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  • 151.
    Yang, Lie
    et al.
    West China Hospital, Sichuan University, China.
    Zhou, Jin
    West China Hospital, Sichuan University, China.
    Ma, Qin
    West China Hospital, Sichuan University, China.
    Wang, Cun
    West China Hospital, Sichuan University, China.
    Chen, Keling
    West China Hospital, Sichuan University, China.
    Meng, Wenjian
    West China Hospital, Sichuan University, China.
    Yu, Yongyang
    West China Hospital, Sichuan University, China.
    Zhou, Zongguang
    West China Hospital, Sichuan University, China.
    Sun, Xiaofeng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Knockdown of PPAR δ Gene Promotes the Growth of Colon Cancer and Reduces the Sensitivity to Bevacizumab in Nude Mice Model2013In: PLOS ONE, E-ISSN 1932-6203, Vol. 8, no 4Article in journal (Refereed)
    Abstract [en]

    The role of peroxisome proliferator – activated receptor- δ (PPAR δ) gene in colon carcinogenesis remains highly controversial. Here, we established nude mice xenograft model using a human colon cancer cell line KM12C either with PPAR δ silenced or normal. The xenografts in PPAR δ-silenced group grew significantly larger and heavier with less differentiation, promoted cell proliferation, increased expression of vascular endothelial growth factor (VEGF) and similar apoptosis index compared with those of PPAR δ-normal group. After treated with the specific VEGF inhibitor bevacizumab, the capacities of growth and proliferation of xenografts were decreased in both groups while still significantly higher in PPAR δ-silenced group than in PPAR δ-normal group. Administration of PPAR δ agonist significantly decreased VEGF expression in PPAR δ-normal KM12C cells but not in PPAR δ-silenced cells. These findings demonstrate that, knockdown of PPAR δ promotes the growth of colon cancer by inducing less differentiation, accelerating the proliferation and VEGF expression of tumor cells in vivo, and reduces tumor sensitivity to bevacizumab. This study indicates that PPAR δ attenuates colon carcinogenesis.

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  • 152.
    Zhang, Dan
    et al.
    Sichuan University, Chengdu, Sichuan Province, China.
    Zhou, Bin
    Sichuan University, Chengdu, Sichuan Province, China.
    Li, Yuan
    Sichuan University, Chengdu, Sichuan Province, China.
    Wang, Mojin
    Sichuan University, Chengdu, Sichuan Province, China.
    Wang, Cun
    Sichuan University, Chengdu, Sichuan Province, China.
    Zhou, Zongguang
    Sichuan University, Chengdu, Sichuan Province, China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Polymorphisms of Glucose-Regulated Protein 78 and Risk of Colorectal Cancer: A Case-Control Study in Southwest China2013In: PLOS ONE, E-ISSN 1932-6203, Vol. 8, no 6Article in journal (Refereed)
    Abstract [en]

    Glucose-regulated protein 78 (GRP78), an endoplasmic reticulum chaperone, up-regulation serves as an efficient mechanism to promote malignant transformation of colorectal cancer (CRC) and protect CRC cells against apoptosis. Recently, the analysis of GRP78 polymorphisms has already determined that GRP78 rs391957 polymorphism could predict clinical outcome in CRC patients. Thus, we tested whether GRP78 polymorphisms are related to the risk of CRC. In this study, we detected two GRP78 polymorphisms (rs391957 (C>T) and rs430397 (G>A)) in 414 CRC cases and 502 hospital-based cancer-free healthy controls in Southwest China using a polymerase chain reaction–restriction fragment length polymorphism technique. Compared with the CC genotype, carriers of CT and TT genotypes of rs391957 polymorphism had higher risks of CRC (odds ratio (OR) = 1.39, 95% confidence interval (CI) = 1.06–1.83 for CT genotype and OR = 2.10, 95% CI = 1.06–4.14 for TT genotype, respectively). In CRC cases, the variant T allele was significantly associated with tumor invasion stage (P = 0.030), but not with status of lymph nodes metastasis (P = 0.052). Compared with the GG genotype, carriers of GA and AA genotypes of rs430397 polymorphism had higher risks of CRC (OR = 1.63, 95% CI = 1.23–2.15 for GA genotype and OR = 2.92, 95% CI = 1.23–6.94 for AA genotype, respectively). The rs430397 polymorphism was not associated with the clinicopathological characteristics of CRC. These data provide the first evidence that GRP78 rs391957 and rs430397 polymorphisms could serve as markers to predict the risk of CRC.

