lung ca by a factor of 10
○ Weaker association with lung adenocarcinoma
• Other factors
○ asbestos - increases risk of lung ca by a factor of 5
§ Smoking and asbestos are synergistic, i.e. a smoker with asbestos exposure has a 10 * 5 = 50 times increased risk
○ arsenic
○ Radon - 2nd leading cause of lung cancer
○ nickel
○ chromate
○ aromatic hydrocarbon
○ cryptogenic fibrosing alveolitis
• Factors that are NOT related
○ coal dust
• Family history (genetic predisposition)
• Other RF: pulmonary scarring, previous radiation, pulmonary fibrosis, chronic infections (eg: TB, HIV)

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2
Q

What is the most potent carcinogen in cigarette smoke?

A

Polycyclic aromatic hydrocarbons

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3
Q

Types of lung cancers

A

Lung cancer is divided into 2 types:
(1) Small Cell Lung Cancer 13%: central location, rapid tumour growth, early metastases and associated with numerous paraneoplastic syndromes

(2) Non-Small Cell Lung Cancer
- Adenocarcinoma (peripheral) - most common 40% and more common in women + non smokers
- Squamous cell carcinoma (central) 20%
- Large cell carcinoma 7%

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4
Q

Features of adenocarcinoma

  • Location
  • Characteristics
A
  • Peripheral
  • Most common form of lung cancer
  • More common in women and non-smokers
  • Associated with mutations in EGFR/ALK/KRAS gene
  • Risks with pulmonary fibrosis
  • Prognosis usually better than other lung cancer
  • Gynaecomastia due to production of HCG (increased risk with large cell carcinoma + poorly differentiated adenocarcinoma)
  • Increased risk with adenocarcinoma: thrombophlebitis migrans, nonbacterial verrucous endocarditis
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5
Q

Features of squamous cell carcinoma

  • Location
  • Characteristics
A
  • Location: central “sentrally located”
  • Strong associations with smoking
  • Cavitations
  • Cavitary lesions arising from hilar bronchus
  • PThrP: hypercalcemia
  • Histology: Intercellular bridges (desmosomes)
    Keratin pearls

C; central location, hypercalcemia, cavitations

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6
Q

Features of large cell carcinoma

  • Location
  • Characteristics
A
  • Location: peripheral
  • Poor response to chemotherapy
  • Early mets
  • Poor prognosis
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7
Q

Features of small cell lung cancer

  • Location
  • Features
A
  • Location: central
  • Strong association with SMOKING-almost all cases are in smokers
  • Very CHEMOTHERAPY SENSITIVE
  • Associated with several PARANEOPLASTIC syndromes
    • Cushing syndrome
    • SIADH
    • Lambert Eaton Syndrome: ab against voltage gated calcium channels
  • Undifferentiated and very aggressive with early metastases
  • Associated mutations: L-myc oncogene
  • Classically bulky lymphadenopathy
  • Chemo+ radiosensitive
  • Doesn’t cause clubbing
  • CNS METS FREQUENT - MRI BRAIN
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8
Q

Staging of SCLC

A

Only 2 stages: limited and extensive

Limited: disease in one haemothorax and ipsilateral mediastinal nodes, encompassable by a single radiation field

Extensive: anything that’s not limited

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9
Q

Treatment for SCLC

A

LIMITED
- Curable (20-30%) with concurrent chemoradiation (CISPLATIN + ETOPOSIDE) and PCI (prophylactic cranial irradiation) in responders as brain is a brain sanctuary site for micromets

EXTENSIVE

  • Generally incurable
  • BUT expect excellent response with chemo/RT even in very unwell patients
  • Median survival 12 months with chemoimmunotherapy

Chemotherapy (CARBOPLATIN + ETOPOSIDE) + ATEZOLIZUMAB (PDL1 inhibitor) improved PFS + OS

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10
Q

Features of mesothelioma

A 
- Asbestos and tobacco related 
10-20x risk of mesothelioma 
Asbestos risk of NSCLC - especially squamous cell carcinoma
- Long latency (30-40 years)
- Usually pleural or peritoneal

Epitheloid more common but sarcomatoid has worse survival

Tx:

  • Generally incurable, role of surgery + radio is limited
  • Radical Tx: extrapleural pneumonectomy
  • Palliative chemo improves survival: cisplatin + pemetrexed

