The liver is one of the most common sites to which malignancies preferentially metastasize. Although a substantial number of liver malignancies are primary tumors, including hepatocellular carcinoma and intrahepatic cholangiocarcinoma, the metastasis of carcinomas to the liver is relatively common and frequently encountered in clinical settings. Representative carcinomas that frequently metastasize to the liver include colorectal carcinoma, breast carcinoma, neuroendocrine tumors, lung carcinoma, and gastric carcinoma. The diagnostic confirmation of suspected metastatic lesions in the liver is generally achieved through a histopathologic examination of biopsy tissues. Although morphology is the most important feature for a pathologic differential diagnosis of metastatic carcinomas, immunohistochemical studies facilitate the differentiation of metastatic carcinoma origins and subtypes. Useful immunohistochemical markers for the differential diagnosis of metastatic carcinomas in the liver include cytokeratins (CK7, CK19, and CK20), neuroendocrine markers (CD56, synaptophysin, and chromogranin A), and tissue-specific markers (CDX2, SATB2, TTF-1, GCDFP-15, mammaglobin, etc.). Here, we provide a brief review about the pathologic differential diagnosis of major metastatic carcinomas in the liver.
Biopsy ; Breast Neoplasms ; Carcinoma, Hepatocellular ; Cholangiocarcinoma ; Colorectal Neoplasms ; Diagnosis, Differential ; Immunohistochemistry ; Keratins ; Liver Neoplasms ; Liver ; Lung ; Neoplasm Metastasis ; Neuroendocrine Tumors ; Pathology ; Synaptophysin

OBJECTIVETo investigate the clinicopathologic features and prognostic factors of gastric neuroendocrine neoplasms(gNENs).

METHODSClinicopathologic data of 104 patients with gastric neuroendocrine neoplasms admitted in Chinese PLA General Hospital between January 2000 and December 2014 were analyzed retrospectively. Tumor proliferation activity classification (G1, G2 and G3) and TNM staging were observed. The clinicopathologic features of the whole group were collected and the univariate and multivariate analysis were determined by Log-rank and Cox proportional hazard model to detect the prognosis-determining features.

RESULTSOf all the patients, 66 cases(63.5%) were neuroendocrine carcinoma, 25 cases(24.0%) were mixed adenoendocrine carcinoma and 12 cases (11.5%) were neuroendocrine tumor. For G grades, 92 cases (88.5%) were G3 grade, 8 cases(7.7%) were G2 grade and 4 cases (3.8%) were G1 grade. TNM staging results showed that stageI( was found in 6 cases (5.8%), stageII(A in 6 cases (5.8%), stageII(B in 9 cases (8.7%), stage III(A in 8 cases (7.7%), stage III(B in 55 cases (52.9%) and stageIIII( in 20 cases (19.2%). For T stage, 7 cases (6.7%) were T1, 12 cases (11.5%) were T2, 24 cases (23.1%) were T3, and 61 cases (58.7%) were T4. Lymph node metastasis occurred in 73 cases (70.2%) and distant metastasis occurred in 20 cases(19.2%). Eighty-six patients were followed up for 6 to 186 months. The median survival was 33.0 months(95% CI: 28.3 to 36.6), and 1-, 3-, and 5-year survival rates were 80%, 49% and 31%. Clinicopathologic features which were considered statistically significant on univariate analysis were selected to Cox proportional hazard model. Univariate analysis showed that risk factors of reducing survival rate included tumor size, pathological type, proliferation activity grades, and depth of invasion (all P<0.05), as well as chromogranin A expression, tumor staging, lymph node metastasis and distant metastasis(all P<0.01). The multivariate analysis showed that the stage of gNEN was the independent risk factor of the prognosis (RR=14.213, 95% CI: 1.316 to 153.524, P=0.029).

CONCLUSIONLate staging is the main clinical feature and a prognostic factor for gNENs.

Carcinoma ; diagnosis ; pathology ; Humans ; Lymphatic Metastasis ; Multivariate Analysis ; Neoplasm Staging ; Neuroendocrine Tumors ; diagnosis ; pathology ; Prognosis ; Proportional Hazards Models ; Retrospective Studies ; Risk Factors ; Stomach Neoplasms ; diagnosis ; pathology ; Survival Rate

OBJECTIVETo study the clinicopathologic characteristics of parathyroid carcinoma (PTC).

METHODSEleven cases of PTC encountered during the period from 1994 to 2012 were enrolled into the study. Forty cases of parathyroid adenoma (PA) were also retrieved for comparison. The clinical manifestations, laboratory results and pathologic features were analyzed, with literature review.