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  • 153.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Ahmadi, Ahmad
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Arbman, G
    Zdolsek, J
    Carstensen, J
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Nordenskjöld, Bo
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Söderkvist, Peter
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Glutathione S-transferase T1 and M1 genotypes in normal mucosa, transitional mucosa and colorectal adenocarcinom.1999In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 84, p. 135-138Article in journal (Refereed)
  • 154.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Arbman, Gunnar
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Codon 201 polymorphism of DCC gene is a prognostic factor in patients with colorectal cancer2003In: Cancer Detection and Prevention, ISSN 0361-090X, E-ISSN 1873-443X, Vol. 27, no 3, p. 216-221Article in journal (Refereed)
    Abstract [en]

    The polymorphism at codon 201 of the "deleted in colorectal carcinoma" (DCC) gene has been liked to susceptibility to colorectal cancer. However, its clinicopathological significance has not been reported. We examined the codon 201 polymorphism and loss of heterozygosity (LOH) by PCR-restriction fragment length polymorphism (PCR-RFLP) in 59 colorectal cancers, 48 samples from transitional mucosa and 67 samples from normal mucosa. The frequencies of the polymorphism did not significantly differ from normal to transitional mucosa and to tumor, but LOH was increased from transitional mucosa to tumor. Almost all of the LOH cases showed the polymorphism. The polymorphism was increased from well/moderately to poorly differentiated and to mucinous carcinoma (P = 0.03). The polymorphism was more frequently seen in advanced stages than in earlier stages (P = 0.02), and further predicted worse survival (P = 0.04). The data suggest that the codon 201 polymorphism of the DCC gene was a target of LOH, and predicted prognosis in colorectal cancer patients. ⌐ 2003 International Society for Preventive Oncology. Published by Elsevier Science Ltd. All rights reserved.

  • 155.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Cell biology.
    Evertsson, Sofia
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Clinicopathological and genetic characteristics of mucinous carcinomas in the colorectal.1999In: International Journal of Oncology, ISSN 1019-6439, E-ISSN 1791-2423, Vol. 14, p. 1057-1061Article in journal (Refereed)
  • 156.
    Zhang, Hong
    et al.
    Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Linköping University, Faculty of Health Sciences.
    Nordenskjöld, Bo
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Dufmats, Monika
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences.
    Söderkvist, Peter
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Sun, Xiao-Feng
    Linköping University, Department of Biomedicine and Surgery, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    K-ras mutations in colorectal adenocarcinomas and neighbouring transitional mucosa.1998In: European Journal of Cancer, ISSN 0959-8049, E-ISSN 1879-0852, Vol. 34, no 13, p. 2053-2057Article in journal (Refereed)
    Abstract [en]

    The K-ras gene in codons 12 and 13 was investigated using allele-specific polymerase chain reaction in matched normal mucosa (n = 106), transitional mucosa (n = 69) and tumours (n = 149) from 149 patients with colorectal adenocarcinomas. K-ras mutations in codon 12 were detected in 41/149 (28%) of tumours and 4/69 (6%) of transitional mucosa samples, but not in the normal mucosa. Further, mutation rates were increased in younger patients (P = 0.001) and in mucinous carcinomas (50%) compared with well differentiated (17%), moderately differentiated (26%) or poorly differentiated (24%) tumours. Our findings indicate that mucinous carcinoma may represent a distinct genetic entity.

