Purpose To investigate clinicopathological features, diagnosis and differential diagnosis of non-sebaceous lymphadenoma of the parotid gland. Methods The histopathological morphology, immunohistochemical profiles and clinicopathological features were an-alyzed in two cases of NSL, along with review the related literatures. Results Two patients were female adults. Microscopically, The tumor was a well-circumscribed mass surrounded by a fibrous capsule of variable thickness and comprised a mixture of proliferating epi-thelium accompanied by a prominent lymphoid component, reactive lymphoid follicles were found in lymphoid stroma. The epithelial component took the form of anastomosing trabeculae, glands, solid basaloid islands or cyst formation. The cysts and glands were lined with luminal cells and abluminal cells, filled with eosinophilic secretions with occasional histiocytes. The epithelial cell was no seba-ceous differentiation, significant cytological atypia and mitotic activity. A fibrous capsule with subcapsular sinus was seen around the mass in one case. Immunohistochemically, the abluminal cells were positive for p63, CK34βE12 and CK5/6, while the epithelial cells were positive for CK(AE1/AE3) and CK7. Conclusion NSL is a very rare benign of salivary gland, which occuring in the lymph node lesions are less reported, knowledge of the wide histological spectrum of this rare tumor is important in order to avoid misdiagno-sis, particularly as malignant tumor.

Abnormal activation of Wnt signaling pathway is closely related to the occurrence of tumor, and T cell factor 4 (Tcf4 ) and beta-catenin are important signal transmission factors of this pathway. The aim of the present study is to explore the significance and correlation between expression of Tcf4, beta-catenin and secreted frizzled related protein 1(SFRP1), suppressor gene of Wnt signaling pathway, in colorectal carcinoma and their correlations to the clinicopathological factors. The expressions of Tcf4, beta-catenin and SFRP1 were performed with immunohistochemistry staining in 97 cases of primary colorectal carcinoma and 40 cases of normal colorectal mucosa tissues. The results showed that the abnormal expression rates of Tcf4 and beta-catenin in colorectal carcinoma were significantly higher than those in the control groups (P<0.01). The positive rate of SFRP1 was significantly lower than those in the control groups (P<0.01). The abnormal expression rates of Tcf4 and beta-catenin were also related to the lymph node metastasis and Dukes stage (P<0.05). A significant correlation was found between the expressions of SFRP1 and Tcf4, beta-catenin (P<0.05). Overexpression of Tcf4 and beta-catenin was related to poor prognosis (P<0.05). But the survival rates of the group with SFRP1 expressions were higher than those in group without SFRP1 expressions (P<0.05). Cox multifactor regression analysis indicated that Dukes stage, expression of beta-catenin and SFRP1 were independent risk factors of colorectal carcinoma (P<0.05). The results suggested that the abnormal expression of Tcf4 and beta-catenin in colorectal cancer may be related to the reduced or absent expression of SFRP1. beta-catenin accumulation in the nuclei formed complexes with Tcf4 is one of the important molecular switch maintaining colorectal malignant phenotype. The combined detection of these indexes may perform an important role in predicting the progression and prognosis of colorectal cancer, and could provide new molecular targets for gene treatment of colorectal cancer.
Carcinoma ; metabolism ; Colorectal Neoplasms ; metabolism ; Disease Progression ; Humans ; Intercellular Signaling Peptides and Proteins ; metabolism ; Lymphatic Metastasis ; Membrane Proteins ; metabolism ; Phenotype ; Prognosis ; Risk Factors ; Transcription Factor 7-Like 2 Protein ; metabolism ; Wnt Signaling Pathway ; beta Catenin ; metabolism

Objective: To investigate the clinicopathological features, diagnosis, and differential diagnosis of gallbladder sarcomatoid carcinoma. Methods: The clinical manifestations and the microscopic and immunohistochemical characteristics of six patients with gallbladder sarcomatoid carcinoma were analyzed with a follow-up period. Related literature was reviewed. Results:Immunohistochemical markers of gallbladder sarcomatoid carcinoma with spindle cell morphology were epithelial and mesenchymal positivity. Conclusion: Gallbladder sarcomatoid carcinoma could be firmly diagnosed by microscopic morphology and immunohistochemistry. Radical resection is currently used to treat such patients. However, more cases with longer follow-up period are needed to discover better treatments and improve the survival of these patients.

