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Abstract Background: Esophageal mixed neuroendocrine-nonneuroendocrine neoplasms (MiNENs) are now known as a neuroendocrine component mixed with a nonneuroendocrine component in a single neoplasm, one of which is in the form of mixed small cell-squamous cell carcinoma. Collision tumors have been excluded from the category of MiNENs, but difference between mixed and collision small cell-squamous cell carcinoma has never been reported. Methods: We collected six cases and reviewed 11 cases of mixed or collision small cell-squamous cell carcinoma (MCSSC); the data from 17 cases of MCSSC were analyzed to observe their clinicopathological features. Results: Most of the MCSSC patients were middle-aged and elderly, with more men than women, and most of the tumors occurred in the middle and lower esophagus. We found that in mixed cancers, the metastases were a mixture of squamous cell carcinoma and small cell carcinoma, whereas metastatic foci in collisional tumors showed simple cancer components; this phenomenon has never been reported before. Mixed cancers account for a higher proportion of small cell carcinomas, a higher pathological stage, and a worse prognosis than collisional cancers. PD-L1 (22C3) was negative in both squamous cell carcinoma and small cell carcinoma regions ( Conclusions: Mixed and collisional small cell-squamous cell carcinomas are essentially distinct tumors. In the clinical diagnostic of MCSSC, the tumor should be clearly identified as mixed or collisional carcinoma to guide the clinical treatment and prognosis more accurately. Keywords: Collision cancer, esophagus, MiNENs, mixed small cell-squamous cell carcinoma, PD-L1, Author(s): Huajun Sun [1]; Yanfen Shi [2]; Dongni Liang [3]; Juan Liu [1]; Gang Xu [1]; Xudan Yang (corresponding author) [1] Introduction Esophageal neuroendocrine neoplasms (NENs) are extremely rare.[sup.[1]] In [...]

Objective To evaluate the value and characteristics of 18F-FDG PET/CT and enhanced CT in primary pulmonary mucinous adenocarcinoma (PPMA), in order to provide reference for the clinical diagnosis and treatment of the disease. Methods Data of enhanced CT and 18F-FDG PET/CT imaging and clinical information of 25 patients with PPMA confirmed by pathology in China-Japan Friendship Hospital from July 2015 to February 2018 were retrospectively reviewed. Results A total of 25 PPMA patients were enrolled. Among them, 25 patients underwent the examination of 18F-FDG PET/CT imaging, and 6 cases underwent enhanced CT scan. Seven cases had one lesion, which morphologically manifested as a solitary lung lesion with lobulation signs, spinous processes on the edge, and uneven uptake of 18F-FDG with low or no uptake in hollow or cystic density areas; 18 cases showed diffuse multiple lesions in both lungs with different distribution, size and shape, including 5 cases with multiple nodules/masses, 5 with consolidations, and 8 with diversified lesions including nodules, masses, cavities, ground glass opacities, patches, and consolidations. Consolidation shadow is the most typical morphological manifestation of diffusely multiple PPMA (11 cases). The density of consolidation foci was extremely uneven, and all of them contain areas of cystic density. They had low CT value(-71-79 Hu), and characteristic features were found, including pulmonary lobe bulging sign (6 cases), pathological air bronchus sign (4 cases), angiographic sign (3 cases) and surrounding ground glass density(7 cases). The uptake of 18F-FDG varied with the density of lesions. The cystic component was lower than the solid component. Contrast-enhanced CT showed heterogeneous enhancement in 4 cases and no enhancement in 2 cases. The degree of 18F-FDG uptake in lesions dominated by nodules, masses or cavities was not linearly correlated with the degree of CT enhancement, but that in lesions dominated by consolidation was positively correlated with the degree of CT enhancement. Conclusions Contrast-enhanced CT shows PPMA lesions with no enhancement or heterogeneous enhancement. PPMA is often manifested as nodules, patchy shadows, and other space-occupying forms mixed with consolidation shadows on 18F-FDG PET/CT imaging, which has characteristic manifestations, including pulmonary lobe bulge and pathological air bronchi. Angiographic signs and the degree of metabolism are positively correlated with the density of lesions, which are used for differential diagnosis of pulmonary infectious diseases.