Nivolumab + ipilimumab in unresectable malignant pleural mesothelioma

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11
Q

Pancoast tumour

A

• Apical lung carcinoma
• Superior sulcus tumour
• Predominantly NSCLC
• May lead to the development of Pancoast Syndrome: constellation of symptoms secondary to the mass effect of the tumour on surrounding structures
○ Cervical sympathetic ganglion (stellate ganglion): Horner syndrome (ipsilateral miosis - small pupil), ptosis, anhidrosis)
○ Brachial Plexus: localised pain in the axilla and shoulder (plexus neuralgia)
- Upper limb motor and sensory deficits (eg: hand muscle weakness and atrophy) - wasting hand muscles (T1)
○ Recurrent laryngeal nerve: hoarseness
○ Brachiocephalic vein
- Unilateral oedema of the arm
- Facial swelling
○ Phrenic Nerve: paralysis of the hemidiaphragm (visible as elevated hemidiaphragm on CX

NOTE:
The right and left recurrent laryngeal nerves are not symmetrical, with the left nerve looping under the aortic arch, and the right nerve looping under the right subclavian artery then traveling upwards.

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12
Q

What are the common sites of metastsis for lung cancer?

A

Lung cancer loves to BLAB

  • Brain
  • Liver
  • Adrenals
  • Bone
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13
Q

Paraneoplastic syndromes of lung cancer

A

Shared paraneoplastic features

  • Cachexia
  • Thrombocytosis + DIC
  • Hypercoagulability
  • Dermatomyositis
  • Acanthosis negricans

NSCLC

  • Hypercalcaemia of malignancy - increased risk with squamous cell
  • Gynaecomastia due to production of HCG (increased risk with large cell carcinoma + poorly differentiated adenocarcinoma)
  • Hypertrophic osteoarthropathy
  • Increased risk with adenocarinoma: thrombophlebitis migrans, nonbacterial verrucous endocarditis

SCLC

  • Cushing syndrome
  • SIADH
  • Lambert eaton syndrome
  • Paraneoplastic cerebellar degeneration
  • Peripheral neuropathy
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14
Q

Clinical features of lung cancer

A

• Pulmonary Symptoms:

  • Cough, haemoptysis
  • Progressive dyspnoea
  • Wheezing
  • Chest pain

• Extrapulmonary Symptoms

  • Constitutional symptoms - weight loss, fever, weakness
  • Signs and symptoms of tumour infiltration and/or compression of neighbouring structures

SVC syndrome: impairs venous backflow to the right atrium, resulting in venous congestion in the head, neck and upper extremities
Treat with steroids
Common in SCLC

Hoarseness: paralysis of the recurrent laryngeal nerve

Dyspnoea and diaphragmatic elevation: paralysis of the phrenic nerve

Dullness on percussion + reduced breath sounds: malignant pleural effusion on the affected side

Dysphagia: oesophageal compression

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15
Q

What should you be concerned about if a patient >40yo has recurrent respiratory infections (eg: pneumonia ) in the same pulmonary region?

A

Lung cancer

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16
Q

Investigation for lung nodule

A
  • <5mm: no follow up if malignancy risk is low
    If high to consider serial CT scans
  • 5-7mm: Serial CT scans
  • > 8mm: PET or biopsy
    If suspicious for malignancy - resection!
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17
Q

Diagnosis for lung cancer

A
  • Central endobronchial lesions: bronchoscopy
  • Peripheral lung lesions: radiology guided core biopsies
  • Central nodes: EBUS (endobronchial US)

Diagnosis: morphology + immunohistochemistry/molecular testing

  • TTF-1 and Napsin A +ve for adenocarcinoma (TANA)
  • Non squamous NSCLC (adenocarcinoma/large cell): EGFR, ALK, ROS1
  • PDL1 expression for all NSCLC (squamous, adeno, large cell)
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18
Q

Imaging for lung cancer

A
  • If CXR raises suspicion –> CT scan
  • PET to stage mediastinum and identify metastatic disease if curative intent is planned for NSCLC
  • Isolated PET positive findings require histological confirmation
  • PET not sensitive for brain - requires ideally MRI Brain
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19
Q

Staging for NSCLC and basic treatment

A

Stage 1: No nodal involvement
- Surgical resection if medically fit - lobectomy vs pneumonectomy
Lobectomy with mediastinal LN dissection is recommended for tumours >2cm
- Stereotactic radiation if non surgical candidate

Stage 2 A+B: Ipsilateral peribronchial and/or hilar LN and intrapulmonary nodes
- Surgical resection + adjuvant chemo

