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Abstract In patients presenting with hyperinsulinemic hypoglycemia with a nonpancreatic neuroendocrine tumor, the diagnosis of an ectopic insulin‐secreting tumor should be considered, and investigated further with confirmatory insulin staining.

A variety of histologies is often mixed in neuroendocrine carcinoma (NEC) called mixed neuroendocrine–non-neuroendocrine neoplasm (MiNEN). However, tumors consisting of both large-cell NEC and squamous cell carcinoma (SCC) are rare. NEC of the large intestine is aggressive; however, an ideal treatment strategy has not been established. In this study, we have reported a case of rectal MiNEN containing large-cell NEC and SCC that was covered by tubulovillous adenoma. A 73-year-old man was referred to our hospital for the treatment of an upper rectal tumor. The results of preoperative biopsy indicated tubulovillous adenoma, whereas computed tomography revealed multiple liver tumors and swollen lymph nodes around the rectum. Laparotomy was performed because of severe dyschezia caused by rectal stenosis. Hartmann's operation was performed because of peritoneal metastases. Histopathological examination of the rectal tumor revealed MiNEN containing large-cell NEC, SCC, well-differentiated adenocarcinoma, and tubulovillous adenoma covering the surface of the tumor. The patient died 73 days after surgery due to liver metastases. It is important to consider NEC in the differential diagnosis and tissue sampling should be performed to ensure appropriate management when pathological findings and clinical diagnosis do not match. More research is required to determine the ideal treatment for these rare and aggressive tumors. [ABSTRACT FROM AUTHOR]

In patients presenting with hyperinsulinemic hypoglycemia with a nonpancreatic neuroendocrine tumor, the diagnosis of an ectopic insulin‐secreting tumor should be considered, and investigated further with confirmatory insulin staining. [ABSTRACT FROM AUTHOR]

Objective: To report the first case in the literature of a primary large-cell undifferentiated carcinoma (LCUC) of the ureter with a very aggressive behavior and dismal prognosis.Clinical Presentation and Intervention: A 60-year-old woman with a history of intermittent macroscopic hematuria and mild to moderate right flank pain was admitted to the Department of Urology. Tissue biopsies and cytological samples were taken. Pathologic examination was consistent with LCUC.Conclusion: LCUC of the ureter is an aggressive tumor with a high proliferation index. Patients might be diagnosed at an advanced stage. LCUC must be considered in the differential diagnosis of urinary tract pathologies. [ABSTRACT FROM AUTHOR]

Non-small cell lung cancer (NSCLC) accounts for >80% of all cases of lung cancer and can be divided into lung adenocarcinoma (LAC), large-cell carcinoma (LCC), and squamous cell carcinoma (SCC). Accumulating evidence suggests that MTSS1, which is a newly discovered protein associated with tumor progression and metastasis, may have differential roles in cancer malignancy. As it has been demonstrated that MTSS1 is overexpressed in NSCLC and may be an independent prognostic factor in patients with SCC, the present study explored the differential roles of MTSS1 in the invasion and proliferation of different subtypes of NSCLC. Stable overexpression and knockdown of MTSS1 was performed in human NSCLC H920 (LAC), H1581 (LCC) and SW900 cell lines (SCC), and western blot, cell invasion, proliferation and FAK activity analyses were used to investigate the effects. Overexpression of MTSS1 enhanced the invasion and proliferation abilities of H920 and H1581 cells, and these effects were abolished by treatment with selective FAK inhibitor 14, which did not affect the expression of MTSS1. Notably, overexpression of MTSS1 inhibited invasion and proliferation in SW900 cells, and this effect was enhanced by the selective FAK inhibitor. Knockdown of MTSS1 decreased the invasion and proliferation abilities of H920 and H1581 cells, whereas knockdown increased invasion and proliferation in SW900 cells. Furthermore, while overexpression of MTSS1 induced FAK phosphorylation and activity in H920 and H1581 cells, MTSS1 overexpression inhibited FAK phosphorylation/activity in SW900 cells. Knockdown of MTSS1 decreased FAK phosphorylation/activity in H920 and H1581 cells, whereas knockdown increased these processes in SW900 cells. To the best of our knowledge, the present study was the first to demonstrate that MTSS1 has differential roles in various subtypes of NSCLC, acting via a FAK-dependent mechanism. The results indicated that MTSS1 may enhance invasion and proliferation in LAC and LCC cells, whereas MTS11 inhibits these processes in SCC cells. These findings provide novel insight into the functional role of MTSS1 in cancer and may help elucidate therapeutic strategies for the treatment of various types of cancer. [ABSTRACT FROM AUTHOR]

