The prediction of clinical recurrence is significantly influenced by the transition from pathological complete response (pCR) to neoadjuvant chemotherapy (NAC). ∼16% of patients who achieve pCR may still encounter disease recurrence, whereas 45% of patients with recurrent disease do not. Longitudinal circulating tumor DNA (ctDNA) testing presents a less invasive method for monitoring the response to treatment in early breast cancer (BC) patients undergoing NAC.
This study aimed to determine whether the status and changes in ctDNA can effectively predict the tumor response to NAC and the likelihood of recurrence in patients with early BC.
This was an observational, retrospective, single-center study to investigate whether ctDNA can predict tumor response to NAC and prognosis in patients with breast cancer. Seventy-four patients received standard-of-care NAC, and 4 were treated with adjuvant therapy.
At diagnosis, baseline blood samples were collected from 44 patients and longitudinally during treatment from 34 patients. Reported outcomes included tumor response and progression. The status and dynamics of ctDNA were correlated with pathologic and radiologic outcomes.
Results indicated that 29 patients with triple-negative breast cancer (TNBC) were ctDNA-positive at baseline, and 6 were ctDNA-negative. Of the 29 patients, early ctDNA clearance by week 6 of NAC was observed in 10 patients, weeks 7-16 in 9 patients, clearance post-surgery in 1 patient, and 3 patients remained ctDNA-positive after surgery. Currently, serial ctDNA testing is underway for the remaining 6 patients.
All patients with TNBC who had a radiological complete response (CR) had early ctDNA clearance. After completion of NAC, there was a radiological partial response (PR) in all patients with persistent ctDNA positivity levels. Of the 9 patients with TNBC with undetectable baseline ctDNA, 33% achieved CR, and 43% achieved pathologic CR. Of the 19 patients with TNBC with ctDNA clearance in response to NAC, 89% (17/19) remained ctDNA-negative, with no evidence of disease.
One patient initially cleared their ctDNA on NAC before turning ctDNA-positive 4 weeks prior to radiological recurrence, and another patient with ctDNA clearance on NAC remained ctDNA post-surgery but experienced recurrence. All (n=3) patients with TNBC with persistent ctDNA positivity levels after curative treatment (NAC and surgery) had disease recurrence. All 6 patients with undetectable baseline ctDNA continued to be ctDNA-negative regardless of their disease status. At diagnosis, 8/9 estrogen receptor (ER)-positive patients were also ctDNA-positive.
Close to 40% of patients who were ER-positive with positive baseline ctDNA had early clearance of ctDNA after NAC. All 3 patients had residual disease on pathology. One-fourth of patients had ctDNA+ after surgery, and neither achieved radiologic CR or pCR. The remaining 3 patients are ongoing NAC.
Monitoring with ctDNA in the early stages of TNBC enables the prediction of tumor response to NAC and the customization of therapeutic regimens.
The persistence of ctDNA can predict early recurrence and help identify patients who may need treatment escalation or enrollment in clinical trials. Despite the limited patient population, the clearance of ctDNA does not serve as a reliable predictor for the response to NAC in ER-positive breast cancer.
The standard first-line treatment for human receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced breast cancer involves a combination of CDK4/6 inhibitors and endocrine therapy (ET). Although disease progression is common in patients with advanced breast cancer, the most effective treatment for those who experience progression on a CDK4/6 inhibitor plus ET is still uncertain.
Real-world evidence indicates that using abemaciclib, an oral CDK4/6 inhibitor with greater selectivity for CDK4, after disease progression on a previous CDK4/6 inhibitor can extend progression-free survival (PFS) in advanced breast cancer. However, other trials with other CDK4/6 inhibitors have produced mixed results.
This study presents the primary outcome analysis of the phase 3 postMONARCH trial (NCT05169567), which evaluated fulvestrant plus abemaciclib or placebo in patients with HR-positive, HER2-negative advanced breast cancer after disease progression on a prior CDK4/6 inhibitor plus ET. The postMONARCH trial was a global, double-blind, placebo-controlled study where patients were randomized 1:1 to receive either abemaciclib plus fulvestrant or placebo plus fulvestrant.
Patients eligible for the study had experienced disease progression on a CDK4/6 inhibitor plus aromatase inhibitor as initial therapy for advanced breast cancer or had a relapse on/after a CDK4/6 inhibitor plus endocrine therapy as adjuvant treatment for early breast cancer.