Stage 3A: ipsilateral mediastinal and/or subcarinal LN
Stage 3B: contralateral mediastinal, hilar, supraclavicular LN
- Resectable: neoadjuvant chemo + surgical resection
- Unresectable: concurrent chemoradiation and DURVALUMAB (PDL1) for 12 months

Stage 4: metastatic disease including malignant pleural effusion + contralateral lung nodules
- Palliative systemic therapy - chemotherapy, targeted therapy and immunotherapy
+ palliative RT

Adjuvant Chemo

  • Consider for all fit stage II-III patients post resection
  • No conclusive benefit for stage IV
  • Generally 4 months of cisplastin + venorelbine
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20
Q

What are the driver mutations in non squamous cell carcinoma (adenocarcinoma, large cell)?
Who should be tested?

A 
Driver Mutations in NSCLC 
- EGFR
- ALK
- ROS 
(EAR)

Who should be tested?

  • All lung ADENOCARCINOMAS
  • All carcinomas with a component of adenocarcinoma, eg: adenosquamous carcinoma
  • Large cell carcinoma
  • Never smokers with squamous cell carcinoma

Driver mutations are absent or extremely rare in

  • Pure squamous cell carcinoma
  • Classic small cell lung cancer
  • Large neuroendocrine carcinoma
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21
Q

Stage IV targeted therapies for lung cancer

A

Factors to Consider

  • Presence of driver mutations: EGFR, ALK rearrangements, ROS 1
  • Presence of PDL-1
  • Squamous vs Non squamous (squamous more aggressive and no therapy available)
  • ECOG
  • RT for palliation + brain mets

EGFR TKIs

  • Erlotinib
  • Gefitinib
  • Afatinib
  • Osimertinib for T790M +ve

ALK TKIs

  • Crizotinib
  • Alectinib

ROS 1 TKI

  • Crizotinib,
  • Entrectinib
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22
Q

EGFR mutations

A 
Osimertinib 
- 1st line 
- For T790M +ve patients 
- 3rd gen 
- Wouldn't give if non exon 19/L85*R 
Gefitinib, Erlotinib - 1st gen 
Afatinib - 2nd gen
  • Most common EGFR activating mutations
    Exon 19 deletion
    Exon 21 point mutation L858R

More common in :

  • Non smokers
  • Females
  • Asian ethnicity
  • Adenocarcinoma

For patients with EGFR mutation, more effective than chemo

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23
Q

Side effects of EGFR inhibitors

Osimertinib, Gefitinib, Afatinib

A 
- Acneform rash - presence of rash is correlated with response to therapy. 
Treat with topical or oral abx (tetracyclines), topical steroids, skin care, sun protection 
- Diarrhoea 
- Macular oedema 
- Alopecia 
- Nail changes
- Pulmonary toxicity 
Don't cause cytopenia

EGFR inhibitor resistance

  • Progression due to resistance common after 6-24 months
  • 60% due to T790M resistance mutation
  • Osimertinib (3rd gen EGFR TKI) highly active
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24
Q

Osimertinib

  • MOA
  • Indication
  • SE
Study These Flashcards
A

MOA: EGFR inhibitor

  • 3rd gen irreversible EGFR-TKI
  • Selectively inhibits both EGFR TKI and EGFR T790M resistance mutations
  • Excellent CNS penetration