Objectives: To assess immunohistochemical (IHC) stains differentially expressed between different types of lung cancer.Methods: We evaluated 16 different IHC stains in 209 prospectively included, surgically treated primary lung cancers, including 121 adenocarcinomas, 65 squamous cell carcinomas, 15 large-cell carcinomas, 5 adenosquamous carcinomas, 2 sarcomatoid carcinomas, and 1 small-cell carcinoma, using the tissue microarray technique.Results: Cytokeratin 5 (CK5) and P63 were both positive in 10% or more of the cells in 97% of the squamous cell carcinomas, with the former being positive (<10% of the cells) in only 2 non-squamous cell carcinomas. Thyroid transcription factor 1 (TTF1) and napsin A were positive in 10% or more of the cells in 88% and 87% of the adenocarcinomas, respectively, with 94% of the adenocarcinomas being positive in at least 1 marker. Fifteen percent of the adenocarcinomas were positive for estrogen receptor.Conclusions: CK5, TTF1, and napsin A are sensitive markers for squamous cell carcinoma and adenocarcinoma of the lung. [ABSTRACT FROM AUTHOR]

Abstract: A 34-year-old Japanese woman presented with left supraclavicular lymph node swelling. Computed tomography scans revealed a mass on the left lower lobe, pulmonary nodules, and pleural effusion. A lymph node biopsy revealed large-cell carcinoma with an epidermal growth factor receptor (EGFR) deletion mutation, L747–T751 in exon 19. Although malignant pleural effusions carried the same EGFR mutation, progressive pleural effusions after treatment with chemotherapy, gefitinib, and erlotinib did not show any EGFR mutation. A cell line established from the pleural effusion 3 days before the patient expired also did not harbor the EGFR mutation. Histological sections of the lymph node of the patient were similar to those of the xenograft tumor of the cell line. There may be genetic heterogeneity in EGFR mutant tumors. [Copyright &y& Elsevier]

Carcinoembryonic antigen, a serum tumor marker, is useful for diagnosing cancer and for following the response to therapy in cancer cases. Serum carcinoembryonic antigen levels are also important as a predictive tool in evaluating prognosis. A 56-year-old man presented with an abnormal shadow on a chest X-ray. His preoperative serum carcinoembryonic antigen was at an elevated level of 1274.0 ng/ml. Chest computed tomography revealed a tumor in the posterior segment of the right lung and a swollen right interlobar lymph node. Right lung pneumonectomy and node dissection were performed. A histological diagnosis determined that the tumor was a large-cell carcinoma at clinical stage IIA. Immunohistochemical analysis detected the production of carcinoembryonic antigen by the tumor cells. Following surgery, the patient's carcinoembryonic antigen levels were maintained within the normal range. This is a rare case of lung cancer with no evidence of recurrence and metastasis for 8 years despite markedly elevated preoperative carcinoembryonic antigen levels. [ABSTRACT FROM AUTHOR]

This report describes a case of large-cell lung carcinoma with neuroendocrine features, presenting with the full clinical picture of paraneoplastic opsoclonus-myoclonus syndrome. The patient had an unexpectedly dramatic resolution of the neurologic dysfunction after receiving antineoplastic treatment. Symptom improvement paralleled a progressive decline of serum ANNA-2 antibody titers to undetectable levels. [ABSTRACT FROM AUTHOR]

Granulocyte colony-stimulating factor ( G- CSF)-producing lung cancers are known to cause extreme leukocytosis. However, acute respiratory distress syndrome ( ARDS) caused by G- CSF-producing lung cancer is extremely rare. We present a case of G- CSF-producing lung cancer with marked leukocytosis, which rapidly led to severe ARDS after the patient developed pneumonia. The present case suggests that extreme leukocytosis may easily lead to ARDS, triggered by infection. Thus, G- CSF-producing lung cancer with marked leukocytosis should be carefully monitored before surgery and during treatment. [ABSTRACT FROM AUTHOR]