Only patients with no prior treatment for advanced breast cancer could participate. The study’s primary endpoint was investigator-assessed PFS, and secondary endpoints included PFS assessed by a blinded independent central review (BICR), overall survival, objective response rate (ORR), and safety.
With an assumed hazard ratio (HR) of 0.7, the study had ∼80% power to detect superiority for abemaciclib while maintaining a cumulative 2-sided type I error of 0.05. The Kaplan-Meier method was utilized to estimate progression-free survival curves, and the treatment effect was estimated using a stratified Cox proportional hazard model.
A total of 368 patients were randomly assigned to receive either abemaciclib plus fulvestrant (n=182) or placebo plus fulvestrant (n=186). Prior use of a CDK4/6 inhibitor included palbociclib (59%), ribociclib (33%), and abemaciclib (8%) in the abemaciclib plus fulvestrant arm and 59%, 33%, and 8%, respectively, in the placebo plus fulvestrant arm.
The interim analysis showed that the study met the predetermined criteria for significantly improved investigator-assessed PFS with abemaciclib plus fulvestrant compared to placebo plus fulvestrant (HR, 0.66; 95% confidence interval [CI], 0.48-0.91; P=.01).
In the primary analysis (HR, 0.73; 95% CI, 0.57-0.95), with PFS rates at 6 months of 50% versus 37% for the abemaciclib and placebo groups, respectively. The ORR was higher with abemaciclib compared to placebo, 17% versus 7% in patients with measurable disease. According to BICR, PFS also showed improvement (HR, 0.55; 95% CI, 0.39-0.77). Safety was consistent with what has been previously reported with abemaciclib, and the discontinuation rate due to adverse events was low (6%).
The combination of abemaciclib and fulvestrant exhibited a notable enhancement in PFS among patients with HR-positive, HER2-negative advanced breast cancer after disease progression on a CDK 4/6 inhibitor.
This combination also consistently improved across key secondary efficacy endpoints, including PFS by BICR and ORR, without any new safety signals in this patient population. This study’s results indicate that patients benefit from continued CDK4/6 inhibition with abemaciclib plus fulvestrant following progression on a CDK 4/6 inhibitor.
Circulating tumor DNA (ctDNA) has the potential to address the constraints associated with tissue biopsy in individuals diagnosed with metastatic breast cancer (mBC). Unlike tissue biopsy, which offers a single snapshot of the tumor’s molecular characteristics at a specific location and moment, ctDNA presents a more comprehensive view of the tumor genome. Serial liquid biopsies can be conveniently collected to monitor clinical responses and the development of resistance over time.
The Individualized Molecular Analyses Guide Efforts in Breast Cancer (IMAGE II) study focuses on assessing the effectiveness of tissue biopsy and serial liquid biopsy techniques in profiling tumor genomics in mBC.
IMAGE II (NCT02965755) is a prospective, multicenter trial designed to assess the clinical effectiveness of liquid biopsy compared with tissue biopsy. Participants included individuals with mBC of any subtype who showed progression necessitating a change in therapy.
As per standard care, tissue biopsy sequencing was mandatory unless a biopsy was not feasible. At the time of enrollment, Foundation Medicine obtained baseline plasma samples for tissue-agnostic comprehensive genomic profiling (CGP).
The results of both liquid biopsy and tissue biopsy sequencing were promptly reviewed by the Johns Hopkins Molecular Tumor Board for treatment recommendations. Serial liquid biopsy samples were collected 1 to 2 weeks after starting the next line of therapy, at the first restaging, and at progression. This analysis reports on the data obtained at enrollment, with the results of serial liquid biopsy samples to be disclosed later.
A total of 199 patients were enrolled, 194 of whom were women (median age, 57 years; age range, 27-86 years). There were 140 hormone receptor (HR)-positive–human epidermal growth factor receptor 2 (HER2)-negative, 4 HR-negative–HER2-positive, 20 HR-positive–HER2-positive, and 35 triple-negative breast cancer cases. Metastases were detected solely in the bone in 19 patients, while in 99, they involved the lung. Additionally, metastases were observed in the liver in 97 patients and the brain in 14 patients.
