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Results are presented from a search for the Higgs boson decay H → Zγ, where Z → ℓ+ℓ− with ℓ = e or μ. The search is performed using a sample of proton-proton (pp) collision data at a center-of-mass energy of 13 TeV, recorded by the CMS experiment at the LHC, corresponding to an integrated luminosity of 138 fb−1. Events are assigned to mutually exclusive categories, which exploit differences in both event topology and kinematics of distinct Higgs production mechanisms to enhance signal sensitivity. The signal strength μ, defined as the product of the cross section and the branching fraction $$ \left[\sigma \left(\textrm{pp}\to \textrm{H}\right)\mathcal{B}\left(\textrm{H}\to \textrm{Z}\upgamma \right)\right] $$ σ pp → H B H → Zγ relative to the standard model prediction, is extracted from a simultaneous fit to the ℓ+ℓ−γ invariant mass distributions in all categories and is measured to be μ = 2.4 ± 0.9 for a Higgs boson mass of 125.38 GeV. The statistical significance of the observed excess of events is 2.7 standard deviations. This measurement corresponds to $$ \left[\sigma \left(\textrm{pp}\to \textrm{H}\right)\mathcal{B}\left(\textrm{H}\to \textrm{Z}\upgamma \right)\right]=0.21\pm 0.08 $$ σ pp → H B H → Zγ = 0.21 ± 0.08 pb. The observed (expected) upper limit at 95% confidence level on μ is 4.1 (1.8), where the expected limit is calculated under the background-only hypothesis. The ratio of branching fractions $$ \mathcal{B}\left(\textrm{H}\to \textrm{Z}\upgamma \right)/\mathcal{B}\left(\textrm{H}\to \upgamma \upgamma \right) $$ B H → Zγ / B H → γγ is measured to be $$ {1.5}_{-0.6}^{+0.7} $$ 1.5 − 0.6 + 0.7 , which agrees with the standard model prediction of 0.69 ± 0.04 at the 1.5 standard deviation level.

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Background: Dual inhibition of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor (VEGF) pathways have demonstrated promising results for treatment of advanced non-small cell lung cancer (NSCLC). We conducted a systematic review and meta-analysis to assess the efficacy and toxicity of combined treatment with EGFR tyrosine kinase inhibitors (TKIs) and VEGF monoclonal antibodies for patients harboring activating EGFR mutations.Methods: The electronic databases PubMed, Cochrane and EMBASE were searched for relevant randomized trials between 2000 and 2019. The primary endpoints were overall survival (OS) and progression-free survival (PFS). Secondary endpoints included objective response rate (ORR), disease control rate (DCR), and grade 3 or higher adverse events (AEs). Pooled hazard ratios (HR) for OS and PFS and odds ratios (OR) for ORR, DCR and toxicity were meta-analyzed using the generic inverse variance and the Mantel-Haenszel methods. Random-effect models were used to compute pooled estimates. Subgroup analyses compared PFS by gender, age, smoking status, type of EGFR mutation, intracranial disease and ECOG performance status.Results: A total of 1,246 patients from 6 trials were evaluated for analyses. Compared to EGFR inhibition alone, combination treatment decreased the risk of disease progression (PFS) (HR¼0.64; 95%CI 0.55-0.75), but not OS (HR¼0.90; 95%CI 0.68-1.19). There were a significantly increased number of AEs reported in the dual treatment arm (OR¼3.55; 95%CI 2.74-4.59), with proteinuria (OR¼14.55; 95%CI 4.47-47.4) and hypertension (OR¼7.02; 95%CI 4.73-10.43) being the most significantly increased AEs. Furthermore, no difference in ORR (OR¼0.86; 95%CI 0.65-1.12) and DCR (OR¼0.75; 95%CI 0.41-1.39) were found. The PFS benefit was consistent across all subgroups.Conclusions: This study suggests combined inhibition of EGFR and VEGF pathways significantly improves PFS, with no OS benefit demonstrated, and increases AEs. Mature OS data are needed to strengthen these results along with results from newer trials exploring this strategy with 3 rd generation EGFR-TKIs.