RESULTSThe main clinical manifestations of PTC included neck mass (11/11), hypercalcemia (11/11) and hyperparathyroidism (11/11). Most patients also had osteoporosis (10/11). In contrast, PA often manifested as hypercalcemia (40/40) and hyperparathyroidism (40/40). Histologic examination of PTC showed that the tumor cells contained clear to eosinophilic cytoplasm and separated by dense bands of fibrosis. The tumor mass was surrounded by thick fibrous capsule. Foci of capsular invasion and vascular permeation were identified at the tumor periphery in all cases. Cellular atypia was not conspicuous but mitotic figures and coagulative necrosis were easily identified. On the other hand, PA were composed of tumor cells with clear to eosinophilic cytoplasm, forming glands, trabeculae or nests. Most of them (35/40) had intact fibrous capsule. Mitotic figures were rarely encountered and tumor necrosis was absent. Immunohistochemical study showed that the tumor cells in PTC were positive for CK19 (11/11), chromogranin A (9/11), synaptophysin (7/11) and parathyroid hormone (11/11). They were negative for thyroglobulin, TTF-1 and calcitonin. The Ki-67 index was less than 10% (range = 2% to 9%). In contrast, the tumor cells in PA were positive (40/40) for CK19, chromogranin A, synaptophysin and parathyroid hormone. They were negative for thyroglobulin, TTF-1 and calcitonin. The Ki-67 index was less than 3%. Follow up-data were available in 9 cases of PTC (duration of follow up = 11 months to 224 months) and 7 of the patients were still alive. Follow up of all PA cases showed no evidence of recurrence.

CONCLUSIONSPTC is a rare malignant endocrine tumor presenting as neck mass. Histologic features suggestive of malignant behavior include presence of coagulative tumor necrosis and capsular/vascular invasion. It needs to be distinguished from other entities such as parathyroid adenoma, papillary thyroid carcinoma and medullary thyroid carcinoma.

Adenoma ; metabolism ; pathology ; Adult ; Carcinoma ; metabolism ; pathology ; Carcinoma, Neuroendocrine ; Carcinoma, Papillary ; Chromogranin A ; metabolism ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Hypercalcemia ; etiology ; Hyperparathyroidism ; etiology ; Immunohistochemistry ; Keratin-19 ; metabolism ; Male ; Middle Aged ; Osteoporosis ; etiology ; Parathyroid Hormone ; metabolism ; Parathyroid Neoplasms ; complications ; metabolism ; pathology ; surgery ; Synaptophysin ; metabolism ; Thyroid Neoplasms ; metabolism ; pathology

Carcinoid Tumor ; diagnosis ; pathology ; Carcinoma, Neuroendocrine ; diagnosis ; pathology ; Ear, Middle ; Humans ; Pharynx

OBJECTIVETo investigate the expression of endothelium tight junction protein Claudin-5 and intercellular adhesion molecule CD99 in solid-pseudopapillary neoplasms (SPN) and neuroendocrine tumors of pancreas (P-NET), and their significance in the differential diagnoses.

METHODSImmunohistochemical staining of Claudin-5 and CD99 was performed in 37 cases SPN and 21 cases of P-NET.

RESULTSMembranous Claudin-5 expression was observed in all cases of SPN but was absent in all cases of P-NET. The difference was significant (P < 0.01). In SPN, 91.9% (34/37) of the cases displayed paranuclear dot-like immunoreactivity for CD99; in contrast, 61.9% (13/21) of the cases of P-NET displayed membranous staining (P < 0.01). There was a positive association between the expression of Claudin-5 and CD99 in SPN (r = 0.421,P = 0.001).

CONCLUSIONSAlthough the macroscopic and microscopic features of SPN are quite characteristic, they may not allow confident differentiation from P-NET in all cases, especially when these characteristics are not classical. If necessary, immunostaining for Claudin-5 and CD99 can help to differentiate between these entities.

12E7 Antigen ; Adolescent ; Adult ; Aged ; Antigens, CD ; metabolism ; Carcinoma, Papillary ; metabolism ; pathology ; Cell Adhesion Molecules ; metabolism ; Child ; Claudin-5 ; metabolism ; Diagnosis, Differential ; Female ; Humans ; Male ; Middle Aged ; Neuroendocrine Tumors ; metabolism ; pathology ; Pancreatic Neoplasms ; metabolism ; pathology ; Retrospective Studies ; Tight Junctions ; metabolism ; Young Adult

OBJECTIVE: To investigate the clinical features, the CT, MRI features and therapeutic strategy of nasal neuroendocrine carcinoma (NEC). METHOD: A retrospective study was carried out on 6 cases of NEC. 2 were female and 4 were male. Routine preoperative CT and MRI examination were performed. In one case,the tumor had invaded the brain and then was treated in department of oncology. Five cases were undertaken tumor resection under nasal endoscope, and combined with postoperative chemoradiation therapy. RESULT: The postoperative pathological report of 1 cases was large cell type, the remaining 4 cases were small cell type. One case treated in department of oncology had lived for 2 month with tumor in his body. One cases relapsed and died at 4 month after postoperation, 1 case was lost and 3 case did not relapse till now. CONCLUSION NEC of paranasal sinuses is malignant, but early detection, early diagnosis and treatment can improve the prognosis of this disease. For limited lesion of NEC, nasal endoscopic operation is an effective, safe and minimally injury method.
Adult ; Carcinoma, Neuroendocrine ; diagnosis ; pathology ; surgery ; Endoscopy ; Female ; Humans ; Male ; Middle Aged ; Paranasal Sinus Neoplasms ; diagnosis ; pathology ; surgery ; Prognosis ; Retrospective Studies

