Non-tumor forming and diffusely spreading invasive pancreatic cancer.

A 78-year-old man presented to our hospital with loss of appetite and epigastric discomfort. Computed tomography (CT) revealed dilation of the main pancreatic duct and three cystic lesions in the pancreatic neck, body, and tail. Endoscopic ultrasonography showed a mural nodule > 5 mm enhanced with Sonazoid in a cyst. Therefore, the patient was diagnosed with intra-ductal papillary mucinous neoplasm (IPMN) and underwent distal pancreatectomy. Macroscopic examination of the cut surface of the resected specimen showed no solid tumors in the pancreatic parenchyma. The histopathological diagnosis of the cysts was IPMN with low-grade dysplasia. Ten months after surgery, the serum carbohydrate antigen 19-9 level was elevated, and CT showed multiple peritoneal and pulmonary nodules, suggesting peritoneal dissemination and lung metastases. Since recurrence of pancreatic cancer was suspected, repeat histopathological examination of the resected specimen was performed, revealing small clusters of atypical epithelial cells diffusely spreading in the pancreatic tissue. The diagnosis was changed to invasive ductal carcinoma (pT2N1bM0, stage IIB). Invasive pancreatic cancer that does not form a solid mass, and shows diffuse spreading with small clusters is extremely rare. Imaging diagnosis and histopathological examination should be carefully performed in such cases.

Diagnosis and clinical implication of collision gastric adenocarcinomas: a case report.

BACKGROUND: Collision tumors are a subtype of simultaneous tumors wherein two unrelated tumors collide or infiltrate each other. Collision gastric adenocarcinomas (CGA) are rare and difficult to diagnose, and their clinical implications remain unclear. Herein, we aimed to reveal diagnostic methods for CGA and provide insight into its implications. CASE PRESENTATION: Among 1041 cases of gastric cancers (GCs) resected between 2008 and 2018, we included cases of confirmed CGA. Patients' backgrounds, preoperative endoscopy findings, macroscopic imaging findings, and histopathology findings [including immunostaining for CK 7, MUC2, and mismatch repair (MMR) proteins] were investigated. The incidence of CGA was 0.5%: 5 of 81 cases having simultaneous multiple GCs. Tumors were mainly in the distal stomach. The CGA in two cases was between early cancers, in two cases was between early and advanced cancers, and in one case was between advanced cancers. There were three cases of collision between differentiated and undifferentiated types and two cases between differentiated types. Immunostaining with CK7 and MUC2 was useful for diagnosing collision tumor when the histology was similar to each other. Among ten GCs comprising CGA, nine tumors (90%) exhibited deficient MMR proteins, suggesting high microsatellite instability (MSI). CONCLUSIONS: CGA is rare and usually found in the distal stomach. Close observation of shape, optimal dissection, and detailed pathological examination, including immunostaining, facilitated diagnosis. CGAs may have high MSI potential.

SMARCA4-deficient rectal carcinoma with a sarcomatoid component: a case report.

A new classification of SMARCA4-deficient tumors was proposed recently for thoracic malignancies, and the tumors have some histopathological characteristics similar to those of carcinosarcoma. We encountered a case of SMARCA4-deficient rectal carcinoma with a sarcomatoid component. A 46-year-old man presented to our hospital with a prolapsing anal mass. Colonoscopy revealed an irregular, nodular, and elevated lesion in the rectum, and the biopsy revealed a moderately differentiated adenocarcinoma. Abdominoperineal resection of the rectum was performed. A macroscopic image of the resected specimen showed a complex tumor 3.5 cm × 3 cm in size with a papillary protrusion and an irregular ulcerative lesion. Histopathological examination revealed that the tumor was composed of moderately/poorly differentiated adenocarcinoma and atypical spindle cells. The adenocarcinoma component was positive for epithelial markers (AE1/AE3 and carcinoembryonic antigen) and showed deletion of SMARCA2 and SMARCA4, while the spindle cells expressed mesenchymal markers (α-smooth muscle actin and vimentin). The pathological diagnosis was poorly differentiated adenocarcinoma with a sarcomatoid component, pT3N2bM0, stage IIIc. Although our case had histological characteristics of carcinosarcoma, immunostaining revealed a deficiency of SMARCA4. This case presented a SMARCA4-deficient colorectal carcinoma with a sarcomatoid component, which was histopathologically similar to carcinosarcoma.

Superficial spreading type of early gastric cancer with diagnostic difficulty and positive surgical margin: a case report.

An 83-year-old man visited our hospital because of difficulty swallowing. Gastroscopy revealed multiple ulcers and a reddish depression in the lesser curvature of the middle stomach. The initial biopsy showed regenerative atypia, so a gastroscopy was repeated every 3 months thereafter because of suspected malignancy. A biopsy performed 12 months after the initial gastroscopy revealed a well-differentiated adenocarcinoma. After determination of the planned oral resection line by two negative biopsies, laparoscopic distal gastrectomy was performed. The resected specimen showed a 0 - IIa + IIc lesion composed of well-to-moderately differentiated tubular adenocarcinoma, including hand-shaking-type gastric cancer. The oral resection margin was positive due to widespread mucosal extension; therefore, an additional total gastrectomy was needed. Cases of well-differentiated adenocarcinoma and its superficial extension may be difficult to diagnose via endoscopy and biopsy.

Mesenchymal-epithelial transition gene amplification and protein overexpression in stage IV pulmonary adenocarcinoma.

BACKGROUND: In non-small cell lung cancer (NSCLC), MET gene copy number gain, including gene amplification and chromosome 7 polysomy, is reportedly associated with patient prognosis. Although relationship between MET copy number gain and poor prognosis has been suggested in surgically resected non-small cell lung cancer, the clinical significance of MET copy number gain and protein overexpression in patients with advanced unresectable tumor is unclear. METHODS: We assessed MET copy number gain and protein expression using fluorescence in situ hybridization and immunohistochemistry in 88 patients with clinical stage IV pulmonary adenocarcinoma receiving chemotherapy, immunotherapy or palliative care. RESULTS: We found MET amplification, polysomy 7 and high MET protein expression in 10.2, 18.2 and 62.5% of 88 cases, respectively. Gene amplification and high protein expression were not significantly associated. A univariate analysis showed that MET amplification-positive patients had increased overall survival (HR 0.335, 95% CI: 0.119-0.945; P = 0.0388). Although it was not statistically significant in the multivariate analysis of the whole cohort, with the removal of patients who did not receive any treatment other than palliative care, MET amplification independently improved the overall survival (HR 0.178, 95% CI: 0.041-0.770; P = 0.0209). Chromosome 7 polysomy and high MET protein expression did not affect the overall survival. CONCLUSIONS: Although MET amplification-positive tumor is considered aggressive, our results suggest that it has a more favorable prognosis than amplification-negative cases in stage IV pulmonary adenocarcinoma with medical treatment.

Trousseau's Syndrome due to Anaplastic Thyroid Carcinoma Presenting with Multiple Ischemic Strokes.

Trousseau's syndrome is characterized by a cerebral or systemic thromboembolism caused by coagulation abnormalities in malignancy. We herein report a case of multiple ischemic strokes as the initial manifestation of anaplastic thyroid carcinoma (ATC). An 86-year-old man was admitted to our hospital due to a sudden-onset weakness of the left limbs. Brain magnetic resonance imaging revealed multiple ischemic lesions in the right middle cerebral artery territory and a mass in the left frontal lobe. Computed tomography revealed a thyroid mass and multiple lung tumors. A diagnosis of ATC was confirmed by a thyroid biopsy. Our case indicates that ATC should be considered as a cause of Trousseau's syndrome.