Table 2 Summary of baseline genomic alterations in patients with valid tissue NGS resulta and by suboptimalb tumor response to treatment or not

From: Candidate mechanisms of acquired resistance to first-line osimertinib in EGFR-mutated advanced non-small cell lung cancer

Gene/mutation, n (%)

All evaluable (N = 104)

Suboptimalb responder (n = 23)

Not suboptimalb responder (n = 81)

TP53 any known/likely

64 (62)

15 (65)

49 (60)

TP53 frameshift/truncation

26 (25)

2 (9)

24 (30)

TP53 splice

9 (9)

2 (9)

7 (9)

TP53 missense

28 (27)

11 (48)

17 (21)

TP53 homozygous deletion

1 (1)

0

1 (1)

EGFR amplification

21 (20)

7 (30)

14 (17)

RB1 any known/likely

12 (12)

4 (17)

8 (10)

RBM10 truncation/splice

5 (5)

4 (17)

1 (1)

SMARCA4 missense/truncation

3 (3)

3 (13)

0

RICTOR amplification

3 (3)

3 (13)

0

HER2 amplification/missense

3 (3)

3 (13)

0

MET amplification

3 (3)

2 (9)

1 (1)

AKT2 any known/likely

2 (2)

2 (9)

0

CDK6 any known/likely

2 (2)

2 (9)

0

FGF23 any known/likely

2 (2)

2 (9)

0

BRCA2 any known/likely

2 (2)

2 (9)

0

APC any known/likely

6 (6)

3 (13)

3 (4)

  1. EGFR epidermal growth factor receptor.
  2. aKnown/likely refers to alterations either known or likely to have a functional impact on a given protein, as determined by the algorithm described in Carr et al.49.
  3. bPatients whose tumors had a suboptimal response were defined by either a best overall response of stable disease or progressive disease with a PFS of <6 months, or non-clearance of plasma ctDNA measured by ddPCR at 6 weeks.
Back to article page