  • 157.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Loss of p27 expression predicts poor prognosis in patients with Dukes' B stage or proximal colorectal cancer.2001In: International Journal of Oncology, ISSN 1019-6439, E-ISSN 1791-2423, Vol. 19, no 1, p. 49-52Article in journal (Refereed)
    Abstract [en]

    p27 is a cyclin-dependent kinase inhibitor which regulates progression of cells from G1 into S phase in a cell cycle. Loss of the negative regulator may contribute to oncogenesis and tumor progression. The aim of this study was to examine p27 expression in normal mucosa, primary and metastatic tumors from patients with colorectal adenocarcinomas and to analyze association of p27 with patient survival and clinicopathological variables. p27 expression was estimated by immunohistochemistry in 178 primary colorectal cancers, 34 lymph node metastases and 48 normal mucosa samples from patients with colorectal adenocarcinoma. Associations of p27 with patient survival, clinicopathological characteristics and expression of p53, p73 and DCC were analyzed. Loss of p27 was found in 51% of primary tumors, 68% of metastases and 56% of normal samples. The intensity of p27 staining was similar in the matched primary tumor, metastasis and normal mucosa. In patients with Dukes' B or with proximal tumors, the loss of p27 predicted poorer prognosis (p = 0.03 and p = 0.05, respectively). However, there were no significant differences in the patients with other individual Dukes' stage or distal tumors. No relationships were found between p27 and patients' gender, age, tumor location, growth pattern and expression of p53, p73 and DCC (p > 0.05). The data suggest that loss of p27 was associated with poor prognosis in patients with Dukes' B tumor or those with proximal tumor. p27 might be a useful marker to identify the more progressive tumors in these groups.

  • 158.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Dermatology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Overexpression of cyclooxygenase-2 correlates with advanced stages of colorectal cancer2002In: American Journal of Gastroenterology, ISSN 0002-9270, E-ISSN 1572-0241, Vol. 97, no 4, p. 1037-1041Article in journal (Refereed)
    Abstract [en]

    OBJECTIVE: We aimed to investigate the associations of cyclooxygenase-2 (COX-2) with pathological features and survival in patients with colorectal cancer. METHODS: The expression of COX-2 was examined by immunohistochemistry in 112 primary colorectal cancers, with 64 samples from the corresponding normal mucosa and 16 metastases in the regional lymph nodes of patients with colorectal cancer. The associations of COX-2 expression with clinico-pathological features, including survival, were analyzed. RESULTS: The frequency and intensity of COX-2 staining were remarkably increased from the normal samples (17%) to the primary tumors (72%) and to the metastases (100%). Expressions of COX-2 were 25%, 74%, 78%, and 67% in Dukes' A, B, C, and D tumors, respectively (p = 0.005), and positively related to proliferative activity (p = 0.003). COX-2 expressions were 80% in colonic tumors and 60% in rectal tumors (p = 0.03). The expression of COX-2 was positively related to the better differentiated tumors in the colon (p = 0.04). We were unable to find any relationship of COX-2 with patient age, sex, tumor growth pattern, apoptosis, and patient survival (p > 0.05). CONCLUSION: We found that the expression of COX-2 was upregulated from normal cells to primary tumors and to metastases, and related to proliferative activity, tumor location, Dukes' stage, and differentiation. These results further support the evidence that COX-2 may be involved in tumorigenesis and development of colorectal cancer. ⌐ 2002 by Am. Coll. of Gastroenterology.

  • 159.
    Zhang, Hong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Synnerstad, Ingrid
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Rosdahl, Inger
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of dermatology and venereology. Östergötlands Läns Landsting, Centre for Medicine, Department of Dermatology and Venerology in Östergötland.
    Importance of FAS-1377, FAS-670, and FASL-844 polymorphisms in tumor onset, progression, and pigment phenotypes of Swedish patients with melanoma: a case-control analysis.2007In: Cancer Journal, ISSN 0765-7846, E-ISSN 1292-8658, Vol. 13, no 4, p. 233-237Article in journal (Refereed)
    Abstract [en]