The median prior lines of metastatic therapy were 2, with 22.1% of patients having been on ≥4 therapies, including antibody–drug conjugates (14 patients), immunotherapy (2), cytotoxic chemotherapy (74), endocrine therapy (88), and targeted therapy (12). At the time of enrollment, 9 patients were newly diagnosed with mBC. Overall, 55% underwent tissue biopsy sequencing.
In the CGP results obtained from 190 patients, the genes that exhibited the highest frequency of alterations were TP53 (90 patients), PIK3CA (63 patients), and ESR1 (54 patients). This study revealed copy number amplifications in FGFR1 (21 patients) and FGFR3 (12 patients) and copy number losses in PTEN (3 patients).
Of 87 individuals whose initial liquid biopsy was analyzed using FoundationOne Liquid CDx to calculate ctDNA tumor fraction, 69 (79.3%) patients exhibited detectable ctDNA tumor fraction. Additionally, ≥1% ctDNA tumor fraction was found in 69% of patients.
The high rate of ctDNA tumor fraction identification in patients suffering from mBC highlights the significance of utilizing liquid biopsy for CGP and enables the detection of multiple alteration classes across different mBC subtypes and metastatic sites.
TROP2, also known as trophoblast cell surface antigen 2, exhibits high expression levels in triple-negative breast cancer (TNBC) and is correlated with poorer survival outcomes. Sacituzumab irinotecan (SKB264/MK-2870) is an antibody–drug conjugate targeting TROP2, which utilizes a unique linker to attach a belotecan-derivative topoisomerase I inhibitor as the payload.
This study presents the findings from a phase 3 clinical trial (OptiTROP-Breast01, NCT05347134) that evaluated the efficacy and safety of sacituzumab tirumotecan in patients with advanced TNBC.
In this phase 3 randomized trial, SKB264 was compared with the chemotherapy choices of eribulin, vinorelbine, capecitabine, or gemcitabine as selected by physicians for patients with locally recurrent or metastatic TNBC (mTNBC) who had undergone ≥2 prior treatments, including ≥1 for metastatic disease. The primary endpoint was progression-free survival (PFS) determined by blinded independent central review (BICR).
This study included 263 patients, 130 of whom received SKB264 and 133 of whom received chemotherapy. The primary endpoint of PFS was achieved based on an interim analysis conducted on June 21, 2023. As assessed by BICR, the median PFS was 5.7 months (95% CI, 4.3-7.2) for patients receiving SKB264 and 2.3 months (95% CI, 1.6-2.7) for those receiving chemotherapy.
In the first planned interim analysis for overall survival (OS), the median follow-up was 10.4 months, and the results showed a statistically significant advantage for SKB264 compared with chemotherapy (hazard ratio, 0.53; 95% CI, 0.36-0.78; P=.0005). The most common grade ≥3 treatment-related adverse events observed were neutrophil count decreased (32.3% with SKB264 vs 47.0% with chemotherapy), anemia (27.7% with SKB264 vs 6.1% with chemotherapy), and white blood cell count decreased (25.4% with SKB264 vs 36.4% with chemotherapy).
Sacituzumab tirumotecan monotherapy exhibited notable improvements in PFS and OS compared with chemotherapy in patients with heavily pretreated advanced TNBC and limited treatment alternatives. Furthermore, it maintained a manageable safety profile.
Disparities in the treatment and outcomes of Black patients with estrogen receptor (ER)-positive, human epidermal growth factor receptor 2 (HER2)-negative metastatic breast cancer (mBC) have been documented. There is a lack of data regarding the racial equity of targeted treatment utilization for patients with ER-positive and HER2-negative mBC.
This study analyzed variances in circulating tumor DNA (ctDNA) genomic alterations between Black and White patients with ER-positive, HER2-negative mBC.
In this retrospective cohort study, 1327 patients with mBC underwent ctDNA testing using the Guardant360 assay at Washington University, Massachusetts General Hospital, and Northwestern University. The patients were stratified based on progesterone receptor (PR) status into ER-positive/PR-positive/HER2-negative and ER-positive/PR-negative/HER2-negative subgroups. Overall, 708 (89%) White patients and 87 (11%) Black patients with an ER-positive/HER2-negative subtype were evaluated in this study.
Patients were assessed based on their self-reported race and their utilization of ptdIns-3-kinase subunit alpha (PIK3CA), cyclin-dependent kinase (CDK)4/6, and mammalian target of rapamycin (mTOR) inhibitors by participating in clinical trials following FDA approval. A multivariate logistic analysis was carried out to identify genomic and prognostic variations across different racial groups, with overall survival (OS) calculated from the time of ctDNA testing.
