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  • 351.
    Zhao, Zeng-Ren
    et al.
    Department of General Surgery Hebei Medical University, Shijiazhuang 050031, P.R. China.
    Zhang, Zhiyong
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi.
    Zhang, Hong
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Dermatologi och venerologi.
    Jiang, Li
    Department of Pathology Tangshan Gongren Hospital, Tangshan 063000, P.R. China.
    Wang, Ming-Wei
    Laboratory Centre Hebei Medical University, Shijiazhuang 050031, P.R. China.
    Sun, Xiao-Feng
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Overexpression of Id-1 protein is a marker in colorectal cancer progression2008Inngår i: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 19, nr 2, s. 419-424Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The inhibitor of differentiation/DNA binding 1 (Id-1), a negative regulator of basic helix-loop-helix transcription factors, plays an important role in the regulation of cell proliferation and differentiation. We examined the Id-1 expression by immunohistochemistry in 9 adenomas, 79 primary colorectal adenocarcinomas matched with 40 adjacent normal mucosa specimens and its relationship with clinicopathological factors. The Id-1 expression was increased in the carcinoma compared to the adjacent normal mucosa either in the unmatched and matched samples or to the adenoma. There was no significant difference in the Id-1 expression between normal mucosa and adenoma. The Id-1 expression of carcinoma was increased from Dukes' stages A to B, to C and to D. The cases with lymph node metastasis had a higher rate of a stronger Id-1 expression than those without lymph node metastasis. In conclusion, Id-1 overexpression plays an important role in colorectal cancer progression.

  • 352.
    Zhou, Bin
    et al.
    Sichuan University.
    Yan, Hui
    Sichuan University.
    Li, Yuan
    Sichuan University.
    Wang, Rong
    Sichuan University.
    Chen, Keling
    Sichuan University.
    Zhou, Zongguang
    Sichuan University.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Centrum för kirurgi, ortopedi och cancervård, Onkologiska kliniken US.
    PNAS-4 expression and its relationship to p53 in colorectal cancer2012Inngår i: Molecular Biology Reports, ISSN 0301-4851, E-ISSN 1573-4978, Vol. 39, nr 1, s. 243-249Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    PNAS-4 is a novel pro-apoptotic protein activated during the early response to DNA damage; however, the molecular mechanisms and pathways regulating PNAS-4 expression in tumors are not well understood. We hypothesized that PNAS-4 is a p53 down-stream target gene and designed this study. We searched online for putative p53-binding sites in the entire PNAS-4 gene and did not find any corresponding information. In HCT116 colon cancer cells, after being transfected with small interfering RNA to silence p53, the expressions of PNAS-4 and other known p53 target gene (Apaf1, Bax, Fas and Dr5) were determined by real-time PCR. We found that PNAS-4 was up-regulated while Apaf1, Bax, Fas and Dr5 were down-regulated. We then examined the expression of PNAS-4 and p53 mutation in colorectal cancer patients. PNAS-4 expressed both in colorectal cancers and normal tissues, but compared with paired control, PNAS-4 was up-regulated in cancers (P = 0.018). PNAS-4 overexpression ratios were correlated to the p53 mutant status (P = 0.001). The mean PNAS-4 expression levels of p53 mutant homozygote group and heterozygote group were higher than that of p53 wild type group (P = 0.013). The expression ratios of PNAS-4 (every sample in relative to its paired normal mucosa) were different between negative lymph node metastasis (66% up-regulated, 34% down-regulated) and positive metastasis (42% up-regulated, 58% down-regulated). Taken together, these findings suggested that PNAS-4 was not a p53 target, but overexpression of PNAS-4 was correlated to p53 inactivity in colorectal cancer.