    PURPOSE: Human skin melanoma at later stages usually has an extremely poor prognosis. It is of importance to search for biologic markers to identify and monitor individuals at risk for melanoma for early diagnosis and to avoid tumor progression. The FAS gene and its natural ligand (FASL) gene initiate the death signal cascade, playing a central role in the apoptotic signaling pathway and tumor growth and metastasis. PATIENTS AND METHODS: In this study, we analyzed polymorphisms in 229 patients with melanoma and 351 age- and gender-matched tumor-free individuals. Genomic DNAs were isolated from mononuclear cells in peripheral vein blood, and the polymorphisms were examined with polymerase chain reaction-restriction fragment length polymorphism techniques. Frequency in distribution of the polymorphisms was compared between the patients with melanoma and the healthy control subjects, and associations with patients' pigment phenotypes, age at diagnosis, and melanoma characteristics were analyzed. RESULTS AND CONCLUSIONS: The FAS-1377, FAS-670, and FASL-844 polymorphisms were not found to be markers of melanoma risk (P > 0.05). In patients with melanoma, frequencies of the FAS-1377, FAS-670, and FASL-844 polymorphisms were different between the patients aged <50 and > or =50 years (P < or = 0.025, P < or = 0.025, and P < or = 0.01). Moreover, the FAS-670 polymorphism correlated with tumor Breslow thickness (P < or = 0.01) and Clark level (P < or = 0.001) and was associated with tumors developing in sun-exposed locations (P < or = 0.001). FAS and FASL were not markers for melanoma risk but might be important in the development and progression of sun-induced melanoma independently of skin type.

  • 160.
    Zhang, Hong
    et al.
    University of Skovde, Sweden .
    Wang, Da-Wei
    University of Skovde, Sweden Hebei Medical University, Peoples R China .
    Adell, Gunnar
    Karolinska University Hospital, Sweden .
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    WRAP53 is an independent prognostic factor in rectal cancer- a study of Swedish clinical trial of preoperative radiotherapy in rectal cancer patients2012In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 12, no 294Article in journal (Refereed)
    Abstract [en]

    Background: Expression of WRAP53 protein has oncogenic properties and it is up regulated in several types of tumors. less thanbrgreater than less thanbrgreater thanMethods: We examined expression of WRAP53 protein in rectal cancers and analyzed its relationship to the response to preoperative radiotherapy and patient survival. The WRAP53 protein was examined by immunohistochemistry in normal mucosa, primary tumors and lymph node metastases from 143 rectal cancer patients participated in a Swedish clinical trial of preoperative radiotherapy. less thanbrgreater than less thanbrgreater thanResults: Frequency of WRAP53 protein expression was increased in primary rectal cancer compared to the normal mucosa (p andlt; 0.05). In non-radiotherapy group positive WRAP53 in primary tumors (p = 0.03, RR, 3.73, 95% CI, 1.13-11.89) or metastases (p = 0.01, RR, 4.11, 95% CI, 1.25-13.14), was associated with poor prognosis independently of stages and differentiations. In radiotherapy group, positive WRAP53 in the metastasis correlated with better survival (p = 0.04). An interaction analysis showed that the correlations of WRAP53 with the prognostic significance with and without radiotherapy in the metastasis differed (p = 0.01). In the radiotherapy group, expression of WRAP53 in metastases gave a better outcome (p = 0.02, RR, 0.32, 95% CI, 0.13-0.84), and an interaction analysis showed significance between the two groups (p = 0.01). less thanbrgreater than less thanbrgreater thanConclusion: WRAP53 may be a new biomarker used to predict prognosis and to select suitable patients for preoperative radiotherapy.

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  • 161.
    Zhang, Hong
    et al.
    University of Skovde.
    Widegren, Emma
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology.
    Wang, Da-Wei
    University of Skovde.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    SPARCL1: a potential molecule associated with tumor diagnosis, progression and prognosis of colorectal cancer2011In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 32, no 6, p. 1225-1231Article in journal (Refereed)
    Abstract [en]