Abstract: In contrast to leukocytosis, paraneoplastic hypereosinophilia is uncommon in lung cancer. We present a patient with large-cell carcinoma of the lung, in which cancer cells generate large amounts of GM-CSF leading to a leukemoid reaction with prominent hypereosinophilia and potentially involved in autocrine tumor stimulation. [Copyright &y& Elsevier]

Background: Primary lung cancer is one of the most common causes of cancer and of death due to cancer worldwide. The tumour node metastases staging for non-small-cell lung cancer (NSCLC) helps to prognosticate and plan for treatment. Most patients have advanced disease at the time of diagnosis. Primary lung malignancy was previously diagnosed mostly in older individuals., Objectives: The primary aim of this study was to determine whether younger age at presentation is a risk factor for more advanced disease. We defined younger age as <45 years., Methods: This was a retrospective analytical study covering 5.5 years. The information was obtained from the lung cancer registry of all patients presented at our Division of Pulmonology weekly combined oncology meeting., Results: A total of 52 of 1 083 patients with lung malignancy were <45 years, and 48 of these had NSCLC. Adenocarcinoma was the predominant type (48%), followed by squamous cell carcinoma (27%), NSCLC not otherwise specified (NOS; 21%) and large-cell carcinoma (4%). Overall, the majority of patients (98%) had advanced disease at presentation. However, there was no statistical difference compared with presenting stage in older patients (odds ratio 0.25, 95% confidence interval (CI) 0.034 - 1.874 and risk ratio 0.27 (95% CI (0.038 - 1.900))., Conclusion: Primary lung malignancy remains a disease of the elderly. This study demonstrated that NSCLC tends to present in advanced stages in younger patients, although the difference was not statistically significant., Competing Interests: Conflicts of interest: None.

Introduction: Patients with pulmonary large-cell carcinoma (LCC) have poor prognosis and limited treatment options. The identification of clinically actionable molecular alterations helps to guide personalized cancer treatment decisions., Patients and Methods: A consecutive cohort of 789 resected NSCLC cases were reviewed. Fifty-nine NSCLC cases lacking morphologic differentiation, accounting for 7.5% of all resected NSCLCs, were identified and further characterized by immunohistochemistry according to the 2015 WHO lung tumor classification. Molecular alterations were investigated by multiple technologies including target capture sequencing, immunohistochemistry, and fluorescence in situ hybridizations., Results: Of 59 NSCLC cases lacking morphologic differentiation, 20 (33.9%) were reclassified as adenocarcinoma (LCC-AD), 14 (23.7%) as squamous cell carcinoma (LCC-SqCC), and 25 (42.4%) as LCC-Null. Approximately 92% of LCC-Null, 95% of LCC-AD, and 86% of LCC-SqCC harbored clinically relevant alterations. Alterations characteristic of adenocarcinoma (EGFR, KRAS, ALK receptor tyrosine kinase [ALK], ROS1, and serine/threonine kinase 11 [STK11]) were detected in the LCC-AD subgroup but not in LCC-SqCC, whereas squamous-lineage alterations (phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit alpha [PIK3CA], SRY-box 2 [SOX2], fibroblast growth factor receptor 1 [FGFR1], and AKT1) were detected in the LCC-SqCC subgroup but not in the LCC-AD group. Although some LCC-Null tumors displayed a genetic profile similar to either adenocarcinoma or squamous-cell carcinoma, more than half of the LCC-Null group were completely devoid of recognizable lineage-specific genetic profiles. High programmed death ligand 1 expression and high frequency of cell cycle regulatory gene alterations were found in the LCC-Null group offering alternative options of targeted therapy., Conclusions: This comprehensive molecular study provided further insight into the genetic architecture of LCC. The presence of clinically actionable alterations in a majority of the tumors allowed personalized treatment to emerge., (Copyright © 2019 International Association for the Study of Lung Cancer. Published by Elsevier Inc. All rights reserved.)