Black patients with PIK3CA single nucleotide variants were significantly less likely to receive targeted therapy than White patients (5.9% vs 28.8% of patients; P=.045), and there was no difference in the detection frequency of PIK3CA mutations between Black (36%) and White (34%) patients. There was no difference in the use of CDK4/6 or mTOR inhibitors. None of the Black patients with PIK3CA mutations were enrolled in clinical trials, compared with 11.5% of White patients.
The likelihood of CCND1 copy number variation was higher in Black patients with ER-positive/PR-positive/HER2-negative tumors than in White patients.
Black patients with PR-negative tumors were more likely to have GATA3 SNV relative to White patients, whereas White PR-negative patients were more likely to harbor a higher KRAS copy number variation prevalence than Black patients.
Among patients with ER-positive/PR-negative/HER2-negative mBC, Black patients had a median OS of 9.1 months, whereas White patients had a median OS of 21 months (P=.00093).
This may be the largest clinic-genomic dataset to date, enabling the comparison of genomic alterations and targeted treatment utilization among different races in mBC.
This analysis revealed notable discrepancies in the use of select inhibitors in Black patients with mBC. The observed differences in OS and participation in clinical trials align with previous studies. Further research is necessary to better understand the drivers of these disparities and ensure all patients have access to treatments.
Lorlatinib, a third-generation ALK tyrosine kinase inhibitor that can penetrate the brain, showed enhanced progression-free survival (PFS) and intracranial (IC) activity compared to crizotinib in treatment-naïve patients with advanced ALK-positive non-small cell lung cancer (NSCLC) in the phase 3 CROWN study. The CROWN study’s long-term efficacy and safety results are now reported after a 5-year follow-up.
In total, 296 patients who had not received any prior treatment and had advanced ALK-positive NSCLC were randomly assigned 1:1 to receive lorlatinib 100 mg once daily (n=149) or crizotinib 250 mg twice daily (n=147). In this post hoc analysis, the efficacy outcomes, safety, and biomarker analyses are reported as assessed by the investigators. No formal statistical testing was conducted.
By October 31, 2023, 74 of 149 patients (50%) were still receiving lorlatinib, while 7 of 142 patients (5%) were still using crizotinib. The median duration of follow-up for progression-free survival (PFS) was 60.2 months (95% CI, 57.4-61.6) for lorlatinib and 55.1 months (95% CI, 36.8-62.5) for crizotinib.
The median PFS (95% CI) was not reached (NR) (NR, 64.3-NR) for lorlatinib, versus 9.1 months (95% CI, 7.4-10.9) for crizotinib (hazard ratio [HR], 0.19; 95% CI, 0.13-0.27). The 5-year PFS (95% CI) was 60% (51-68) for lorlatinib and 8% (3-14) for crizotinib.
The median time to IC progression (95% CI) was not reached (NR; NR-NR) for lorlatinib and 16.4 months (95% CI, 12.7-21.9) for crizotinib (HR, 0.06; 95% CI, 0.03-0.12). In patients without baseline brain metastases in the lorlatinib group, brain progression was observed in 4 of 114 patients, all within the initial 16 months of therapy. Grade 3/4 adverse events (AEs) were reported in 77% of patients receiving lorlatinib and 57% of those on crizotinib.
Treatment-based AEs led to treatment discontinuation in 5% and 6% of patients in the lorlatinib and crizotinib groups, respectively. The safety profile remained consistent with previous analyses, and no new ALK mutations were detected in circulating tumor DNA after lorlatinib treatment (n=31).
After a 5-year follow-up, the lorlatinib arm had not reached the median PFS, setting a record for the longest PFS reported in advanced NSCLC. These results, combined with the absence of any new safety issues, demonstrate the extraordinary improvement in outcomes for individuals with advanced ALK-positive NSCLC.
The EVOKE-01 study, a phase 3 trial with an open-label design, compared sacituzumab govitecan (SG) to docetaxel as a standard-of-care treatment for metastatic non–small cell lung cancer (mNSCLC) patients who had experienced disease progression following platinum-based chemotherapy, anti–programmed death-ligand 1 (PD-L1) therapy, and targeted treatment for actionable genomic alterations (AGAs). These are the primary analysis results.