    We investigated whether SPARCL1 played an essential role in tumor initiation, formation and progression of colorectal carcinomas. In this study, we examined expression of SPARCL1 protein in the normal colorectal mucosa, adjacent normal mucosa and primary and lymph node metastases from colorectal cancer patients. In matched patients, we found that SPARCL1 was negative in the distant normal colorectal mucosa, weakly expressed in the adjacent normal mucosa, strongly expressed in primary colorectal adenocarcinomas and slightly expressed in their lymph node metastases. A similar pattern was observed in the SPARCL1 expression from our series of non-matched colorectal cancer patients. The strongest expression and highest frequency of the SPARCL1 protein were found in the primary cancers. Interestingly, in the primary tumors, the frequency of SPARCL1 expression was significantly increased from the Dukes A to Dukes B tumors and then decreased gradually from the Dukes B to C and D tumors. There was no difference in the intensity of SPARCL1 expression between the central areas and invasion margins of the primary tumors. Moreover, the SPARCL1 protein was more strongly expressed in the highly differentiated tumors than the lower differentiated ones. The patients with positive expression of SPARCL1 in their tumors had worse prognosis than the patients with SPARCL1-negative ones, even after the analyses by Multivariate and Interaction method. Expression of SPARCL1 protein might be a valuable biomarker for early diagnosis in colorectal cancers and further predicting patients prognosis.

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  • 162.
    Zhang, Hong-Zhen
    et al.
    Hebei Medical University.
    Li, Xue-Hui
    Hebei Medical University.
    Zhang, Xia
    Hebei Medical University.
    Zhang, Zhi-Yong
    Tangshan Gongren Hospital.
    Meng, Ya-Li
    Hebei Medical University.
    Xu, Shu-Wen
    Hebei Medical University.
    Zheng, Yan
    Hebei Medical University.
    Zhu, Zhen-Long
    Hebei Medical University.
    Cui, Dong-Sheng
    Hebei Medical University.
    Huang, Li-Xia
    Hebei Medical University.
    Yan, Bao-Yong
    Hebei Medical University.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    PINCH Protein Expression in Normal Endometrium, Atypical Endometrial Hyperplasia and Endometrioid Endometrial Carcinoma2010In: CHEMOTHERAPY, ISSN 0009-3157, Vol. 56, no 4, p. 291-297Article in journal (Refereed)
    Abstract [en]

    Background: Particularly interesting new cysteine-histidine rich protein ( PINCH), as an adapter protein of the LIM family for signal transduction in the integrin and growth factor pathway, is upregulated in the stroma of several common types of cancers and involved in promoting tumor progression. In the present study, we examined PINCH expression in normal endometrium, atypical endometrial hyperplasia and endometrioid carcinoma, and further studied the relationships of PINCH expression with clinicopathological variables in cancer patients. Methods: PINCH expression was examined by immunohistochemistry in 23 normal endometrial samples, 18 atypical endometrial hyperplasias and 48 endometrioid endometrial carcinomas. Results: The PINCH expression in the stroma of cancer (71%) was significantly increased compared to either normal endometrium (17%, p andlt; 0.0001) or atypical hyperplasia (39%, p = 0.017), along with 9 cancers that had stronger PINCH expressions at the invasive margin of the cancers compared to the inner cancers. PINCH expression in cancer was higher in the patients with hypertension (p = 0.041) and estrogen exposure time andgt;30 years (p = 0.021). On the other hand, PINCH expression was not related to menopausal status, gravid status, blood sugar/lipid, family background of cancer, histological grade, myometrial invasion, cervical involvement, lymph nodal metastases, growth pattern, estrogen and progestogen receptors (p andgt; 0.05). Conclusion: The results suggest that PINCH seems to play a role, presently unknown, in the tumorigenesis and development of endometrial cancer that merits further study.