SE

  • Skin toxicity (less skin toxicity than others)
  • DIarrhoea
  • pneumonitis
  • Cardiac impairment - more prolonged QT
25
ALK Mutations - anaplastic lymphoma kinase translocation | ALECTINIB is 1st line
- Fusion oncogene EML4-ALK - Inversion in Chromosome 2P that fuses EML4 gene with ALK gene Occurs in: - Adrenocarcinoma - Non smokers - Younger patients - Crizotinib: 1st gen - Alectinib: 3rd gen, improved 1st line DFS and better CNS penetration than crizotinib - Lorlatinib: 2nd gen TKI failure Following progression with an ALK inhibitor other than crizotinib ALECTINIB is 1st line - less toxic, better CNS respones SE: - Hypercholesterolemia - Hypertriglyceridemia - Cognitive and mood effects - Visual changes - Neutropenia - Fluid retention - Prolonged QT
26
ROS1 Rearrangement
- Occur in adenocarcinoma, non squamous NSCLC Tends to occur in: - Younger patients - Non smokers Respond to crizotinib (1st line), lorlatinib, entrectinib
27
KRAS G12C mutation
KRAS mutation NSCLC - Occurs in 15-30% of lung adenocarcinomas Common in - Smokers Western background Sotorasib for KRAS
28
If there is no driver mutation - treatment
Stage 3B NSCLC: consolidation DURVALUMAB Stage 4 Wildtype NSCLC - Check PDL1 levels - PDL 1> 50%: prembolizumab single agent - PDL1 < 50% - prebolizumab + platinum + pemetrexed Stage IV non small cell lung cancer with PDL1: Platinum Doublet + PD1 or PDL1 inhibitors <50 - Pembrolizumab + Chemo - Atezolizumab + bevacizumab + chemo for non squamous cell cancer only - Nivolumab + Ipilimumab with chemo for squamous cell cancer only >50 - Pembrolizumab as single agent (preferred) - Pembrolizumab with chemo - Atezoliumab + bevaciziumab + chemo for non squamous cell cancer - Platinum Doublet: cisplatin + etoposide or cisplatin + vinorelbine) - Note: pemetrexed (non squamous NSCLC) PD1 Inhibitors: Nivolumab, Prembolizumab PDL1 Inhibitors: Atezolizumab, Durvalumab
29
General treatment for NSCLC
Stage 3: Consolidation durvalumab Stage 4: - PD1/PDL1 antibody for everyone is first line if wildtype with no contraindications - Monotherapy or in combination with chemo depends on PDL1 - Generally doses work well in EGFR/ALK mutated patients
30
Systemic therapy for locally advanced and metastatic non small cell lung cancer.
- EGFR mutations: Osimertinib - ALK rearrangements: Alectinib or Brigatinib - ROS1 rearrangements: Crizotinib - BRAF V600E mutations: Dabrafenib + trametinib - NTRK alterations: Larotrectinib PDL 1 score - >50%: Pembrolizumab as single agent - <50% Prebolizumab + platinum + pemetrexed
31
Mechanism of action of EGFR inhibitors with respect to cell cycle
Epidermal growth factor inhibitors (EGFRi) such as erlotinib (used in nonsmall cell lung cancer) and cetuximab (used in colorectal cancer and head/neck cancer) block the progression of a cell from the G1 phase to the S phase.
32
Features of the cell cycle
The cell cycle can be divided into two phases: interphase and mitosis. Interphase is further divided into the G1 (gap 1), S (synthesis), and G2 (gap 2) phases, which prepare the cell for division. - G1 Phase: proteins and cell organelles are synthesized. - S Phase: DNA is replicated in the S phase. - G2 Phase: DNA replication errors are repaired. - Mitosis (M) or cell division. - There are various checkpoints within the cell cycle that ensure the cell is ready to enter the next phase (G1, G2, and M checkpoints). - Only proliferating cells pass through the cell cycle. - Most mature tissue cells are in a resting phase, the G0 phase. - These cells are differentiated, with each performing a specific function. - Mature differentiated cells do not divide
33
Predictive vs prognostic biomarker