Patients were randomly assigned 1:1 and stratified by histology, superior response to the previous anti–PD-L1-containing regimen, and whether AGA treatment was received to either SG (one 10 mg/kg intravenous [IV] infusion on days 1 and 8) or docetaxel (one 75 mg/m2 IV infusion on day 1) in 21-day cycles.
The primary focus of the study was overall survival (OS), while key secondary endpoints included investigator-assessed progression-free survival (PFS), objective response rate, patient-reported symptom assessment, and safety.
In the intent-to-treat population, which consisted of 299 patients in the SG group and 304 patients in the docetaxel group, 55.4% had received 1 previous line of therapy. The median follow-up period was 12.7 months, ranging from 6 to 24 months.
Although the primary endpoint was not achieved, OS for SG improved compared to docetaxel, with a median OS of 11.1 months versus 9.8 months, respectively (hazard ratio [HR], 0.84; 95% confidence interval [CI], 0.68-1.04], 1-sided; P=.0534). This trend was consistent across squamous and nonsquamous histologies.
The median PFS was 4.1 months for SG and 3.9 months for docetaxel (HR, 0.92; 95% CI, 0.77-1.11). An OS benefit was noted for SG in comparison to docetaxel among patients with mNSCLC who were nonresponsive to the last anti–PD-L1-containing regimen, showing a 3.5-month median OS increase and an HR of 0.75 (95% CI, 0.58-0.97), which was consistent across different histologies.
The discontinuation rate due to treatment-related adverse events (TRAEs) was 6.8% for SG and 14.2% for docetaxel, respectively, with TRAEs leading to death in 1.4% and 1.0% of patients, respectively.
Despite not reaching statistical significance, SG improved OS compared to docetaxel, which was consistent across different histologies. A clinically significant enhancement in OS was observed in patients with mNSCLC who did not respond to the last anti–PD-L1-containing regimen.
SG demonstrated better tolerability than docetaxel and maintained its established safety profile, with no new safety concerns identified.
The bispecific antibody, ivonescimab (AK112/SMT112), acts as an anti–programmed death-1 (PD-1)/vascular endothelial growth factor (VEGF) agent. Promising results from phase 1/2 clinical trials have indicated its potential efficacy in patients with non-small cell lung cancer (NSCLC) accompanied by epidermal growth factor receptor (EGFR) mutations who had previously undergone unsuccessful EGFR-tyrosine kinase inhibitor (TKI) therapies.
This phase 3 study was conducted to investigate further and confirm the effectiveness and safety of combining ivonescimab with chemotherapy instead of chemotherapy alone. This study enrolled patients who were randomly assigned 1:1 to ivonescimab (20 mg/kg) plus pemetrexed (500 mg/m2) and carboplatin or placebo in combination with chemotherapy.
This treatment was administered once every 3 weeks for 4 cycles. Stratification was done based on the use of third-generation EGFR-TKI (received/not received) and the presence or absence of brain metastases. Following the initial cycles, patients underwent maintenance therapy with either ivonescimab and pemetrexed or placebo and pemetrexed.
The study’s main objective was to evaluate progression-free survival (PFS) in the intent-to-treat population. An independent radiographic review committee (IRRC) conducted this assessment using RECIST (version 1.1) criteria.
A total of 322 patients were randomly assigned to either the ivonescimab plus chemotherapy arm (161 patients) or the placebo plus chemotherapy arm (161 patients). The percentage of patients who had received third-generation EGFR-TKIs treatment was 86.3% versus 85.1%, respectively, and the percentage of patients with brain metastases was 21.7% versus 23.0%, respectively.
As of March 10, 2023, the median follow-up time was 7.89 months. PFS was significantly more effective in the ivonescimab plus chemotherapy arm (hazard ratio [HR], 0.46 [0.34, 0.62]; P<.0001).
The median PFS (95% confidence interval) by IRRC was 7.06 months (5.85, 8.74) in the ivonescimab arm compared to 4.80 months (4.21, 5.55) in the chemotherapy arm. Subgroup analyses indicated that PFS benefit favored patients receiving ivonescimab over placebo in almost all subgroups, including those who progressed on third-generation EGFR-TKIs therapy, those with brain metastases, those with EGFR mutation of deletion 19 (HR, 0.48; 0.32-0.73), and patients who were T790M mutation-positive.