Objective To evaluate the clinical value and toxicities of docetaxel plus capecitabine in the first-line treatment of metastatic breast cancer (MBC),and compare the outcomes among different molecular subtypes.Methods A total of 108 patients with MBC who received docetaxel plus capecitabine combination treatment between January 1,2012 and December 31,2015 in Bejing Chaoyang District Sanhuan Cancer Hospital were retrospectively analyzed,and 104 cases were available for evaluation.The clinicopathological characteristics,clinical value and toxicities of these patients were evaluated.Results The patients were divided into 3 molecular subtypes,among 104 patients,85 patients in Luminal subtype,14 patients in triple negative breast cancer (TNBC) subtype,and 5 patients in human epidermal growth factor receptor-2 (HER-2) over expression subtype.The treatment achieved objective responses (OR) in 55 patients (52.9％),and the disease control rate (DCR) was 88.5％,including complete response (CR) in 4 patients,partial response (PR) in 51 patients,stable disease (SD) in 37 patients,and progressive disease (PD) in 12 patients.In Luminal subtype,4 patients achieved CR,43 PR,33 SD,and 5 PD.In TNBC subtype,6 patients achieved PR,3 SD,5 PD.In the HER-2 over expression subtype,2 patients achieved PR,1 SD,2 PD.There was no significant difference in the short-term therapeutic effect among 3 molecular subtypes (x2 =4.429,P =0.106).As a result,the progression-free survival (PFS) of the 104 patients was 1.5-121.0 months,and the median PFS was 10.0 months.The median PFS was 11.0 months in Luminal subtype,4.0 months in TNBC subtype and 10.3 months in HER-2 over expression subtype,with a significant difference (x2 =7.510,P =0.006).The most common adverse events were hand-foot syndrome (HFS),nausea or vomiting,neutropenia,anaemia,diarrhea and so on.The incidence of grade 2/3 HFS was 44.2％ (46/104),and the grade 3/4 neutropenia was 39.4％ (41/104).Conclusion The first-line treatment of MBC using docetaxel plus capecitabine is effective,and the toxicities can be tolerable,especially in the Luminal subtype.

OBJECTIVETo investigate the correlation between infection with L-form of Helicobacter pylori (Hp-L) and the expressions of macrophage migration inhibition factor (MIF), matrix metalloproteinase 9 (MMP9), and vascular endothelial growth factor (VEGF) in gastric cancer.

METHODSHp-L was examined in 80 gastric carcinoma and 50 adjacent normal tissues by Gram staining and immunohistochemical staining, and the expressions of MIF, MMP9 and VEGF were detected by immunohistochemical staining; the expression of MIF mRNA was detected by RT-PCR and the expression of MIF, MMP9 and VEGF proteins were detected by Western blotting in 30 fresh gastric cancer tissues and the corresponding adjacent tissues.

RESULTSOf the 80 gastric carcinoma tissues, 57 (71.25%) showed Hp-L positivity detected by both Gram staining and immunohistochemical staining, as compared with a rate of only 14% in the adjacent normal tissues (P<0.05). The gastric carcinoma tissues showed higher expression levels of MIF, MMP9 and VEGF proteins than the corresponding adjacent normal mucosa; the positivity MIF, MMP-9 and VEGF proteins were significantly higher in Hp-L-positive gastric carcinoma than in Hp-L-negative cases (P<0.05). Positive correlations were found between Hp-L positivity and the expressions of MIF, MMP-9 and VEGF (r=0.598, 0.292, 0.341, respectively, P<0.05). The 30 fresh gastric cancer tissues showed also significantly higher MIF mRNA expression and MIF, MMP-9 and VEGF protein expressions than the adjacent tissues (t=3.729, P<0.01). The expressions of MIF and MMP-9 were also related to the clinicopathological factors including lymph node metastasis and depth of invasion (P<0.05).

CONCLUSIONInfection with L-form of Hp-L can be an important factor that contributes to the invasion and metastasis of gastric carcinoma, the mechanism of which involves up-regulated expressions of MIF, MMP-9 and VEGF.

Adult ; Aged ; Aged, 80 and over ; Female ; Helicobacter Infections ; metabolism ; pathology ; Helicobacter pylori ; Humans ; L Forms ; Lymphatic Metastasis ; Macrophage Migration-Inhibitory Factors ; metabolism ; Male ; Matrix Metalloproteinase 9 ; metabolism ; Middle Aged ; Stomach Neoplasms ; metabolism ; microbiology ; pathology ; Vascular Endothelial Growth Factor A ; metabolism

Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00%(6/30), 24.24%(8/33), and 21.05%(16/76), respectively;χ2=0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells. Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00%(6/30), 24.24%(8/33), and 21.05%(16/76), respectively;χ2=0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells. Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

OBJECTIVETo investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC).

