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Front Oncol: Exploration of the efficacy of different treatment strategies for patients with MET amplification after EGFR-TKI treatment progresses in EGFR-mutant NSCLC patients

 Last Update: 2021-10-10
 Source: Internet
 Author: User

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The standard treatment for patients with advanced EGFR-mutant non-small cell lung cancer is EGFR-TKI inhibitors
.

But it is inevitable that the problem of drug resistance

The standard treatment for patients with advanced EGFR-mutant non-small cell lung cancer is EGFR-TKI inhibitors

The study included patients with advanced NSCLC with EGFR mutations who were treated in the hospital between March 2015 and March 2020
.

All patients received first-line or second-line treatment with EGFR-TKI, NGS analysis was performed after progression, and patients with EGFR mutations and MET amplification were subjected to final analysis

The study included patients with advanced NSCLC with EGFR mutations who were treated in the hospital between March 2015 and March 2020

A total of 70 patients were included in the study, of which 38 were treated with EGFR-TKI+crizotinib, 10 were treated with crizotinib alone, and 22 were treated with chemotherapy

Among the 38 patients who received EGFR-TKI and crizotinib combination therapy, only 35 patients could be evaluated for efficacy

Efficacy and prognosis

The median real-world PFS (rwPFS) of patients receiving EGFR-TKI combined with crizotinib was compared with crizotinib monotherapy (5.
0 vs.
2.
3 months; p = 0.
007; HR = 0.
88, 95% CI (0.
42-2.
42) ), adjusted p = 0.
036) and chemotherapy (5.
0 vs.
2.
9 months; p = 0.
038; HR = 0.
72, 95% CI (0.
32, 2.
06), adjusted p = 0.
024) were significantly longer
.

However, the median OS of patients receiving EGFR-TKI combined with crizotinib was higher than that of crizotinib alone (10 vs.

The median real-world PFS (rwPFS) of patients receiving EGFR-TKI combined with crizotinib was compared with crizotinib monotherapy (5.

Patients with TP53 mutations, who received EGFR-TKI + crizotinib (n = 17) for median rwPFS bicrizotinib monotherapy (n = 8) (6.

Prognosis with TP53 mutation

The median rwPFS of patients with EGFR amplification who received EGFR-TKI + crizotinib (n = 13) was longer than that of crizotinib alone (5.
0 vs 1.
2 months, p = 0.
017, adjp = 0.
046), The median OS was also significantly longer (10.
0 vs.
3.
0 months, p = 0.
02, adjp = 0.
019)
.

Compared with chemotherapy (n = 12) treatment, median rwPFS (5.

The median rwPFS of patients with EGFR amplification who received EGFR-TKI + crizotinib (n = 13) was longer than that of crizotinib alone (5.

Prognosis of combined EGFR amplification

Potential acquired resistance mechanisms after EGFR-TKI+crizotinib treatment include: EGFR-T790M (n= 2), EGFR- 1718q (n=1), EGFR-s645c (n=1), MET-D1228H ( n=1), BRAF-V600E(n=1), NRAS-Q61H(n=1), KRAS-amp(n=1), ERBB2-amp(n=1), CDK4-amp(n=1), MYC-amp (n=1)
.

The most common treatment-related toxicities are neutropenia (n = 16, 22.
9%) and fatigue (n = 13, 18.
6%)
.
In 38 patients treated with EGFR-TKI combined with crizotinib, grade 1-2 neutropenia (n=5), grade 1-3 transaminase elevation (n=4), grade 1-2 vomiting (n=4), grade 1-2 diarrhea (n=4) and grade 1-3 rash (n=4) are the most common adverse reactions
.
Among the 10 patients who received crizotinib monotherapy, the most common adverse reactions were grade 1-2 vomiting (n = 3) and diarrhea (n = 2)
.
Among 22 patients who received chemotherapy, grade 1-3 neutropenia (n = 10) and fatigue (n = 8) were the most common adverse reactions
.
Six patients receiving EGFR-TKI combined with crizotinib (15.
8%) and three patients receiving chemotherapy (13.
6%) observed treatment-related toxicity of grade 3 or above (p = 0.
591)
.
No adverse events of grade IV, fatal or unexpected were observed
.

Adverse reactions

In summary, this real-world retrospective study table shows that dual inhibition of EGFR and MET may be an effective treatment after EGFR-TKI treatment resistance
.

In summary, this real-world retrospective study table shows that dual inhibition of EGFR and MET may be an effective treatment after EGFR-TKI treatment resistance
.
This real-world retrospective study table shows that dual inhibition of EGFR and MET may be an effective treatment after EGFR-TKI treatment of drug resistance
.
This real-world retrospective study table shows that dual inhibition of EGFR and MET may be an effective treatment after EGFR-TKI treatment of drug resistance
.

Original source:

Liu L, Qu J, Heng J, Zhou C, Xiong Y, Yang H, Jiang W, Zeng L, Zhu S, Zhang Y, Tan J, Hu C, Deng P and Yang N (2021) A Large Real-World Study on the Effectiveness of the Combined Inhibition of EGFR and MET in EGFR-Mutant Non-Small-Cell Lung Cancer After Development of EGFR-TKI Resistance.
Front.
Oncol.
11:722039.
doi: 10.
3389/fonc.
2021.
722039

Liu L, Qu J, Heng J, Zhou C, Xiong Y, Yang H, Jiang W, Zeng L, Zhu S, Zhang Y, Tan J, Hu C, Deng P and Yang N (2021) A Large Real-World Study on the Effectiveness of the Combined Inhibition of EGFR and MET in EGFR-Mutant Non-Small-Cell Lung Cancer After Development of EGFR-TKI Resistance Front Oncol 11:.
.
.
722039 doi:.
10.
3389 / fonc.
2021.
722039 in this message

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