  • 353.
    Zhou, X.
    et al.
    Sichuan University.
    Li, Y.
    Sichuan University.
    Ding, J.
    Sichuan University.
    Wang, L.
    Sichuan University.
    Wang, R.
    Sichuan University.
    Zhou, B.
    Sichuan University.
    Gu, J.
    Sichuan University.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Zhou, Z.
    Sichuan University.
    Down-regulation of tumor necrosis factor-associated factor 6 is associated with progression of acute pancreatitis complicating lung injury in mice2009Inngår i: Tohoku Journal of Experimental Medicine, ISSN 0040-8727, Vol. 217, nr 4, s. 279-285Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Acute lung injury is one of the critical complications of acute pancreatitis (AP). Tumor necrosis factor-associated factor 6 (TRAF6) is a key adaptor that regulates various inflammatory signaling pathways, including those mediated by Toll-like receptors (TLRs). This study was performed to investigate the potential role of TRAF6 in the pathogenesis of AP and pancreatitis-associated acute lung injury using a mouse model of caerulein-induced AP (CAP). CAP was induced by intraperitoneal injection of caerulein hourly for 7 times (50 µg/kg), and control mice were treated with saline of the same volume. Typical pancreatic and lung inflammation was observed in the early stage (1 h) of CAP, as judged by morphological changes. Likewise, in CAP mice, the pancreatic myeloperoxidase activity and serum levels of interleukin-6 add interleukin-10 were significantly increased after 2 h, peaked it 4h, and then decreased by 24 h. The expression of TRAF6 was then studied by real time-PCR, immunohistochemistry, and Western blot analysis. Compared with control group, TRAF6 mRNA level was decreased in CAP group within the first 12 h, and then significantly increased after 24 h, which was in accordance with the protein level detected by Western blot analysis and immunohistochemistry. Moreover, TRAF6 protein was expressed in both pancreatic acinar cells and lung bronchial epithelial cells. In conclusion, the down-regulation of TRAF6 was associated with increased inflammatory severity in the pancreas and lung, suggesting that TRAF6 is involved in the anti-inflammatory process during AP. TRAF6 may be a potential molecular target for treating AP.

  • 354.
    Zhou, Xiang-Yu
    et al.
    Sichuan University.
    Zhou, Zong-Guang
    Sichuan University.
    Ding, Jun-Li
    Sichuan University.
    Wang, Ling
    Sichuan University.
    Wang, Rong
    Sichuan University.
    Zhou, Bing
    Sichuan University.
    Gu, Jun
    Sichuan University.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Li, Yuan
    Sichuan University.
    TRAF6 as the Key Adaptor of TLR4 Signaling Pathway Is Involved in Acute Pancreatitis2010Inngår i: PANCREAS, ISSN 0885-3177, Vol. 39, nr 3, s. 359-366Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objectives: To study the potential role of tumor necrosis factor receptor-associated factor 6 (TRAF6) as the key adaptor of the toll-like receptor 4 (TLR4) signaling pathway in acute pancreatitis (AP) in mice. Methods: Acute pancreatitis was induced by 7 intraperitoneal injections of cerulein in TLR4-deficient (TLR4-Def) and TLR4 wild-type (TLR4-WT) mice. Inflammatory severity was scored and evaluated based on pathological study. TRAF6 expression was determined by reverse transcriptase polymerase chain reaction, Western blot, and immunohistochemistry. Results: Acute pancreatitis was successfully induced in both mice strains, but the inflammatory progression was different. In TLR4-Def mice, pancreatic inflammation was blunt and mild first, then became increasingly intensive and peaked at the later stage, whereas in the TLR4-WT mice, the response was fast initiated and peaked at the early stage of AP, then alleviated gradually. TRAF6 expression in TLR4-Def mice was significantly higher than that in the TLR4-WT mice. Immunohistochemistry located TRAF6 expressed mainly in the pancreatic acinar cells. Conclusions: The TLR4-TRAF6 signaling pathway is critically involved in AP. Other signaling pathways beyond TLR4 may participate in the pancreatic inflammatory process via TRAF6. As a convergence point of the TLR4-dependent and the TLR4-independent signaling pathways, TRAF6 plays an important role in AP.

