Adenocarcinoma, Clear Cell ; complications ; metabolism ; pathology ; surgery ; Adenoma ; pathology ; Adnexal Diseases ; pathology ; Adult ; Carcinoma, Renal Cell ; pathology ; secondary ; Cystadenoma, Papillary ; complications ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Fallopian Tube Neoplasms ; complications ; metabolism ; pathology ; surgery ; Female ; Follow-Up Studies ; Humans ; Keratin-7 ; metabolism ; Kidney Neoplasms ; pathology ; secondary ; Mucin-1 ; metabolism ; von Hippel-Lindau Disease ; complications ; metabolism ; pathology ; surgery

Metaplastic breast carcinoma is very rare, and metaplastic carcinoma with chondroid differentiation is even rarer. Here, we report a case of metaplastic carcinoma with extensive chondroid differentiation mimicking chondrosarcoma that was challenging to diagnose. The tumor was characterized by an abundant chondromyxoid matrix. The definitive area of classic invasive ductal carcinoma was minimal. The peripheral portion of the tumor showed increased cellularity with pleomorphism and definitive invasive growth. Tumor cells in the chondrosarcomatous areas were diffusely immunoreactive for S-100 protein, patchy positive for cytokeratin, but negative for epithelial membrane antigen (EMA). Tumor cells in carcinomatous areas were diffusely positive for cytokeratin, S-100 protein, and patchy positive for EMA. In both areas, tumor cells were negative for smooth muscle actin (SMA) and CD34, while oncoprotein p53 was overexpressed. When pathologists encounter breast tumors with chondroid differentiation, careful sampling and immunohistochemistry for cytokeratin and SMA are most helpful to differentiate metaplastic carcinoma from malignant phyllodes tumor and malignant adenomyoepithelioma.
S100 Proteins/chemistry ; Neoplasm Metastasis ; Muscle, Smooth/pathology ; Middle Aged ; Metaplasia ; Keratins/metabolism ; Immunohistochemistry ; Humans ; Female ; Cell Differentiation ; Carcinoma/*complications/metabolism/pathology ; CA-15-3 Antigen/metabolism ; Breast Neoplasms/complications/metabolism/*pathology ; Antigens, CD34/biosynthesis ; Actins/metabolism

OBJECTIVETo study the clinicopathologic features and differential diagnosis of dyshormonogenetic goiter.

METHODSThe clinical features, histopathologic findings and immunohistochemistry of four cases of dyshormonogenetic goiter were reviewed.

RESULTSAmongst the cases of dyshormonogenetic goiter studied, three were females and one male. The age of disease onset ranged from 6 to 12 years and the age at operation ranged from 13 to 28 years. Three patients presented with symptoms of hypothyroidism and one patient had normal thyroid function. On gross examination, the thyroid was multinodular and covered by fibrous capsule. Histologically, three patterns were observed. The predominant pattern was microfollicular/trabecular, with hyperplastic follicular cells associated with scanty colloid material. The second pattern was macrofollicular, the follicular cells were cuboid in shape, with inconspicuous mitotic figures. The third pattern was microcystic, with papillary component frequently seen. No normal intervening thyroid parenchyma was found. All the patients were on long-term thyroxine replacement therapy after operation and remained well.

CONCLUSIONSDyshormonogenetic goiter is considered as a form of thyroid hyperplasia due to enzymatic defects in hormone synthesis. The architectural polymorphism and cellular atypia may mimic thyroid neoplasms and cause difficulties in differential diagnosis.

Adolescent ; Adult ; Carcinoma, Papillary ; pathology ; Diagnosis, Differential ; Female ; Goiter ; complications ; pathology ; surgery ; Humans ; Hypothyroidism ; complications ; pathology ; surgery ; Male ; Thyroid Gland ; metabolism ; pathology ; surgery ; Thyroid Neoplasms ; pathology ; Thyroidectomy ; Thyroiditis ; pathology ; Thyrotropin ; metabolism ; Young Adult

Carcinoma, Mucoepidermoid ; complications ; metabolism ; pathology ; DNA-Binding Proteins ; metabolism ; Diagnosis, Differential ; Eosinophilia ; complications ; metabolism ; pathology ; Epithelial Cells ; pathology ; Female ; Hashimoto Disease ; metabolism ; pathology ; surgery ; Humans ; Keratin-19 ; metabolism ; Membrane Proteins ; metabolism ; Middle Aged ; Thyroid Gland ; metabolism ; pathology ; surgery ; Thyroid Nodule ; metabolism ; pathology ; surgery ; Transcription Factors ; beta Catenin ; metabolism

