Radical gastrectomy for gastric cancer results in various post-operative complications, and the influencing factors are complicated. The diagnosis, treatment and prevention of common complications have been reported in many literatures. However, there are few reports on the prevention and treatment of rare complications. Rare complications after radical gastrectomy are often overlooked due to their low incidence. In addition, there are few guidelines and expert consensus regarding to the rare complications. Therefore, clinicians may lack experience in the diagnosis, treatment and prevention of rare complications after radical gastrectomy. Based on the literature review and the author's experience, this article systematically reviews seven rare complications after radical gastrectomy (duodenal stump fistula, pancreatic fistula, chyle leakage, esophagomediastinal fistula, internal hernia, gastroparesis, and intussusception). This article aims to provide a comprehensive reference for the diagnosis, treatment and prevention of rare complications after radical gastrectomy for gastric cancer patients.
Humans ; Stomach Neoplasms/complications* ; Gastrectomy/methods* ; Postoperative Complications/etiology* ; Duodenal Diseases ; Laparoscopy/adverse effects* ; Retrospective Studies

Humans ; Sarcoma ; NFATC Transcription Factors ; RNA-Binding Protein EWS

Humans ; Colon, Descending ; Dendritic Cell Sarcoma, Follicular

Animals ; Mice ; Colon ; Histological Techniques

Humans ; Carcinoma, Squamous Cell/pathology* ; Chromosomal Proteins, Non-Histone/genetics* ; Ear, Middle/pathology* ; Poly-ADP-Ribose Binding Proteins ; Nuclear Proteins

Objective: To investigate the clinicopathological features, immunophenotype, molecular features and differential diagnosis of primary synovial sarcoma of the lung (PSSL). Methods: Twelve cases of PSSL were collected at Henan Provincial People's Hospital, during May 2010 and April 2021, and their clinicopathological parameters were summarized. SS18-SSX, H3K27Me3, and SOX2 were added to the original immunomarkers to evaluate their diagnostic value for PSSL. Results: The age of 12 patients when diagnosed ranged from 32 to 75 years (mean of 50 years). There were 7 males and 5 females, 2 left lung cases and 10 right lung cases. Of the 6 patients who underwent surgical resection, five cases were confined to lung tissue (T1), one case had mediastinal invasion (T3), two cases had regional lymph node metastasis (N1), and none had distal metastasis. Microscopically, 11 cases showed monophasic spindle cell type and one case showed biphasic type composed of mainly epithelial cells consisting of cuboidal to columnar cells with glandular and cribriform structures. It was difficult to make the diagnosis by using the biopsy specimens. Immunohistochemistry (IHC) showed CKpan expression in 8 of 12 cases; EMA expression in 11 of 12 case; TLE1 expression in 8 of 12 cases; S-100 protein expression in two of 12 cases; various expression of bcl-2 and vimentin in 12 cases, but no expression of SOX10 and CD34 in all the cases. The Ki-67 index was 15%-30%. The expression of SS18-SSX fusion antibody was diffusely and strongly positive in all 12 cases. SOX2 was partially or diffusely expressed in 8 of 12 cases, with strong expression in the epithelial component. H3K27Me3 was absent in 3 of 12 cases. SS18 gene translocation was confirmed by fluorescence in situ hybridization (FISH) test in all 12 samples. Six cases underwent surgery and postoperative chemotherapy, while the other six cases had chemotherapy alone. Ten patients were followed up after 9-114 months, with an average of 41 months and a median of 26 months. Five patients survived and five died of the disease within two years. Conclusions: PSSL is rare and has a broad morphological spectrum. IHC and molecular tests are needed for definitive diagnosis. Compared with current commonly used IHC markers, SS18-SSX fusion antibody has better sensitivity to PSSL, which could be used as an alternative for FISH, reverse transcription-polymerase chain reaction or next generation sequencing in the diagnosis of PSSL.
Male ; Female ; Humans ; Adult ; Middle Aged ; Aged ; Biomarkers, Tumor/analysis* ; Sarcoma, Synovial/diagnosis* ; In Situ Hybridization, Fluorescence ; Histones/genetics* ; Proto-Oncogene Proteins/metabolism* ; Oncogene Proteins, Fusion/genetics* ; Repressor Proteins/metabolism* ; Lung/pathology* ; Lung Neoplasms

Humans ; Anaplastic Lymphoma Kinase ; Histiocytosis, Langerhans-Cell ; Receptor Protein-Tyrosine Kinases ; Lymphoma, Large-Cell, Anaplastic/pathology*

Female ; Humans ; Ovarian Neoplasms/surgery* ; Sex Cord-Gonadal Stromal Tumors/surgery* ; Myxoma/surgery*

Objective: To investigate the clinicopathological features, molecular genetic features, differential diagnosis and prognosis of ELOC mutated renal cell carcinoma. Methods: From January 2015 to June 2022, 11 cases of renal cell carcinoma with clear-cell morphology, expression of CAⅨ and CK7 and no 3p deletion were collected. Two cases of ELOC mutant renal cell carcinoma were diagnosed using whole exome sequencing (WES). The clinical features, morphology, immunophenotype, FISH and WES results were analyzed. The relevant literature was reviewed. Results: The two patients were both male, aged 29 and 51 years, respectively. They were both found to have a renal mass by physical examination. The maximum diameters of the tumors were 3.5 cm and 2.0 cm, respectively. At the low magnification, the tumors were well-defined. The tumor cells showed a pushing border and were separated by thick fibrous bands, forming nodules. The tumor cells were arranged in a variety of patterns, including tubular, papillary, solid nest or alveolar. At high magnification, the tumor cells were large, with well-defined cell borders and clear cytoplasm or fine eosinophilic granules. CAⅨ was diffusely box-like positive in both cases. Case 1 was partially and moderately positive for CK7, strongly positive for CD10, diffusely and moderately positive for P504S, and weakly positive for 34βE12. In case 2, CK7 and CD10 were both partially, moderately positive and P504s were diffusely positive, but 34βE12 was negative. FISH results showed that both cases had no 3p deletion. ELOC c.235T>A (p.Y79N) mutation was identified using WES in case 1, while ELOC c.236_237inv (p.Y79C) mutation was identified in case 2. Conclusions: As a new clinical entity, ELOC mutated renal cell carcinoma may be underdiagnosed due to its overlap with clear cell renal cell carcinoma in morphology and immunophenotype. The diagnosis of renal cell carcinoma with ELOC mutation should be confirmed by morphology, immunohistochemistry, FISH and gene mutation detection. However, more additional cases are needed to explain its biological behavior and prognosis.
Humans ; Male ; Biomarkers, Tumor/genetics* ; Carcinoma, Renal Cell/pathology* ; Chromosome Aberrations ; Kidney Neoplasms/pathology* ; Molecular Biology ; Mutation ; Prognosis