  • 355.
    Zhou, X.-L.
    et al.
    Department of Molecular Medicine, Karolinska Institutet, S-171 76 Stockholm, Sweden.
    Djureinovic, T.
    Department of Molecular Medicine, Karolinska Institutet, S-171 76 Stockholm, Sweden.
    Werelius, B.
    Department of Molecular Medicine, Karolinska Institutet, S-171 76 Stockholm, Sweden.
    Lindmark, G.
    Department of Surgery, Helsingsborg Hospital, S-251 87 Helsingborg, Sweden.
    Sun, Xiao-Feng
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Lindblom, A.
    Department of Molecular Medicine, Karolinska Institutet, S-171 76 Stockholm, Sweden, Department of Molecular Medicine, CMM L8:02, Karolinska Institutet, S-171 76 Stockholm, Sweden.
    Germline mutations in the MYH gene in Swedish familial and sporadic colorectal cancer2005Inngår i: Genetic Testing, ISSN 1090-6576, E-ISSN 1557-7473, Vol. 9, nr 2, s. 147-151Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Biallelic germline mutations in the base excision repair gene MYH have been shown to predispose to a proportion of multiple colorectal adenomas and cancer. To evaluate the contribution of MYH mutations to non-FAP, non-HNPCC familial colorectal cancer, 84 unrelated Swedish individuals affected with colorectal cancer from such families were screened for germline mutations in the coding sequence of the gene. None of the cases was found to carry any pathogenic sequence change. We then determined the prevalence of the two most common pathogenic MYH mutations found in Caucasians, Y165C and G382D, in 450 Swedish sporadic colorectal cancer cases and 480 Swedish healthy controls. The frequency of both variants in Swedish cases and controls was similar to those previously reported. In addition, we found that previously unknown sequence variations at the position of amino acid 423 (R423Q, R423P, and R423R) appear to occur more frequently in cases than in controls (p = 0.02), a finding that warrants future studies. © Mary Ann Liebert, Inc.

  • 356.
    Zhu, Zhen-Long
    et al.
    The First Hospital of Hebei Medical University, China.
    Yan, Bao-Yong
    The First Hospital of Hebei Medical University, China.
    Zhang, Yu
    Clinical College of Hebei Medical University, China.
    Yang, Yan-Hong
    The First Hospital of Hebei Medical University, China.
    Wang, Zheng-Min
    The First Hospital of Hebei Medical University, China.
    Zhang, Hong-Zhen
    The First Hospital of Hebei Medical University, China.
    Wang, Ming-Wei
    The First Hospital of Hebei Medical University, China.
    Zhang, Xiang-Hong
    Graduate School of Hebei Medical University, China.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Centrum för kirurgi, ortopedi och cancervård, Onkologiska kliniken US.
    Cytoplasmic expression of p33(ING1b) is correlated with tumorigenesis and progression of human esophageal squamous cell carcinoma.2013Inngår i: Oncology letters, ISSN 1792-1074, Vol. 5, nr 1, s. 161-166Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    p33(ING1b), a newly discovered candidate tumor suppressor gene and a nuclear protein, belongs to the inhibitor of growth gene family. Previous studies have shown that p33(ING1b) is involved in the restriction of cell growth and proliferation, apoptosis, tumor anchorage-independent growth, cellular senescence, maintenance of genomic stability and modulation of cell cycle checkpoints. Loss of nuclear p33(ING1b) has been observed in melanoma, seminoma, papillary thyroid carcinoma, oral squamous cell carcinoma, breast ductal cancer and acute lymphoblastic leukemia. Inactivation and/or decreased expression of p33(ING1b) have been reported in various types of cancer, including head and neck squamous cell, breast, lung, stomach, blood and brain malignancies. Since little is known about the clinicopathological significance of p33(ING1b) in esophageal squamous cell carcinoma (ESCC), this study aimed to investigate the association of p33(ING1b) expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in patients with ESCC. p33(ING1b) expression was examined by immunohistochemistry in 20 normal esophageal mucosa and in 64 ESCC specimens. The results revealed that the positive expression of p33(ING1b) protein in normal squamous cells was localized in the nucleus alone and the positive rate was 95%, while in ESCCs, the positive expression was mainly in the cytoplasm, together with nuclear expression, and the positive rate was 36% (P<0.0001). Furthermore, the cases with lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P=0.001). The cytoplasmic expression of p33(ING1b) was positively related to PINCH expression (P<0.0001) in ESCC, and the cases positive for both proteins had a high lymph node metastasis rate (P=0.001). In conclusion, p33(ING1b) cellular compartmental shift from the nucleus to the cytoplasm may cause loss of normal cellular function and play a central role in the tumorigenesis and metastasis of ESCC.

