Table 1 Clinicopathological characteristics for the study cohort.

From: Clonal dynamics of BRAF-driven drug resistance in EGFR-mutant lung cancer

Patient ID

Sex

Age

Biopsy

EGFR mutation

BRAF mutation

Co-mutations

01

F

70

TB

E746_A750del, T790M

V600E

Class I

Acquired (osimertinib)

Persistent T790M

02

F

71

TB

E746_A750del, T790M

S605C

Not classified

Initial

TP53 R273H

03

M

61

TB

L858R

K601E

Class II

Initial

DDR2 R279M

04

M

72

TB

E746_A750del, T790M

V600E

Class I

Acquired (osimertinib)

loss of T790M

05

M

77

TB

L861Q

G466A

Class III

Acquired (afatinib)

ERBB2 G815A, TP53 S166*

06

M

66

TB

L858R, V834L

V600E

Class I

Acquired (osimertinib)

loss of EGFR mutations

07

F

84

TB

L858R

V600E

Class I

Initial

08

F

74

TB

L858R

G466E

Class III

Acquired (gefitinib)

09

M

50

TB

E746_A750del

V600E

Class I

Acquired (osimertinib)

CCDC6-RET

10

F

67

TB

L747_P753delinsS

G466E

Class III

Initial

KRAS A59E

11

F

75

TB

E746_A750del

S605N

Not classified

Initial

12

F

61

LB

E746_A750del, 790M, C797S, C797G

V600E

Class I

Acquired (osimertinib)

TP53 splice

13

M

50

LB

L747_S752del

K601E

Class II

Acquired (osimertinib)

TP53 R248G

14

F

70

TB

L858R, T790M, C797S

V600E

Class I

Acquired (osimertinib)

TP53 K120E, BRCA S237Y (VUS)

15

M

52

TB

L747_A750delinsP T790M, C797G

V600E

Class I

Acquired (osimertinib)

CTNNB1 S37C, ATM R1437K (VUS)

  1. Patients with lung adenocarcinoma harboring activating EGFR mutations and co-occurring BRAF mutations were collected from three different cancer centers. Class I and class II (RAS-independent) BRAF mutations result in activation of the BRAF kinase and the MAPK pathway. Class III (RAS-dependent) BRAF mutations result in impaired BRAF kinase activity and amplify ERK signaling based upon upstream activating signals. BRAFS605C/N mutations (variants) lie within the kinase domain of the BRAF protein, they are not yet functionally classified. TB tissue biopsy, LB liquid biopsy.