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

Objective: To investigate the clinical value of plasma scaffold protein SEC16A level and related models in the diagnosis of hepatitis B virus-related liver cirrhosis (HBV-LC) and hepatocellular carcinoma (HBV-HCC). Methods: Patients with HBV-LC and HBV-HCC and a healthy control group diagnosed by clinical, laboratory examination, imaging, and liver histopathology at the Third Hospital of Hebei Medical University between June 2017 and October 2021 were selected. Plasma SEC16A level was detected using an enzyme-linked immunosorbent assay (ELISA). Serum alpha-fetoprotein (AFP) was detected using an electrochemiluminescence instrument. SPSS 26.0 and MedCalc 15.0 statistical software were used to analyze the relationship between plasma SEC16A levels and the occurrence and development of liver cirrhosis and liver cancer. A sequential logistic regression model was used to analyze relevant factors. SEC16A was established through a joint diagnostic model. Receiver operating characteristic curve was used to evaluate the clinical efficacy of the model for liver cirrhosis and hepatocellular carcinoma diagnosis. Pearson correlation analysis was used to identify the influencing factors of novel diagnostic biomarkers. Results: A total of 60 cases of healthy controls, 60 cases of HBV-LC, and 52 cases of HBV-HCC were included. The average levels of plasma SEC16A were (7.41 ± 1.66) ng/ml, (10.26 ± 1.86) ng/ml, (12.79 ± 1.49) ng /ml, respectively, with P < 0.001. The sensitivity and specificity of SEC16A in the diagnosis of liver cirrhosis and hepatocellular carcinoma were 69.44% and 71.05%, and 89.36% and 88.89%, respectively. SEC16A, age, and AFP were independent risk factors for the occurrence of HBV-LC and HCC. SAA diagnostic cut-off values, sensitivity, and specificity were 26.21 and 31.46, 77.78% and 81.58%, and 87.23% and 97.22%, respectively. The sensitivity and specificity for HBV-HCC early diagnosis were 80.95% and 97.22%, respectively. Pearson correlation analysis showed that AFP level was positively correlated with alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBil), and γ-glutamyltransferase (GGT) with P < 0.01, while the serum SEC16A level was only slightly positively correlated with ALT and AST in the liver cirrhosis group (r = 0.268 and 0.260, respectively, P < 0.05). Conclusion: Plasma SEC16A can be used as a diagnostic marker for hepatitis B-related liver cirrhosis and hepatocellular carcinoma. SEC16A, combined with age and the AFP diagnostic model with SAA, can significantly improve the rate of HBV-LC and HBV-HCC early diagnosis. Additionally, its application is helpful for the diagnosis and differential diagnosis of the progression of HBV-related diseases.
Humans ; Carcinoma, Hepatocellular/pathology* ; Liver Neoplasms/pathology* ; alpha-Fetoproteins/metabolism* ; Endoplasmic Reticulum/metabolism* ; Golgi Apparatus/metabolism* ; Vesicular Transport Proteins ; Liver Cirrhosis/complications* ; Hepatitis B/complications* ; ROC Curve ; Hepatitis B virus/metabolism* ; Biomarkers, Tumor

Hepatitis C virus (HCV) is a leading etiology of hepatocellular carcinoma (HCC). The interaction of HCV with its human host is complex and multilayered; stemming in part from the fact that HCV is a RNA virus with no ability to integrate in the host's genome. Direct and indirect mechanisms of HCV-induced HCC include activation of multiple host pathways such as liver fibrogenic pathways, cellular and survival pathways, interaction with the immune and metabolic systems. Host factors also play a major role in HCV-induced HCC as evidenced by genomic studies identifying polymorphisms in immune, metabolic, and growth signaling systems associated with increased risk of HCC. Despite highly effective direct-acting antiviral agents, the morbidity and incidence of liver-related complications of HCV, including HCC, is likely to persist in the near future. Clinical markers to selectively identify HCV subjects at higher risk of developing HCC have been reported however they require further validation, especially in subjects who have experienced sustained virological response. Molecular biomarkers allowing further refinement of HCC risk are starting to be implemented in clinical platforms, allowing objective stratification of risk and leading to individualized therapy and surveillance for HCV individuals. Another role for molecular biomarker-based stratification could be enrichment of HCC chemoprevention clinical trials leading to smaller sample size, shorter trial duration, and reduced costs.
Biomarkers, Tumor/genetics/metabolism ; Carcinoma, Hepatocellular/*etiology ; Hepacivirus/genetics/*pathogenicity ; Hepatitis C/complications/pathology/virology ; Humans ; Liver Neoplasms/*etiology ; Risk

OBJECTIVETo investigate the effects of different clinicopathologic variables on serum protein fingerprint in hepatocellular carcinoma (HCC) patients.

