Immune checkpoint inhibitor therapy in Asian population with metastatic diseaseEfficacy and safety in gastric cancer patients have been proven, but the efficacy and safety in the western real world are still lacking
.
Therefore, a multicenter retrospective real-world study was carried out abroad to evaluate the efficacy and safety of immune checkpoint inhibitors in Western patients with previously treated metastatic gastric cancer
.
The results were published in the journal BMC Cancer
.
.
Therefore, a multicenter retrospective real-world study was carried out abroad to evaluate the efficacy and safety of immune checkpoint inhibitors in Western patients with previously treated metastatic gastric cancer
.
The results were published in the journal BMC Cancer
.
immunitystomach cancer
Overall, between November 2015 and April 2020, 50 patients with metastatic gastric/gastroesophageal junction (GEJ) cancer who received nivolumab or pembrolizumab palliatively were included
.
The median age was 58, with a range from 27 to 87
.
A quarter of the patients were 65 years or older
.
Most (84%) patients had ECOG=1
.
DNA mismatch repair deficiency was detected in 16% of patients, and PD-L1 positive expression was detected in 48% of patients
.
In the nivolumab subgroup (n = 19), PD-L1 positivity and microsatellite instability were 32% (n = 6) and 5% (n = 1), respectively
.
In the pembroli-zumab subgroup (n = 31), PD-L1 positivity and microsatellite instability were 58% (n = 18) and 23% (n = 7), respectively
.
.
The median age was 58, with a range from 27 to 87
.
A quarter of the patients were 65 years or older
.
Most (84%) patients had ECOG=1
.
DNA mismatch repair deficiency was detected in 16% of patients, and PD-L1 positive expression was detected in 48% of patients
.
In the nivolumab subgroup (n = 19), PD-L1 positivity and microsatellite instability were 32% (n = 6) and 5% (n = 1), respectively
.
In the pembroli-zumab subgroup (n = 31), PD-L1 positivity and microsatellite instability were 58% (n = 18) and 23% (n = 7), respectively
.
The ORR for treatment was 10% (n = 5), while the DCR was 32% (n = 16)
.
The median PFS and OS for the entire cohort were 2.
1 months (95% CI: 1.
4-2.
8) and 6.
3 months (95% CI: 3.
3-9.
3), respectively
.
.
The median PFS and OS for the entire cohort were 2.
1 months (95% CI: 1.
4-2.
8) and 6.
3 months (95% CI: 3.
3-9.
3), respectively
.
The ORR for treatment was 10% (n = 5), while the DCR was 32% (n = 16)
.
The median PFS and OS for the entire cohort were 2.
1 months (95% CI: 1.
4-2.
8) and 6.
3 months (95% CI: 3.
3-9.
3), respectively
.
OS and PFS
OS and PFSBy microsatellite status (MSS: 6.
3 vs.
MSI: 11.
5 months; HR = 1.
21, 95% CI: 0.
5-3.
1; p = 0.
69) or PD-L1 status (negative: 9.
3 months vs.
positive: 7.
2 months ; HR = 0.
87, 95% CI : 0.
4-2.
1; no p = 0.
74) difference in median OS statistical significance
.
3 vs.
MSI: 11.
5 months; HR = 1.
21, 95% CI: 0.
5-3.
1; p = 0.
69) or PD-L1 status (negative: 9.
3 months vs.
positive: 7.
2 months ; HR = 0.
87, 95% CI : 0.
4-2.
1; no p = 0.
74) difference in median OS statistical significance
.
statistics
By microsatellite status (MSS: 2.
5 months vs.
MSI: 7.
7 months; HR = 1.
71, 95% CI: 0.
7-4.
3; p = 0.
26) or PD-L1 status (negative: 2.
1 vs.
positive: 4.
4 months ; HR = 1.
01, 95% CI: 0.
5-2.
3; p = 0.
90), the difference in median PFS was not statistically significant
.
5 months vs.
MSI: 7.
7 months; HR = 1.
71, 95% CI: 0.
7-4.
3; p = 0.
26) or PD-L1 status (negative: 2.
1 vs.
positive: 4.
4 months ; HR = 1.
01, 95% CI: 0.
5-2.
3; p = 0.
90), the difference in median PFS was not statistically significant
.
The prognosis of patients with GEJ tumors was significantly better than that of patients with primary gastric tumors (median OS, 12.
6 vs 6.
2 months; HR = 0.
47, 95% CI: 0.
2 -0.
9; p = 0.
03)
.
There was no significant difference in prognosis between patients with different pathological types (intestinal type: 3.
5 months versus signet ring cells: 7.
2 months versus nonspecific adenocarcinoma: 16.
3 months; p = 0.
06)
.
6 vs 6.
2 months; HR = 0.
47, 95% CI: 0.
2 -0.
9; p = 0.
03)
.
There was no significant difference in prognosis between patients with different pathological types (intestinal type: 3.
5 months versus signet ring cells: 7.
2 months versus nonspecific adenocarcinoma: 16.
