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PHAM02 > lung cancer SD > Flashcards

lung cancer SD Flashcards

1
Q

RF for lung cancer

A

cigarette smoking

passive smoking

occupational
- asbestos
- ionising radiation
- occupational RF
- air pollution

genetic predisposition

previous malignancies

genetic RF - old age, obesity, poor diet, physical inactivity, alcohol

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2
Q

Sx

A

chest discomfort/pain
trouble breathing
wheezing
blood in sputum
hoarseness
trouble swallowing
loss of appetite
weight loss for no reason
very tired
cough thatdoesn’t go away/worse over time
swelling in face/veins in neck

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3
Q

scans that can be used

A

x-ray

CT scan

PET-CT scan (positron emission tomography)

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4
Q

What scan is used to locate mass in a lung?

A

CT

PET-CT

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5
Q

bronchoscopy

A
  • bronchoscope inserted through nose/mouth into trachea and lungs
  • biopsy can be taken from lung for analysis
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6
Q

classifications of lung cancer

A

SCLC

NSCLC

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7
Q

small cell lung cancer

A
  • mostly caused by smoking
  • highly maligant
  • spreads rapidly
  • metastases when diagnosis made
  • located in central airway
  • tumours smaller in size compared to NSCLC
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8
Q

non-small cell lung cancer types

A

most common types:

  1. squamous cell carcinoma
  2. adenocarcinoma
  3. large cell cancers
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9
Q

squamous cell carcinoma

A

cancer in epithelial cells lining the lungs

typically in central portion of the lung and in airways

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10
Q

adenocarcinoma

A
  • tumour originated from bronchial/alveolar epithelium
  • most common type of LC in women who ever smoked
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11
Q

large cell cancers

A
  • originate in larger cells of the lungs
  • peripherally located
  • eg. large clear cells
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12
Q

staging of lung cancer tumour

A

stage 1: <3cm, not spread, small

stage 2: 3-5cm, in lymph nodes in lungs,

stage 3: 5-7cm, in lymph nodes away from primary tumour, other organs/tissues, invading into chest wall/breast bone

stage 4: >7cm, spread to other lung, in many lymph nodes, metastasised to ANOTHER ORGAN

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13
Q

What are micro metastases?

A

metastses in another organ that can’t be seen on x-ray or CT scan

don’t have eough biomarkers yet

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14
Q

What can be used to diagnose LC if pathology not clear?

A

IHC - immuno histo chemistry

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15
Q

What are paraneoplastic syndromes assocated with LC?

A

secondary effetcs of the cancer

producing chemicals and hormones

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16
Q

paraneoplastic syndromes with LC

A
  • ADH: inducing HYPONATRAEMIA
  • ACTH: CUSHING syndrome
  • parahormone, PTH related peptide, PGE, cytokines: HYPERCALCAEMIA
  • calcitonin: HYPOPCALCAEMIA
  • gonadotropins: GYNECOMASTIA
  • serotonin, bradykinin: CARCINOID syndrome
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17
Q

common oncogenes in LC

A

KRAS
EGFR

18
Q

tumour suppressor genes that are lost in LC

A

p53

RB1

p16

multiple loci on chromosome 3 (lots of tumour suppressor genes)

19
Q

% of cases p53 lost in SCLC and NSCLC

A

SCLC 90%

NSCLC 50%

20
Q

most prominent genetic alteration in LC

A

EGFR mutations

21
Q

targeted therapies in NSCLC to target EGFR?

A

EGFR inhibitors

-> TKIs

22
Q

How does EGFR drive cancer growth?

A
  • activated oncogene
  • drives cancer growth
  • decreases apoptosis
  • increased angiogenesis
23
Q

TKIs and MAB used in NSCLC

A

Erlotinib

Gefitinib

Osimertinib

Cetuximab (MAB against EGFR)

24
Q

How does cetuximab work?

A
  • binds to outside of EGFR
  • stops EGFR from dimerising
  • inhibits KRAS
  • slows down EGFR signalling & cellular growth
  • leads to cell apoptosis
25
Q

When does cetuximab become ineffective?

A
  • if there’s mutant KRAS
  • it becomes ineffective
  • cancer cell will survive and proliferate
26
Q

1st line Tx for NSCLC

A
  • initially cetuzimab
  • when that fails use TKIs
  • 1st TKI = erlotinib
27
Q

How does erlotinib work?

A
  • TKI
  • prevents EGFR phosphorylation
  • inhibits MAPK
  • tumour regression
  • resistance in 10-14 mths
28
Q

What mutation causes erlotinib resistanace?

A

T790M mutation

29
Q

Where does T790M mutation occur?

A

in the ATP binding pocket

30
Q

most common cause for TKI resistance (erlotinib, gefitinib, afatinib)

A

T790M mutation

31
Q

Tx for T790M mutation

A
  • Osimertinib (Targrisso)
  • can bind to EGFR T790M
  • binds to the mutated R
32
Q

advantage with Osimertinib (Tagrisso)

A
  • doesn’t bind to WT (wild type) EGFR
  • only effects cancer cells and not normal cells
33
Q

What type of drug is Osimertinib (Tagrisso)

A

irreversible EGFR-TKI

34
Q

resistance mechanisms to Osimertinib (Tagrisso)

A
  1. MET-amplification
  2. EGFR C797S mutation
  3. HER2-amplification, PIK3CA and RAS mutations
35
Q

EML4-ALK marker in NSCLC

A

ALK - R
EML - structural protein

NSCLC: genetic mutation activates ALK, leads to hyperphosphorylation & activation

genetic change forms a fusion protein:
- ALK fuses to EML4
- EML4-ALK fusion protein drives the protein fxn

EML4-ALK activates proliferation

-> 2 separate genes forming 1 gene

36
Q

problem with EML4-ALK fusion protein

A
  • it bypasses EGFR blockade
  • inc proliferation and cell cycle
  • dec apoptosis
37
Q

TKI to target EML4-ALK

A

Crizotinib

Alectinib

38
Q

drug used in LC if it has Ras mutation (G12C mutation)

A

Sotorasib (Ras inhibitor)

39
Q

examples of immunotherapy that inhibit PD1 and activate the immune system to attack tumours producing antigens

A

Pembrolizumab (Keytruda)

Nivolumab (Opdivo)

40
Q

Why can tumour cells express PD1?

A

to suppress T cells

41
Q

PD-L1 inhibitors in LC

A
  • tumour cells express PD-L1 to suppress T cells (PD-1 on T cell)
  • PDL = programme death ligand
  • PD-L1 inhibitors bind to PD-L1 and stop it binding to T cell
  • activate immune system to attack tumours

PHAM02 (32 decks)

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