METHODSThe expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting.

RESULTSAll the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00% (6/30), 24.24% (8/33), and 21.05% (16/76), respectively; Χ² =0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells.

CONCLUSIONAberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

Carcinogenesis ; Carcinoma, Hepatocellular ; metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus ; Cytoplasm ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Hepatocytes ; metabolism ; Humans ; Immunohistochemistry ; Liver Cirrhosis ; Liver Neoplasms ; metabolism ; Membrane Glycoproteins ; metabolism ; Receptors, Immunologic ; metabolism ; Triggering Receptor Expressed on Myeloid Cells-1 ; Up-Regulation

Objective To investigate the correlation between infection with L-form of Helicobacter pylori (Hp-L) and the expressions of macrophage migration inhibition factor (MIF), matrix metalloproteinase 9 (MMP9), and vascular endothelial growth factor (VEGF) in gastric cancer. Methods Hp-L was examined in 80 gastric carcinoma and 50 adjacent normal tissues by Gram staining and immunohistochemical staining, and the expressions of MIF, MMP9 and VEGF were detected by immunohistochemical staining;the expression of MIF mRNA was detected by RT-PCR and the expression of MIF, MMP9 and VEGF proteins were detected by Western blotting in 30 fresh gastric cancer tissues and the corresponding adjacent tissues. Results Of the 80 gastric carcinoma tissues, 57 (71.25%) showed Hp-L positivity detected by both Gram staining and immunohistochemical staining, as compared with a rate of only 14% in the adjacent normal tissues (P<0.05). The gastric carcinoma tissues showed higher expression levels of MIF, MMP9 and VEGF proteins than the corresponding adjacent normal mucosa;the positivity MIF, MMP-9 and VEGF proteins were significantly higher in Hp-L-positive gastric carcinoma than in Hp-L-negative cases (P<0.05). Positive correlations were found between Hp-L positivity and the expressions of MIF, MMP-9 and VEGF (r=0.598, 0.292, 0.341, respectively, P<0.05). The 30 fresh gastric cancer tissues showed also significantly higher MIF mRNA expression and MIF, MMP-9 and VEGF protein expressions than the adjacent tissues (t=3.729, P<0.01). The expressions of MIF and MMP-9 were also related to the clinicopathological factors including lymph node metastasis and depth of invasion (P<0.05). Conclusion Infection with L-form of Hp-L can be an important factor that contributes to the invasion and metastasis of gastric carcinoma, the mechanism of which involves up-regulated expressions of MIF, MMP-9 and VEGF.

Objective To investigate the correlation between infection with L-form of Helicobacter pylori (Hp-L) and the expressions of macrophage migration inhibition factor (MIF), matrix metalloproteinase 9 (MMP9), and vascular endothelial growth factor (VEGF) in gastric cancer. Methods Hp-L was examined in 80 gastric carcinoma and 50 adjacent normal tissues by Gram staining and immunohistochemical staining, and the expressions of MIF, MMP9 and VEGF were detected by immunohistochemical staining;the expression of MIF mRNA was detected by RT-PCR and the expression of MIF, MMP9 and VEGF proteins were detected by Western blotting in 30 fresh gastric cancer tissues and the corresponding adjacent tissues. Results Of the 80 gastric carcinoma tissues, 57 (71.25%) showed Hp-L positivity detected by both Gram staining and immunohistochemical staining, as compared with a rate of only 14% in the adjacent normal tissues (P<0.05). The gastric carcinoma tissues showed higher expression levels of MIF, MMP9 and VEGF proteins than the corresponding adjacent normal mucosa;the positivity MIF, MMP-9 and VEGF proteins were significantly higher in Hp-L-positive gastric carcinoma than in Hp-L-negative cases (P<0.05). Positive correlations were found between Hp-L positivity and the expressions of MIF, MMP-9 and VEGF (r=0.598, 0.292, 0.341, respectively, P<0.05). The 30 fresh gastric cancer tissues showed also significantly higher MIF mRNA expression and MIF, MMP-9 and VEGF protein expressions than the adjacent tissues (t=3.729, P<0.01). The expressions of MIF and MMP-9 were also related to the clinicopathological factors including lymph node metastasis and depth of invasion (P<0.05). Conclusion Infection with L-form of Hp-L can be an important factor that contributes to the invasion and metastasis of gastric carcinoma, the mechanism of which involves up-regulated expressions of MIF, MMP-9 and VEGF.