The objective response rates were 50.6% and 35.4% for the 2 groups. Grade ≥3 treatment-emergent adverse events (TEAEs) were observed in 99 (61.5%) patients receiving ivonescimab plus chemotherapy versus 79 (49.1%) patients receiving placebo plus chemotherapy. The most common grade ≥3 TEAEs were adverse events (AEs) related to chemotherapy.
Grade ≥3 immune-related AEs were reported in 10 (6.2%) patients versus 4 (2.5%) patients, respectively. Additionally, grade ≥3 AEs related to VEGF blocking occurred in 5 patients (3.1%) versus 4 patients (2.5%), respectively.
Ivonescimab, in combination with chemotherapy, demonstrated a notable enhancement in PFS among patients who had previously experienced treatment failure with EGFR-TKIs. Importantly, this treatment approach maintained a manageable safety profile.
Epidermal growth factor receptor (EGFR) mutations are found in nearly one-third of patients with unresectable, stage III non-small cell lung cancer (NSCLC). The standard of care for patients who do not experience progression after concurrent chemoradiotherapy (cCRT) is consolidation durvalumab.
However, the effectiveness of consolidation immunotherapy, specifically for EGFR mutation (EGFRm) NSCLC, is still uncertain due to limited available data. Osimertinib (osi), a third-generation central nervous system-active EGFR-tyrosine kinase inhibitor (TKI), is recommended for advanced/metastatic EGFRm NSCLC and as adjuvant therapy for resectable EGFRm NSCLC.
Consolidation durvalumab is the standard of care in unresectable stage III NSCLC following CRT without progression. However, the benefit of consolidation durvalumab in EGFRm NSCLC is not certain based on the subgroup analysis from the PACIFIC study.
The efficacy of EGFR-TKIs is supported by the phase 2 RECEL study and real-world data. However, prospective phase 3 studies are needed, and no approved targeted therapies are available for unresectable stage III EGFRm NSCLC.
The primary results are reported from the global, double-blind, placebo-controlled phase 3 LAURA study (NCT03521154), which evaluated the efficacy and safety of osi in unresectable stage III EGFRm NSCLC patients without progression after definitive CRT (dCRT).
Patients who met the eligibility criteria, which included being aged ≥18 years (≥20 years in Japan), having a World Health Organization performance status of 0 or 1, and having unresectable stage III EGFRm (Ex19del/L858R) NSCLC, were enrolled in the study.
The patients were stratified based on the type of CRT received (cCRT vs sequential), the stage of their disease (IIIA vs IIIB/IIIC), and their nationality (Chinese vs non-Chinese).
They were then randomly assigned in a 2:1 ratio to receive either osi 80 mg or placebo once daily until disease progression or discontinuation, as confirmed by a blinded independent central review. Imaging, including brain magnetic resonance imaging, was required at baseline, every 8 weeks up to week 48, and then every 12 weeks until disease progression, as determined by the central review.
The study’s primary endpoint was progression-free survival (PFS), which was assessed by blinded independent central review (BICR) using RECIST (version 1.1) criteria. Secondary endpoints included overall survival (OS) and safety.
A total of 216 participants were randomly assigned to 2 treatment groups: osi, with 143 patients, and placebo (PBO), with 73 patients. The baseline characteristics were generally similar between the osi and PBO groups. The results showed that osi significantly improved PFS compared to PBO, as assessed by BICR. The median PFS was 39.1 months (95% confidence interval [CI], 31.5, not estimable) for osi compared to 5.6 months (95% CI: 3.7, 7.4) for PBO (hazard ratio [HR], 0.16; 95% CI, 0.10-0.24; P<.001). The interim OS analysis (20% maturity) indicated a trend in favor of osi, although not statistically significant (HR, 0.81; 95% CI, 0.42-1.56; P=.530).
Notably, 81% of participants in the PBO arm received osi after disease progression. Adverse events (AEs) were reported in a higher percentage of participants in the osi group compared to the PBO group (98% versus 88%, respectively). Grade 3 or higher AEs were also more common in the osi group (35%) compared to the PBO group (12%).
Osi, after dCRT, showed a significant and clinically meaningful improvement in PFS for unresectable stage III EGFRm NSCLC., There were no unexpected safety signals observed during the study. These findings firmly establish osi as the new standard of care for EGFRm NSCLC in this specific setting.
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