  • 357.
    Zhu, Zhen-Long
    et al.
    Hebei Medical University, Peoples R China.
    Yan, Bao-Yong
    Hebei Medical University, Peoples R China .
    Zhang, Yu
    Hebei Medical University, Peoples R China .
    Yang, Yan-Hong
    Hebei Medical University, Peoples R China .
    Wang, Zheng-Min
    Hebei Medical University, Peoples R China .
    Zhang, Hong-Zhen
    Hebei Medical University, Peoples R China .
    Wang, Ming-Wei
    Hebei Medical University, Peoples R China .
    Zhang, Xiang-Hong
    Hebei Medical University, Peoples R China .
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Centrum för kirurgi, ortopedi och cancervård, Onkologiska kliniken US.
    PINCH expression and its clinicopathological significance in gastric adenocarcinoma2012Inngår i: Disease Markers, ISSN 0278-0240, E-ISSN 1875-8630, Vol. 33, nr 4, s. 171-178Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: Particularly interesting new cysteine-histidine rich protein (PINCH) is an important component of the local adhesion complexes and upregulated in several types of malignancies, and involved in the incidence and development of tumours. PINCH expression is also independently correlated with poorer survival in patients with colorectal cancer. However, there is no study of PINCH in gastric cancer, therefore, the aim of this project was to investigate PINCH expression and its clinicopathological significance in gastric adenocarcinoma. less thanbrgreater than less thanbrgreater thanPatients and methods: PINCH expression was immunohistochemically examined in normal gastric mucous (n = 30) and gastric adenocarcinoma (n = 73), from gastric cancer patients. less thanbrgreater than less thanbrgreater thanResults: PINCH expression in the associated-stroma of gastric cancers was heterogeneous, and its positive rate (75%) was higher than that of normal gastric mucosa (43%, X-2 = 9.711, p = 0.002). The stronger staining was observed at the invasive edge of tumour when compared to the inner area of tumour. The rate of positive PINCH (88%) in the cases with lymph node metastasis was higher than that (52%) in the cases without metastasis (X-2 = 11.151, p = 0.001). PINCH expression was not correlated with patients gender, age, tumour size, differentiation and invasion depth (p andgt; 0.05). less thanbrgreater than less thanbrgreater thanConclusion: PINCH protein might play an important role in the tumourigenesis and metastasis of gastric adenocarcinoma.

