EGFR receptors- missing lecture Flashcards Preview

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Flashcards in EGFR receptors- missing lecture Deck (16)
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1
Q

____ cancers overexpress HER2 than EGFR

A

fewer

2
Q

small molecule EGFR approaches?

A

gefitinib

erlotinib

3
Q

mAb approaches to EGFR

A

Cetuximab

panitumumab

4
Q

cetuximab is commonly used in ______ therapy with?

A

combination

radiotherapy

5
Q

what can reduce the effectiveness of EGFR inhibitors

A

if theyre K-RAS mutant

6
Q

what happens in K-RAS mutations?

A

it stops the feedthrough at the receptor so the EGFR drug doesn’t have an effect
active despite whats happening upstream

7
Q

what is cetuximab lisenced for treatment in?

A

bowel cancer

head and neck cancer

8
Q

what do patients need to be screened for prior to recieving cetuximab?

A

K-Ras mutation

9
Q

which patients respond well to small molecule EGFR inhibitors?

A

mutated EGFR

10
Q

Is simple over-expression of EGFR enough to tell us if the patient will respond to a small molecule inhibitor?

A

no

11
Q

why does mutated EGFR show an increased response to blocking?

A

as the tumour becomes reliant on the increased EGFR signalling so blocking this shows good results

12
Q

major differences between mutated and wild type EGFR:

regarding 1. activation

A

wild type is activated by ligands (homodimerisation and autophosphorylation)

mutant can be active in the absence of the lingand

13
Q

major differences between mutated and wild type EGFR:

regarding 1. Pathways/ signalling cascades

A

enhanced with mutant EGFR

14
Q

major differences between mutated and wild type EGFR:

regarding 1. sensitivity to TKI’s?

A

context dependent in wild type but the mutant EGFR is sensitised

15
Q

major differences between mutated and wild type EGFR:

regarding 1. Ubiquitin mediated degradation

A

ubiquitin- mediated degradation of wild ytpe EGFR is ligand induced

mutant EGFR shows elevated ubiquitinylation

16
Q

EGFR mutations are common in which groups?

A

non smokers
adenocarcinoma histology
females
asians