Ibrutinib plus rituximab vs ibrutinib monotherapy in patients with Waldenström macroglobulinemia: a pooled analysis.

However, the benefit of adding rituximab remains unclear, and a prospective trial to compare these two regimens has not been undertaken.

然而，添加利妥昔单抗的益处仍不明确，且尚未进行比较这两种方案的前瞻性试验。

Therefore, we performed a pooled analysis of prospective studies to compare their effectiveness.

因此，我们对前瞻性研究进行了汇总分析，以比较它们的有效性。

Patient-level demographic, response, and survival data were pooled from three prospective studies (ClinicalTrials.gov identifiers: NCT01614821, NCT02604511, NCT02165397).

从三项前瞻性研究（ClinicalTrials.gov标识符：NCT01614821、NCT02604511、NCT02165397）中汇总了患者级别的人口统计学、反应和生存数据。

We included patients treated with I+R or I, excluding those without MYD88 mutations.

我们纳入了接受I+R或I治疗的患者，排除了没有MYD88突变的患者。

Among 174 patients (58 I+R, 116 I), very good partial response (VGPR) rates were comparable across treatment groups (38% I+R vs 28% I; P = .21).

在174名患者中（58名接受I+R治疗，116名接受I治疗），非常好的部分缓解（VGPR）率在治疗组之间是可比的（38%的I+R组对比28%的I组；P = .21）。

The 48-month progression-free survival(PFS) rate was 74% with I+R vs 61% with I (P = .22).

48个月无进展生存（PFS）率在I+R组为74%，而在I组为61%（P = .22）。

The 48-month overall survivalrate was 94% vs 89% (P = .45).

48个月总生存率在两组间分别为94%和89%（P = .45）。

In patients with CXCR4 mutations, I+R trended toward higher VGPR (27% vs 11%; P = .10), and had a superior 48-month PFS rate (72% vs 43%; P = .03).

在携带CXCR4突变的患者中，I+R治疗趋向于更高的完全缓解率（27%对比11%；P = .10），并且在48个月时具有更优越的无进展生存率（72%对比43%；P = .03）。

CXCR4 mutations were associated with inferior VGPR (42% vs 17%; P = .001) and 48-month PFS in the I arm (43% vs 72%; P = .002).

CXCR4突变与I治疗组中较低的完全缓解率（42%对比17%；P = .001）和48个月的无进展生存率（43%对比72%；P = .002）相关。

In the I+R arm, CXCR4 mutations were associated with numerically inferior VGPR (47% vs 27%; P = .12), but the 48-month PFS rate was not impacted (74% vs 72%; P = .96).

在接受I+R治疗的患者中，CXCR4突变与较低的VGPR（47%对比27%；P = .12）相关，但48个月的PFS率并未受影响（74%对比72%；P = .96）。

I+R significantly improved PFS over I in patients with CXCR4-mutated WM, along with a nonsignificant increase in VGPR in this subgroup.

对于携带CXCR4突变的WM患者，I+R显著改善了PFS，同时在这一亚组中，VGPR的增加并不显著。

These results support routine CXCR4 testing in patients with WM, and clinical trials of rituximab with covalent or noncovalent Bruton tyrosine kinase inhibitors.

这些结果支持在WM患者中常规进行CXCR4检测，并进行利妥昔单抗与共价或非共价布鲁顿酪氨酸激酶抑制剂的临床试验。