METHODSSerum samples were collected from 112 HCC patients, Special serum protein or peptide spectra was determined by surface enhanced laser desorption/ionization-time of flight-mass spectrometry (SELDI-TOF-MS) measurement after treating the sample onto weak cation exchange (WCX2) protein chip for each case. The serum protein profiles were compared by BioMarker Wizard Software among the patients stratified according to gender, AFP, presence of portal vein tumor thrombus (PVTT), tumor size, tumor number, presence of cirrhosis, respectively.

RESULTSAccording to serum protein fingerprints of 112 HCC patients, a total of 100 protein peaks were identified at the m/z value ranging from 1100 to 30,000. (1) Sixteen significant differential proteins were found between the groups of HCC with single tumor and those with multiple tumors (P < 0.01). (2) Only one significant differential protein was found between the groups of HCC with tumor size > 3 cm and those with tumor size 5 cm and those with tumor size 10 cm and those with tumor size

CONCLUSIONSPVTT, tumor number and tumor size had significant effects on serum protein fingerprint, while no significant effect on serum protein from gender, presence of cirrhosis and AFP. The most profound impact on the serum protein was attained when cutoff was chosen to be presence of Ma-PVTT compared to less effect from Mi-PVTT and 5cm for tumor size.

Adult ; Aged ; Blood Proteins ; metabolism ; Carcinoma, Hepatocellular ; blood ; complications ; pathology ; Female ; Humans ; Liver Cirrhosis ; complications ; Liver Neoplasms ; blood ; complications ; pathology ; Male ; Middle Aged ; Neoplastic Cells, Circulating ; Peptide Mapping ; Sex Factors ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization ; alpha-Fetoproteins ; metabolism

OBJECTIVEThis study was designed to investigate the expression and significance of NET-1 in hepatocellular carcinoma (HCC) and analyze the relationship between NET-1 gene expression and clinicopathologic factors in HCC.

METHODSNET-1 gene protein expression was detected by Western blot, fluorescence immunocytochemistry, confocal laser scanning microscopy and immunohistochemistry in 8 cases of HCC tissues, human hepatoma cell line SMMC-7721, and paraffin-embeded sections from 130 cases of HCC.

RESULTSNET-1 gene protein expressed in 8 cases of HCC tissues by Western blot. The NET-1 gene protein positively located in the cytoplasm as irregular granules near Golgi apparatus in SMMC-7721cells, detected by fluorescent immunocytochemistry and observed by confocal laser scanning microscopy. The positive rate of NET-1 protein expression revealed by immunohistochemistry was 96.9% in HCC (126/130). NET-1 Protein expression in HCC was clearly correlative with HCC cytological variants, there were pronounced higher expressions in clear cell type, pleomorphic cell type, and sarcomatous change than that in hepatocytic type (P < 0.05). NET-1 Protein expression in HCC was positively correlative with the histopathologic grading, clinical stages and HCC with hepatitis and cirrhosis (P < 0.05), respectively, and negatively correlated with the presence of patches of necrosis (P < 0.05). But NET-1 protein expression was not associated with AFP level, tumor size and growth patterns, respectively.

CONCLUSIONNET-1 protein is expressed in cytoplasm of HCC cells as irregular granules near Golgi apparatus. NET-1 gene expression may promote the uncontrolled proliferation and abnormal differentiation in HCC cells.

Adult ; Aged ; Carcinoma, Hepatocellular ; complications ; metabolism ; pathology ; virology ; Cell Line, Tumor ; Cell Proliferation ; Cytoplasm ; metabolism ; Female ; Gene Expression Regulation, Neoplastic ; Golgi Apparatus ; metabolism ; Hepatitis B ; metabolism ; Hepatocytes ; metabolism ; Humans ; Liver Cirrhosis ; complications ; metabolism ; Liver Neoplasms ; complications ; metabolism ; pathology ; virology ; Male ; Middle Aged ; Neoplasm Staging ; Oncogene Proteins ; metabolism ; alpha-Fetoproteins ; metabolism

Actins ; metabolism ; Adult ; Antigens, CD34 ; metabolism ; Carcinoma, Renal Cell ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Glomus Tumor ; metabolism ; pathology ; Hemangiopericytoma ; metabolism ; pathology ; Humans ; Hypertension ; etiology ; Juxtaglomerular Apparatus ; metabolism ; pathology ; surgery ; ultrastructure ; Kidney Neoplasms ; complications ; metabolism ; pathology ; surgery ; ultrastructure ; Nephrectomy ; Wilms Tumor ; metabolism ; pathology