PREDICTIVE: provides information on OUTCOME with regards to SPECIFIC THERAPY PROGNOSTIC: provides information on OUTCOME, INDEPENDENT OF THE THERAPY that is used PREDICTIVE BIOMARKER: identify subgroups most likely to respond - provides information on the probability of obtaining a response to treatment - Allows for therapeutic decisions - EG: HER2/EGFR --> predicts will respond to treatment KRAS mutated --> predicts resistance to treatment PDL1 >50% --> predicts better response to immunotherapy BRAF in melanoma is PREDICTIVE not prognostic of response to BRAF inhibitors PROGNOSTIC BIOMARKER: provides information on course of disease - informs about a likely cancer outcome (eg, disease recurrence, disease progression, death) independent of treatment received. - reflects the underlying biology and natural history - treatment benefit similar for biomarker-positive and biomarker negative patient, but the biomarker will still be associated with a differential outcome depending on whether it is present or absent - the biomarker positive patients have a better survival than biomarker negative patients, independent of treatment group EG: EGFR IN LUNG CANCER
34
Hallmarks of Cancer
1. Evading growth suppressors - Cyclin dependent kinase inhibitors, eg: CK 4/6 inhibitors in breast cancer 2. Avoid immune destruction - AntiCTLA-4 mAB 3. Enabling replicative immortality - Telomerase inhibitors 4. Tumour promoting inflammation - Selective anti-inflammatory drugs 5. Activating invasion and metastasis - Inhibitors of HGF-c-Met 6. Inducing angiogenesis - Inhibitors of VEGF signalling 7. Genome instability and mutation - PARP inhibitors 8. Resisting cell death - Proapoptotic BH3 mimetics 9. Deregulating cellular energetics/ epigeneitcs - Aerobic glycolysis inhibitors 10. Sustaining proliferative signalling EGFR inhibitors
35
Side effects of immunotherapies
- Related to autoimmunity - immune checkpoint blockade enhances T cell responses throughout the body - Can occur anywhere in the body - Thyroid dysfunction: hypothyroid> hyperthyroid - Pneumonitis - steroids, if worsening hypoxia will require infliximab or mycophenolate - Colitis - more common in CTLA4 >PD1 - Renal dysfunction - Hepatotoxicity * PD1: Thyroid, lung, autoimmune diabetes * CTLA4: Colitis, rash, hypophysitis * SE occur normally within 4-12 weeks * Endocrinopathies can occur anytime * Can also occur after medications are ceased
35
What is pseudoprogression/hyperprogression
Immunotherapy - the following are exclusive to immunotherapy - Pseudoprogression: immune storm, tumour site increases in size - Hyperprogression: tumour growth increases significantly
36
How do you treat colitis which has occurred secondary to immunotherapy?
CTLA4 > PD1 G1: <4 stools more than baseline - LOPERAMIDE G2: 4-6 stools more than baseline WH immunotherapy Add IV methpred and then taper with oral or can start with oral G3: >7 stools more than baseline WH immunotherapy IV pred If refractory over 3-4 days - add infliximab G4: perforation Permanently discontinue immunotherapy Add IV methylpred Infliximab and surgical review
37
Mutations associated with - Colorectal cancer - Lung cancer - Melanoma - Breast cancer
- Colorectal Cancer: EGFR overexpressed in ~80% --> KRAS wild type/not mutated - Lung Cancer: EGFR 10-30% KRAS pG12C mutations - Melanoma BRAF in 50% - Breast Cancer HER2
38
Which group of individuals are EGFR mutations more likely to be found?
Non smoker Female Asian Adenocarcinoma
39
How do you manage diarrhoea in - chemotherapy - targeted therapy - immunotherapy
Chemotherapy - Infection screen + IVF - Loperamide - Codeine - Octreotide infusion - Neutropenic colitis ?abx - C difficle Targeted Therapy - Infection screen + IVF - WH medication + Loperamide ``` Immunotherapy - Infection screen + IVF - Grade 1-2 : oral steroids - Grade 3: IV steroids - Colonoscopy - Infliximab Think colitis for immunotherapy ```
40
Side effects of the following chemotherapy - Taxanes: paclitaxel (breast), oxaliplatin (bowel), docetaxel (prostate) - 5FU/Capecitabine - Anthracyclines: doxorubicin (breast), epirubicin - Alkylating agents: temozolamide, ifosfamide - Vinca alkaloids: vincristine Topoisomerase I inhibitors: Irinotecan (bowel)
- Taxanes: paclitaxel (breast), oxaliplatin (bowel), docetaxel (prostate) Peripheral neuropathy Paclitaxel: hypersensitivity infusion reactions - 5FU/Capecitabine Diarrhoea Hand/foot syndrome - Anthracyclines: doxorubicin (breast), epirubicin Cardiotoxicity Chemo induced N+V - Alkylating agents: temozolamide, ifosfamide, cyclophosphamide Ovarian insufficiency Nausea Thrombocytopenia IFOS - encephalopathy - treat with methylene blue Mesna always given with ifosfamide to protect bladder and prevent irritation and bleeding. - Vinca alkaloids: vincristine Peripheral neuropathy Topoisomerase I inhibitors: Irinotecan (bowel) Diarrhoea