Simple Summary: Thymic neuroendocrine tumors (Th-NETs) are rare, with limited research on prognostic markers and treatments. Our retrospective study evaluated clinicopathological characteristics and therapeutic strategies for Th-NETs, filling gaps in existing studies. We highlighted the importance of biomarkers such as serum neuron-specific enolase, inflammatory factors, and oxygen 6-methylguanine-DNA methyltransferase, as well as the roles of surgical interventions, postoperative therapies, and temozolomide-based chemotherapy in improving patient survival. Our findings confirmed the crucial role of surgical treatment and the potential benefits of postoperative adjuvant radiotherapy. Furthermore, temozolomide-based chemotherapy demonstrated efficacy in Th-NETs treatment, with the neutrophil-to-lymphocyte ratio and serum neuron-specific enolase proving to be valuable prognostic markers necessitating further research. Background: Thymic neuroendocrine tumors (Th-NETs) are rare and aggressive, with a scarcity of research on predicting patient prognosis. Our study aimed to assess the impact of prognostic markers and temozolomide (TMZ)-based chemotherapy on survival in Th-NETs. Methods: We retrospectively reviewed the medical records of patients diagnosed with Th-NETs between 2013 and 2023 at our institution. We collected clinicopathological data, including tumor pathological grading, staging, serum concentrations of neuron-specific enolase (NSE) and pro-gastrin-releasing peptide, levels of inflammatory factors, and expression of oxygen 6-methylguanine-DNA methyltransferase (MGMT). Treatment details (such as surgery and chemotherapy) and survival outcomes were also documented. Results: A total of 32 patients were included in our study after excluding those without complete available information. The median progression-free survival (PFS) was 12.5 months (95%CI, 8–16 months) for 19 patients who received TMZ-based chemotherapy. Twenty-one patients underwent surgery as the primary treatment, demonstrating a median disease-free survival (DFS) of 51.0 months. The inflammatory factor neutrophil-to-lymphocyte ratio (NLR) was an independent prognostic indicator of DFS in postoperative patients and PFS in TMZ-treated patients. The overall 3-, 5-, and 10-year survival rates were 86.6%, 69.5%, and 33.8%, respectively. Ki67 level exceeding 10% (p = 0.048) and absence of surgical resection (p = 0.003) were significantly associated with worse overall survival (OS). Conclusion: Surgical treatment was currently the primary method for treating Th-NETs, and postoperative adjuvant therapy was an essential consideration for specific patient cohorts. Despite widespread positive MGMT expression, TMZ-based chemotherapy showed promise. Some potential prognostic biomarkers such as NLR and NSE need more attention. [ABSTRACT FROM AUTHOR]

ERK3/MAPK6 activates MAP kinase‐activated protein kinase (MK)‐5 in selected cell types. Male MK5 haplodeficient mice show reduced hypertrophy and attenuated increase in Col1a1 mRNA in response to increased cardiac afterload. In addition, MK5 deficiency impairs cardiac fibroblast function. This study determined the effect of reduced ERK3 on cardiac hypertrophy following transverse aortic constriction (TAC) and fibroblast biology in male mice. Three weeks post‐surgery, ERK3, but not ERK4 or p38α, co‐immunoprecipitated with MK5 from both sham and TAC heart lysates. The increase in left ventricular mass and myocyte diameter was lower in TAC‐ERK3+/− than TAC‐ERK3+/+ hearts, whereas ERK3 haploinsufficiency did not alter systolic or diastolic function. Furthermore, the TAC‐induced increase in Col1a1 mRNA abundance was diminished in ERK3+/− hearts. ERK3 immunoreactivity was detected in atrial and ventricular fibroblasts but not myocytes. In both quiescent fibroblasts and "activated" myofibroblasts isolated from adult mouse heart, siRNA‐mediated knockdown of ERK3 reduced the TGF‐β‐induced increase in Col1a1 mRNA. In addition, intracellular type 1 collagen immunoreactivity was reduced following ERK3 depletion in quiescent fibroblasts but not myofibroblasts. Finally, knocking down ERK3 impaired motility in both atrial and ventricular myofibroblasts. These results suggest that ERK3 plays an important role in multiple aspects of cardiac fibroblast biology. [ABSTRACT FROM AUTHOR]