A malignant gastrointestinal neuroectodermal tumor (GNET) is rare, and it is therefore yet to be completely understood. This study aimed to present the clinicopathologic features of GNET, including treatment information. We included 19 patients with GNET with a mean tumor size of 4.2 cm. The most common site of tumor origin was the small intestine (57.9%), followed by the stomach (15.8%), colon (10.5%), ileocecal junction (5.3%), lower esophagus (5.3%), and anal canal (5.3%). Microscopically, the tumors were composed of epithelioid cells with eosinophilic or clear cytoplasm arranged in nest, sheet-like, papillary, or pseudoalveolar patterns and/or spindle tumor cells with eosinophilic cytoplasm arranged in a fascicular pattern. Immunohistochemically, the tumor cells stained positively for S100 (19/19,100%), SOX10 (14/15, 93.3%), vimentin (17/17, 100%), synaptophysin (Syn) (7/17, 41.2%), CD56 (4/13, 30.8%), CD99 (1/5, 20%), and CD117 (1/15, 6.7%), and negatively for HMB45, Melan A, DOG1, CD34, AE1/AE3, CAM5.2, chromogranin A, smooth muscle actin, and desmin. In total, 14/15 (93.3%) cases showed split Ewing sarcoma breakpoint region 1 gene (EWSR1) signals consistent with a chromosomal translocation involving EWSR1. Within a mean follow-up of 29.7 months (range: 3 to 63 mo), 2/15 (13.3%) patients died of disease, 5 (33.3%) were alive with disease, and 8 (53.3%) had no evidence of disease. Two and 1 patients showed partial response to apatinib and anlotinib, respectively. In conclusion, GNET has distinctive morphologic, immunohistochemical, and molecular genetic features and should be distinguished from other gastrointestinal tract malignancies. Apatinib and anlotinib might be effective for the treatment of advanced GNET and could prolong patient survival.
ObjectiveTo evaluate the 2017 implementation of China’s 2009 healthcare price reforms on Beijing’s secondary and tertiary traditional Chinese medicine (TCM) hospitals.DesignWe employed a panel-interrupted time-series model with hospital fixed effects to estimate the impact of the price reforms.SettingBeijing, April 2014 to April 2018.ParticipantsAll TCM hospitals in Beijing.Outcome measuresOur dependent variables comprised the monthly outpatient and inpatient revenues, the number of monthly outpatient visits and inpatient admissions, the average total expenditures per outpatient visit and per inpatient admission, the average drug expenditures (except herbal medicines) per outpatient visit and per inpatient admission and the average medical service expenditures per outpatient visit and per inpatient admission.ResultsIn tertiary hospitals, the price reforms led to significant reductions in the number of outpatient visits (23.1%), inpatients admission (4.6%) and drug expenditures (except herbal medicines) per inpatient admission (14.0%), and an instant raise in average total expenditure per outpatient (22.0%), medical service expenditures per outpatient visit (58.2%) and inpatient admission (19.0%). There was no significant association between the price reforms and the monthly outpatient and inpatient revenues. After the price reforms, the previous upward trend in medical service expenditures per outpatient visit rose more sharply (from 0.5% to 1.6%). In secondary hospitals, the price reforms decreased the level of drug expenditures (except herbal medicines) per outpatient visit (13.0%) and per inpatient admission (20.8%), but increased medical service expenditures per inpatient admission by 19.0%.ConclusionThe Beijing price reforms adjusted the cost structures in secondary and tertiary TCM hospitals without negatively impacting the operation of the hospitals, and through the increased hierarchical medical service fee, shifted patient choices away from tertiary to other health facilities, especially for patients with minor illnesses.
MCST shows a unique morphology with characteristic immunophenotype. β-catenin expression in the nucleus and β-catenin mutations were identified in the majority of cases, which suggests that the Wnt/β-catenin pathway may play a crucial role in the tumorigenesis of MCST.
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