3 months; p = 0.
06)
.
The prognosis of patients with GEJ tumors was significantly better than that of patients with primary gastric tumors (median OS, 12.
6 vs 6.
2 months; HR = 0.
47, 95% CI: 0.
2 -0.
9; p = 0.
03)
.
The prognosis of patients with GEJ tumors was significantly better than that of patients with primary gastric tumors (median OS, 12.
6 vs 6.
2 months; HR = 0.
47, 95% CI: 0.
2 -0.
9; p = 0.
03)
.
There was no significant difference in prognosis between patients with different pathological types (intestinal type: 3.
5 months versus signet ring cells: 7.
2 months versus nonspecific adenocarcinoma: 16.
3 months; p = 0.
06)
.
Median OS was significantly shorter in patients with ECOG PS ≥ 2 than in patients with ECOG PS ≤ 1 (2.
7 versus 8.
2 months; HR = 2.
50, 95% CI: 1.
1–5.
9; p = 0.
03)
.
The prognosis was better with first- or second-line PD-1 inhibitor therapy than with later-line therapy (19.
0 versus 4.
7 months; HR = 0.
32, 95% CI: 0.
1–0.
8; p = 0.
01)
.
7 versus 8.
2 months; HR = 2.
50, 95% CI: 1.
1–5.
9; p = 0.
03)
.
The prognosis was better with first- or second-line PD-1 inhibitor therapy than with later-line therapy (19.
0 versus 4.
7 months; HR = 0.
32, 95% CI: 0.
1–0.
8; p = 0.
01)
.
Median OS was significantly shorter in patients with ECOG PS ≥ 2 than in patients with ECOG PS ≤ 1 (2.
7 versus 8.
2 months; HR = 2.
50, 95% CI: 1.
1–5.
9; p = 0.
03)
.
The prognosis was better with first- or second-line PD-1 inhibitor therapy than with later-line therapy (19.
0 versus 4.
7 months; HR = 0.
32, 95% CI: 0.
1–0.
8; p = 0.
01)
.
Median OS was significantly shorter in patients with ECOG PS ≥ 2 than in patients with ECOG PS ≤ 1 (2.
7 versus 8.
2 months; HR = 2.
50, 95%CI: 1.
1–5.
9; p = 0.
03)
.
The prognosis was better with first- or second-line PD-1 inhibitor therapy than with later-line therapy (19.
0 versus4.
7 months; HR = 0.
32, 95% CI: 0.
1–0.
8; p = 0.
01)
.
Different subgroup analysis of OS
Different Subgroup Analysis OS Different Subgroup Analysis OS Different Subgroup Analysis OSMetastasis time points (synchronous: 6.
3 months vs.
metachronous: 8.
2 months; HR = 1.
19, 95% CI: 0.
6-2.
3; P = 0.
60), peritoneal metastases (No: 6.
2 months vs.
Yes: 7.
2 months; HR = 1.
24, 95% CI: 0.
6-2.
5; p = 0.
54) and HER2 status (negative: 7.
0 months vs positive: 3.
0 months; HR = 0.
9, 95% CI: 0.
4-2.
2; p = 0.
83) There was no significant effect on median OS
.
3 months vs.
metachronous: 8.
2 months; HR = 1.
19, 95% CI: 0.
6-2.
3; P = 0.
60), peritoneal metastases (No: 6.
2 months vs.
Yes: 7.
2 months; HR = 1.
24, 95% CI: 0.
6-2.
5; p = 0.
54) and HER2 status (negative: 7.
0 months vs positive: 3.
0 months; HR = 0.
9, 95% CI: 0.
4-2.
2; p = 0.
83) There was no significant effect on median OS
.
Taken together, this study supports immune checkpoint inhibitor therapy in previously treated patients with metastatic gastric or gastroesophageal junction (GEJ)
.
.
This study supports immune checkpoint inhibitor therapy in previously treated patients with metastatic gastric or gastroesophageal junction (GEJ)
.
This study supports immune checkpoint inhibitor therapy in previously treated patients with metastatic gastric or gastroesophageal junction (GEJ)
.
Original source:
Original source:Schlintl V, Huemer F, Rinnerthaler G, Melchardt T, Winder T, Reimann P, Riedl J, Amann A, Eisterer W, Romeder F, Piringer G, Ilhan-Mutlu A, Wöll E, Greil R, Weiss L.
Checkpoint inhibitors in metastatic gastric and GEJ cancer: a multi-institutional retrospective analysis of real-world data in a Western cohort.
BMC Cancer.
2022 Jan 10;22(1):51.
doi: 10.
1186/s12885-021-09115-6.
PMID: 35012477; PMCID: PMC8744304.
Checkpoint inhibitors in metastatic gastric and GEJ cancer: a multi-institutional retrospective analysis of real-world data in a Western cohort.
BMC Cancer.
2022 Jan 10;22(1):51.
doi: 10.
1186/s12885-021-09115-6.
PMID: 35012477; PMCID: PMC8744304.
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