Collision tumors of the colon are rare. A 54-year-old man was referred to our hospital for the evaluation of hematochezia. Colonoscopy demonstrated the presence of about 3 cm sized mass in the rectosigmoid junction. After surgical resection, the colonic lesion was histologically composed of two discrete lesions: adenocarcinoma in the superficial layer and poorly differentiated neuroendocrine carcinoma in the deeper layer. We report this case of colonic collision tumor (adenocarcinoma and neuroendocrine carcinoma) with a review of the literature.
Adenocarcinoma/*diagnosis/pathology ; Antigens, CD/metabolism ; Antigens, Differentiation, T-Lymphocyte/metabolism ; Carcinoma, Neuroendocrine/*diagnosis/pathology ; Colonic Neoplasms/*diagnosis/pathology ; Colonoscopy ; Humans ; Male ; Middle Aged ; Positron-Emission Tomography and Computed Tomography ; Synaptophysin/metabolism ; Tomography, X-Ray Computed

Antigens, CD20 ; metabolism ; CD79 Antigens ; metabolism ; Carcinoma, Neuroendocrine ; metabolism ; pathology ; Carcinoma, Renal Cell ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Kidney Neoplasms ; metabolism ; pathology ; Leukocyte Common Antigens ; metabolism ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Middle Aged ; Neoplasms, Multiple Primary ; metabolism ; pathology ; Nephrectomy ; PAX5 Transcription Factor ; metabolism ; Wilms Tumor ; metabolism ; pathology

OBJECTIVETo study the clinicopathologic features and histologic differential diagnosis of small cell neuroendocrine carcinoma (SmCC) of kidney.

METHODSThe clinicopathologic features of 12 cases of SmCC of kidney encountered during the period from 1999 to 2010 were retrospectively reviewed.

RESULTSSix cases of primary and 6 cases of metastatic SmCC involving kidney were identified. Amongst the primary renal SmCC, 2 were located in renal parenchyma and 4 in renal pelvis. Chest X-ray showed negative findings. Five of them underwent radical nephrectomy. On gross examination, the tumor was located centrally around the renal pelvis in 4 cases and peripherally in renal parenchyma in 1 case. On the other hand, 4 of the 6 cases of metastatic SmCC were discovered during therapy for pulmonary SmCC. Two of these patients presented with abdominal pain and gross hematuria, with lung and renal tumor masses identified simultaneously. The diagnosis of all the 6 cases of metastatic SmCC was confirmed by fine needle aspiration biopsy. Microscopically, pure SmCC was demonstrated in the 2 cases of primary renal parenchymal SmCC and 6 cases of metastatic SmCC. The 4 primary renal pelvic SmCC coexisted with urothelial carcinoma component. On immunohistochemical study, all cases were positive for cytokeratin, synaptophysin and CD56. All metastatic cases and 4 primary cases were also positive for TTF-1. Of six patients with primary SmCC two died 4 and 9 months after operation, and two were alive with a follow-up of 25 and 138 months, respectively. Five of six cases with metastatic SmCC died 3 - 8 months after diagnosis. The other 3 cases were failed to follow-up.

CONCLUSIONSBoth primary and metastatic SmCC can be found in the kidney. Although rare, primary SmCC is located either in renal parenchyma or in pelvis. The diagnosis of SmCC relies on morphologic examination and immunohistochemical study. TTF-1 immunostaining cannot reliably distinguish primary from metastatic SmCC in kidney. Correlation with clinicoradiologic findings and demonstration of coexisting urothelial carcinoma component (if any) is helpful in delineation of the tumor origin.

Adult ; Aged ; CD56 Antigen ; metabolism ; Carcinoma, Neuroendocrine ; metabolism ; pathology ; secondary ; surgery ; Carcinoma, Renal Cell ; metabolism ; pathology ; Carcinoma, Small Cell ; metabolism ; pathology ; secondary ; surgery ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Keratins ; metabolism ; Kidney Neoplasms ; metabolism ; pathology ; secondary ; surgery ; Lung Neoplasms ; pathology ; secondary ; Lymphoma ; metabolism ; pathology ; Male ; Middle Aged ; Nephrectomy ; Nuclear Proteins ; metabolism ; Retrospective Studies ; Sarcoma, Ewing ; metabolism ; pathology ; Synaptophysin ; metabolism ; Thyroid Nuclear Factor 1 ; Transcription Factors ; metabolism ; Treatment Outcome ; Wilms Tumor ; metabolism ; pathology

Adult ; Carcinoma, Neuroendocrine ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Hodgkin Disease ; metabolism ; pathology ; Humans ; Ki-1 Antigen ; metabolism ; Leukocyte Common Antigens ; metabolism ; Lung Neoplasms ; metabolism ; pathology ; surgery ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; surgery ; Melanoma ; metabolism ; pathology ; Mucin-1 ; metabolism ; Pneumonectomy ; Poly(A)-Binding Proteins ; metabolism ; Receptor Protein-Tyrosine Kinases ; metabolism ; T-Cell Intracellular Antigen-1