  • 358.
    Zhu, Zhenlong
    et al.
    Department of Pathology, The First Hospital of Hebei Medical University, China.
    Yang, Yanhong
    Department of Pathology, The First Hospital of Hebei Medical University, China.
    Zhang, Yu
    Clinical College, Hebei Medical University, China.
    Wang, Zhengmin
    Department of Pathology, The First Hospital of Hebei Medical University, China.
    Cui, Dongsheng
    Central Laboratory, The First Hospital of Hebei Medical University, China.
    Zhang, Jinting
    Central Laboratory, The First Hospital of Hebei Medical University, China.
    Wang, Mingwei
    Central Laboratory, The First Hospital of Hebei Medical University, China.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    PINCH expression and its significance in esophageal squamous cell carcinoma2008Inngår i: Disease Markers, ISSN 0278-0240, E-ISSN 1875-8630, Vol. 25, nr 2, s. 75-80Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Particularly interesting new cysteine-histidine rich protein (PINCH), as a newly discovered protein of LIM family members, may play a role in signal transduction of integrin and growth factor, and involved in the incidence and development of tumors. PINCH protein is overexpressed in tumor-associated stroma of several types of tumors. However, there is no study of the PINCH in esophageal cancer, therefore we investigated PINCH expression in esophageal squamous cell carcinomas and its clinicopathogical significance in the patients. PINCH expression was immunohistochemically examined in 20 normal esophageal samples and 64 esophageal squamous cell carcinomas. The results showed that PINCH expression in the stroma of cancers was heterogeneous, and its positive rate (56%) was higher than that of normal esophageal mucosa (5%, p<0.0001). The stronger staining was observed at the invasive edge of tumor when compared to the inner area of tumor. The rate of positive PINCH (90%) in the cases with lymph node metastasis was higher than that (41%) in the cases without metastasis (p<0.0001). PINCH expression was not correlated with patients’ gender, age, tumor location, size and differentiation (p>0.05). The results suggest that PINCH protein may be a marker of tumor associated-stroma involving tumor development, and predicting the ability of invasion and metastasis of esophageal squamous cell carcinoma.

  • 359.
    Zhu, Zhen-Long
    et al.
    Hebei Medical University.
    Zhao, Zeng-Ren
    Hebei Medical University.
    Zhang, Yu
    Hebei Medical University.
    Yang, Yan-Hong
    Hebei Medical University.
    Wang, Zheng-Min
    Hebei Medical University.
    Cui, Dong-Sheng
    Hebei Medical University.
    Wang, Ming-Wei
    Hebei Medical University.
    Kleeff, Joerg
    Technical University of Munich.
    Kayed, Hany
    University of Heidelberg.
    Yan, Bao-Yong
    Hebei Medical University.
    Sun, Xiao-Feng
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Onkologi. Linköpings universitet, Hälsouniversitetet. Östergötlands Läns Landsting, Kirurgi- och onkologicentrum, Onkologiska kliniken US.
    Expression and significance of FXYD-3 protein in gastric adenocarcinoma2010Inngår i: DISEASE MARKERS, ISSN 0278-0240, Vol. 28, nr 2, s. 63-69Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Objective: FXYD-3, also known as Mat-8, is a member of the FXYD protein family. It was reported that this protein can associate with and modify the transport properties of Na, K-ATPase, and may play an important role in a variety of physiological and pathological states. This protein is up-regulated in certain types of cancers (such as breast, prostate and pancreatic cancer), but down-regulated in other types of cancers (such as colon and kidney cancer). No study has been performed in gastric cancer; therefore, the aim of this project was to investigate FXYD-3 expression and its clinicopathological significance in gastric adenocarcinoma. Patients and methods: FXYD-3 protein was examined by immunohistochemistry in normal gastric mucous (n = 29) and gastric adenocarcinoma (n = 51), obtained from surgical resection of gastric cancer patients. Results: FXYD-3 protein was present in the cytoplasm of normal gastric epithelial cells or gastric cancer cells. The rate of FXYD-3 strong expression was significantly higher in cancer (51% of 51) than in normal mucosa (10% of 29, X-2=13.210, p andlt; 0.0001). FXYD-3 expressed strongly in ulcerative/infiltrating types of cancers compared to polypoid/fungating ones (X-2 = 5.765, p = 0.016). However, FXYD-3 expression was not correlated with patients gender, age, tumor size, lymph node status and histological grade (p andgt; 0.05). Conclosion: Up-regulated expression of FXYD-3 protein may be involved in tumourgenesis and invasion of gastric adenocarcinoma.

5678 351 - 359 of 359
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