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The standard treatment for patients with EGFR-mutant advanced NSCLC is EGFR-TKI.
Although it is effective, resistance will inevitably occur eventually
.
After progression on EGFR-TKI therapy, the optimal follow-up treatment is unclear
The standard treatment for patients with EGFR-mutant advanced NSCLC is EGFR-TKI.
We screened patients with advanced NSCLC with EGFR mutations diagnosed between January 2015 and December 2020, who received chemotherapy-antiangiogenic or chemotherapy-immunotherapy combination therapy after EGFR-TKI resistance
.
Patient information was collected and objective response rate (ORR), disease control rate (DCR), and progression-free survival (PFS) were assessed
We screened patients with advanced NSCLC with EGFR mutations diagnosed between January 2015 and December 2020, who received chemotherapy-antiangiogenic or chemotherapy-immunotherapy combination therapy after EGFR-TKI resistance
A total of 144 patients were included, the median age of all patients was 61 years (range, 19-76 years), and 52.
Of the 144 patients, 131 (91.
The ORR and DCR of all patients treated with EGFR-TKIs were 60.
After progression on EGFR-TKI therapy, chemotherapy-immune combination therapy resulted in a higher objective response rate (ORR) than chemotherapy-antiangiogenic combination therapy (29.
In subgroup analysis, ORR and PFS were not significantly different in patients with 19del and L858R mutations who received chemotherapy-antiangiogenic combination therapy (ORR: 10.
9% vs.
11.
8%, P=1.
000; median PFS: 7.
74 vs.
7.
30 month, P=0.
702, HR=0.
920, 95% CI: 0.
594 1.
426)
.
In addition, T790m-positive and T790m-negative patients had similar ORR and PFS after TKI resistance (ORR: 9.
In subgroup analysis, ORR and PFS were not significantly different in patients with 19del and L858R mutations who received chemotherapy-antiangiogenic combination therapy (ORR: 10.
For patients receiving combined immunochemotherapy, ORR and PFS were better in the EGFR L858R mutation group than in the 19del mutation group, but not significantly different (ORR: 33.
3% vs.
22.
7%, P=0.
438; median PFS: 7.
59 vs.
5.
65 month, P=0.
798, HR=0.
899, 95% CI: 0.
392-2.
059)
.
3% vs.
22.
7%, P=0.
438; median PFS: 7.
59 vs.
5.
65 month, P=0.
798, HR=0.
899, 95% CI: 0.
392-2.
059)
.
For patients receiving combined immunochemotherapy, ORR and PFS were better in the EGFR L858R mutation group than in the 19del mutation group, but not significantly different (ORR: 33.
However, patients with secondary T790M mutation after EGFR-TKI treatment were less likely to benefit from the combination chemotherapy-immunotherapy (ORR: 14.
Multivariate analysis showed that in the chemotherapy-antiangiogenesis group, only platelet count ≤ 373 10 9 /L was independently associated with prolonged PFS (P=0.
037, HR =0.
334, 95% CI: 0.
119 0.
937)
.
In the chemotherapy-immunotherapy group, platelet count ≤ 264 10 9 /L was independently associated with prolonged PFS (P=0.
028, HR =0.
256, 95% CI: 0.
076 0.
865)
.
037, HR =0.
334, 95% CI: 0.
119 0.
937)
.
In the chemotherapy-immunotherapy group, platelet count ≤ 264 10 9 /L was independently associated with prolonged PFS (P=0.
028, HR =0.
256, 95% CI: 0.
076 0.
865)
.
Multivariate analysis showed that in the chemotherapy-antiangiogenesis group, only platelet count ≤ 373 10 9 /L was independently associated with prolonged PFS (P=0.
037, HR =0.
334, 95% CI: 0.
119 0.
937)
.
In the chemotherapy-immunotherapy group, platelet count ≤ 264 10 9 /L was independently associated with prolonged PFS (P=0.
028, HR =0.
256, 95% CI: 0.
076 0.
865)
.
In conclusion, the study shows that the efficacy of chemotherapy-immunotherapy combination therapy is comparable to that of chemotherapy-antiangiogenesis combination therapy after EGFR-TKI treatment failure
.
For patients with EGFR T790M mutation, chemotherapy-antiangiogenic combination therapy may be the preferred treatment option
.
Furthermore, platelet count may be a potential prognostic factor in patients after EGFR-TKI treatment failure
.
.
For patients with EGFR T790M mutation, chemotherapy-antiangiogenic combination therapy may be the preferred treatment option
.
Furthermore, platelet count may be a potential prognostic factor in patients after EGFR-TKI treatment failure
.
Studies have shown that the efficacy of chemotherapy-immunotherapy combination therapy is comparable to that of chemotherapy-antiangiogenic combination therapy after EGFR-TKI treatment failure
.
For patients with EGFR T790M mutation, chemotherapy-antiangiogenic combination therapy may be the preferred treatment option
.
Furthermore, platelet count may be a potential prognostic factor in patients after EGFR-TKI treatment failure
.
Studies have shown that the efficacy of chemotherapy-immunotherapy combination therapy is comparable to that of chemotherapy-antiangiogenic combination therapy after EGFR-TKI treatment failure
.
For patients with EGFR T790M mutation, chemotherapy-antiangiogenic combination therapy may be the preferred treatment option
.
Furthermore, platelet count may be a potential prognostic factor in patients after EGFR-TKI treatment failure
.
Original source:
Original source:Yu X, Li J, Ye L, Zhao J, Xie M, Zhou J, Shen Y, Zhou F, Wu Y, Han C, Qian J, Chu T, Su C.
Real-world outcomes of chemo-antiangiogenesis versus chemo- immunotherapy combinations in EGFR-mutant advanced non-small cell lung cancer patients after failure of EGFR-TKI therapy.
Transl Lung Cancer Res 2021;10(9):3782-3792.
doi: 10.
21037/tlcr-21-681
Real-world outcomes of chemo-antiangiogenesis versus chemo- immunotherapy combinations in EGFR-mutant advanced non-small cell lung cancer patients after failure of EGFR-TKI therapy.
Transl Lung Cancer Res 2021;10(9):3782-3792.
doi: 10.
21037/tlcr-21-681 Leave a comment here