PATIENTS AND METHODS: A total of 657 patients with EGFR-mutated (exon 19 deletions or L858R) locally advanced or metastatic NSCLC after disease progression on osimertinib were randomized 2 : 2 : 1 to receive amivantamab-lazertinib-chemotherapy, chemotherapy, or amivantamab-chemotherapy. The dual primary endpoints were progression-free survival (PFS) of amivantamab-chemotherapy and amivantamab-lazertinib-chemotherapy versus chemotherapy. During the study, hematologic toxicities observed in the amivantamab-lazertinib-chemotherapy arm necessitated a regimen change to start lazertinib after carboplatin completion.
RESULTS: All baseline characteristics were well balanced across the three arms, including by history of brain metastases and prior brain radiation. PFS was significantly longer for amivantamab-chemotherapy and amivantamab-lazertinib-chemotherapy versus chemotherapy [hazard ratio (HR) for disease progression or death 0.48 and 0.44, respectively; P < 0.001 for both; median of 6.3 and 8.3 versus 4.2 months, respectively]. Consistent PFS results were seen by investigator assessment (HR for disease progression or death 0.41 and 0.38 for amivantamab-chemotherapy and amivantamab-lazertinib-chemotherapy, respectively; P < 0.001 for both; median of 8.2 and 8.3 versus 4.2 months, respectively). Objective response rate was significantly higher for amivantamab-chemotherapy and amivantamab-lazertinib-chemotherapy versus chemotherapy (64% and 63% versus 36%, respectively; P < 0.001 for both). Median intracranial PFS was 12.5 and 12.8 versus 8.3 months for amivantamab-chemotherapy and amivantamab-lazertinib-chemotherapy versus chemotherapy (HR for intracranial disease progression or death 0.55 and 0.58, respectively). Predominant adverse events (AEs) in the amivantamab-containing regimens were hematologic, EGFR-, and MET-related toxicities. Amivantamab-chemotherapy had lower rates of hematologic AEs than amivantamab-lazertinib-chemotherapy.
CONCLUSIONS: Amivantamab-chemotherapy and amivantamab-lazertinib-chemotherapy improved PFS and intracranial PFS versus chemotherapy in a population with limited options after disease progression on osimertinib. Longer follow-up is needed for the modified amivantamab-lazertinib-chemotherapy regimen.
METHODS: A literature search was performed on PUBMED, SCOPUS AND EMBASE. The following keywords were used: ethmoidal artery; anterior ethmoidal artery; anterior ethmoidal canal; ethmoid sinus; ethmoid roof; skull base. The search was conducted over a period of 6 months between October 2016 and April 2017.
RESULTS: 105 articles were retrieved. 76 articles which were either case reports or unrelated topics were excluded. Out of the 29 full text articles retrieved, 16 articles were selected; 3 were cadaveric dissection, 5 combined cadaveric dissection and computed tomography (CT) and the rest were of CT studies. All studies were of level III evidence and a total of 1985 arteries were studied. Its position at the skull base was influenced by the presence of supraorbital ethmoid cell (SOEC) and length of the lateral lamella of cribriform plate (LLCP). Inter population morphological variations contribute to the anatomical variations.
CONCLUSIONS: The average diameter of AEA was 0.80 mm and the intranasal length was 5.82 mm. 79.2% was found between the second and third lamellae, 12.0% in the third lamella, 6% posterior to third lamella and 1.2% in the second lamella. Extra precaution should be taken in the presence of a well-pneumatized SOEC and a long LLCP as AEA tends to run freely below skull base.
METHODS: A cross-sectional study of 252 AEA identified by computed tomography (CT) of the paranasal sinuses. The multiplanar CT images were acquired from SOMATOM® Definition AS+ and reconstructed to axial, coronal and sagittal view at 1 mm slice thickness.
RESULTS: 42.5% of AEA was within skull base (grade I), 20.2% at skull base (grade II) and 37.3% coursed freely below skull base (grade III). The prevalence of supraorbital ethmoid cell (SOEC) and suprabullar cell (SBC) was 29.8% and 48.0%. The position of AEA at skull base has significant association with SOEC (p