41
Metastatic testicular cancer chemo treatment and side effect
BEP - Bleomycin: pneumonitis, ILD - Etoposide - Cisplastin: peripheral neuropathy, tinnitus, N+V, renal impairment/electrolyte derangement
42
``` Pathophysiology of chemotherapy induced N+V involves activation of neurotransmitters in the brain. What is the receptor for substance? A. H-hydroxytryptamine-3 B. Dopamine 2 C. Gamma aminobutyric acid A D. HIstamine 1 E. Neurokinin 1 ```
E. Neurokinin 1
43
MOA of the following anti-emetics - Metoclopramide - Ondansetron/Palonestron - Aprepitant - Targin - Cyclizine
- Metoclopramide: D2 antagonist - Ondansetron/Palonestron: 5HT3 - Aprepitant: Neurokinin 1 - Targin: reduces opioid associated constipation without reducing opioid effiaccy - Cyclizine: H1 antagonist, anticholinergic action
44
What is chromogranin A a marker of ?
Neuroendocrine tumours
45
What is the most common SE for immunotherapy?
Most common toxicities: skin toxicities | Most common significant or serious toxicities: GI toxicity
46
Endocrinopathies associated with immunotherapy
Pituitary Gland - Hypophysitis - ACTH decrease - Secondary adrenal insufficiency Thyroid Gland - Hyperthyroidism - Hypothyroidism - TSH increase or decrease - Thyroiditis - Free thyroxine increase or decrease - Autoimmune thyroiditis Adrenal glands - Primary adrenal insufficiency Pancreas - Diabetes
47
What does the following biomarkers predict: HER2 amplication KRAS mutation
HER2 amplication predicts response to trastuzumab KRAS mutation in colorectal cancer predicts lack of response to cetuximab (EGFRI) - only works for wild type KRAS
48
What cancers are the following VEGF receptor inhibitors used for? - Sorafenib - Sunitinib, pazopanib, cabozantinib - Lenvatinib, vendetanib
- Sorafenib: HCC, thyroid, clear cell RCC - Sunitinib, pazopanib, cabozantinib: clear cell RCC - Lenvatinib, vendetanib: radio-iodine refractory differentiated thyroid
49
EGFR Inhibitors - EGFR (mab) - EGFR (TKI) - EGFR - activity against T790M
EGFR (mab) - Cetuximab/Panitumumab - CRC (KRAS WILD TYPE) - Head and Neck SCC EGFR (TKI) - Erlotinib, Gefitinib, Afatinib - NSCLC EGFR + EGFR - activity against T790M - Osimertinib - NSCLC EGFR T790M + - SE: more prolonged QT SE: EGFR = rash, diarrhoea
50
HER2 inhibitor - HER2 (MAB) - HER2/EGFR (TKI) - HER2 (ADC)
HER2 (MAB) - Trastuzumab, Pertuzumab - Breast cancer HER 2+ - Cardiotoxicity, diarrhoea (Pertuzumab) HER2/EGFR (TKI) - Lapatinib - Breast cancer HER2+ - Rash diarrhoea, cardiotoxicity HER2 (ADC) - antibody drug conjugate - T-DM1: trastuzumab emtansine - Thrombocytopenia, transaminitis
51
ALK rearrangement inhibitors
- Alectinib, Certinib, Crizotinib - NSCLC ALK+ SE - N+V - Diarrhoea - Visual disturbance - Hepatitis - Pneumonitis - Bradycardia - Alectinib - better tolerated than crizotinib and now new standard of care
52
BRAF inhibitors
- Dabrafenib, Vemurafenib - BRAF TKI - Melanoma BRAF V600E+ SE: - Fever - Skin: secondary cutaneous malignancies, hyperkeratosis, rash, photosensitivity - Skin toxicities improved if given with MEK inhibtor - Hair changes - Arthralgia
53
MEK inhibitor
- Trametinib, Cobimetinib - Melanoma BRAF V600E inhibitor SE: - Rash - Diarrhoea - Peripheral oedema - Fever - Retinopathy
54
VEGF inhibitor | VEGFR inhibitor and multi-kinase TKI
VEGF inhibitor: bevacizumab for CRC VEGFR inhibitor: sunitinib, axitinib Hypertension, hand-foot syndrome, diarrhoea, hypothyroidism, hepatitis, cardiotoxicity
55
cKIT (TKI)
Imatinib GIST tumour SE - Muscle cramps - Maculopapular rash - N+V - Diarrhoea - Fatigue
56
Everolimus
- mTOR - Breast Cancer ER+PR+ Pancreatic NET Clear Cell RCC SE - Mucositis - Diarrhoea - Fatigue - Hyperglycaemia - Rash - Pneumonotis - Myelosuppression
57
CDK4/6 inhibitor
Ribociclib Breast cancer ER+PR+ SE: - Neutropenia - Diarrhoea - Transaminitis
58
PARP inhibitor
Olaparib BRCA1/2 germline mutation + Serous ovarian cancer ``` SE: N/V Diarrhoea Fatigue Taste/smell changes Myelosuppresion ```

Oncology (7 decks)

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