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Table 2 Resistant mechanism, individual therapy strategy and efficacy in PG

From: Chemotherapy versus personalized therapy for EGFR mutant lung adenocarcinoma resistance to EGFR-tyrosine kinase inhibitors: a retrospective dual-center study

Rsistance mechanism

Drugs

Number

ORR

DCR

PFS (m)

MET amplification

MET plus EGFR-TKIs

27

40.7%

87.7%

4.2

SCLC transformation

Etoposide plus platinum or carboplatin

16

37.5%

75.0%

3.9

BRAF mutation

Dabrafenib, trametinib and EGFR-TKIs,

3

33.3%

33.3%

2.9

ERBB2 amplification

Trastuzumab, chemotherapy and EGFR-TKIs

4

0%

100%

-

RET fusion

LOXO-292 plus EGFR-TKIs

1

0%

0%

0.9

T790M-trans-C797S

the 1st and 3rd EGFR-TKIs

2

0%

50%

0.7

  1. PG Personalized group, ORR Objective response rate, DCR Disease control rate, PFS Progression-free survival