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  • 163.
    Zhang, Jiao
    et al.
    West China Hospital, Sichuan University, Chengdu, China.
    Zhou, Bin
    IWest China Hospital, Sichuan University, Chengdu, China.
    Liu, Yinghua
    DWest China Hospital, Sichuan University, Chengdu, China.
    Chen, Keling
    West China Hospital, Sichuan University, Chengdu, China.
    Bao, Pingqian
    West China Hospital, Sichuan University, Chengdu, China.
    Wang, Yi
    West China Hospital, Sichuan University, Chengdu, China.
    Wang, Jiaxiang
    First Affiliated Hospital of Zhengzhou University, Henan, China.
    Zhou, Zongguang
    West China Hospital, Sichuan University, Chengdu, China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology. nstitute of Digestive Surgery, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
    Li, Yuan
    West China Hospital, Sichuan University, Chengdu, China.
    Wnt inhibitory factor-1 functions as a tumor suppressor through modulating Wnt/β-catenin signaling in neuroblastoma2014In: Cancer Letters, ISSN 0304-3835, E-ISSN 1872-7980, Vol. 348, no 1–2, p. 12-19Article in journal (Refereed)
    Abstract [en]

    Neuroblastoma is the most common extracranial solid tumor in childhood and is associated with serious morbidity and mortality. The effective treatment of neuroblastoma remains one of the major challenges in pediatric oncology. The Wnt signaling pathway has been shown to play a significant role in the pathogenesis of adult and pediatric tumors. WIF-1 has been identified as an important Wnt antagonist which inhibits Wnt/β-catenin signaling by directly binding to Wnt proteins. However, the expression and function of WIF-1 in neuroblastoma remains unknown. The present study showed that WIF-1 was downregulated with high level promoter methylation in neuroblastoma cells, and was significantly upregulated after exposure to demethylating agent. This finding suggests that downregulation of WIF-1 was associated with its promoter methylation in neuroblastoma. To further study the potential function of WIF-1 in neuroblastoma, we constructed a plasmid that over-expressed WIF-1 and transfected the plasmid into one neuroblastoma cell line SK-N-SH. We found that restoration of WIF-1 inhibited the growth and proliferation of neuroblastoma cells in vitro. Morever, Wnt/β-catenin signaling activity and target genes expression were reduced by WIF-1 restoration. These results provide support that WIF-1 is downregulated and functions as a tumor suppressor by antagonizing Wnt/β-catenin signaling in neuroblastoma, suggesting a potential role as a therapeutic target in neuroblastoma.

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  • 164.
    Zhang, Jin-Ting
    et al.
    Department of Stomatology Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Wang, Da-Wei
    Department of Stomatology Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Li, Qing-Xing
    Department of Stomatology Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Zhu, Zhen-Long
    Department of Pathology Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Wang, Ming-Wei
    Central Laboratory Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Cui, Dong-Sheng
    Central Laboratory Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Yang, Yan-Hong
    Department of Pathology Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Gu, Yu-Xin
    Department of Stomatology Hebei Medical University, Shijiazhuang 050031, Hebei Province, China.
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Nuclear to cytoplasmic shift of p33ING1b protein from normal oral mucosa to oral squamous cell carcinoma in relation to clinicopathological variables2008In: Journal of Cancer Research and Clinical Oncology, ISSN 0171-5216, E-ISSN 1432-1335, Vol. 134, no 3, p. 421-426Article in journal (Refereed)
    Abstract [en]

    Purpose: p33ING1b, as a candidate tumour suppressor gene, has been found to be expressed a proportion of oral squamous cell carcinomas (OSCCs), however, its clinicopathological significance is not studied yet. Our aim was to investigate association of p33ING1b expression with clinicopathological variables and particularly interesting new cysteine-histidine rich protein (PINCH) in OSCCs. Methods: p33ING1b expression was immumohistochemically examined in 20 normal oral mucosa specimens and 49 OSCCs. Results: Normal squamous cells showed only p33ING1b nuclear expression (no cytoplasmic expression), with a rate of 90% positive cases. While 24% of OSCCs appeared cytoplasmic expression (11 of them with weak nuclear staining) and the rest tumours (76%) were negative for p33 ING1b. Furthermore, the cases having lymph node metastasis showed a higher frequency of positive cytoplasmic expression than those without metastasis (P = 0.03). The p33ING1b cytoplasmic expression was positively related to PINCH expression (P = 0.04), the cases positive for both proteins had a high rate of the metastasis (P = 0.03). Conclusions: The transfer of p33ING1b protein from the nucleus to the cytoplasm may result in loss of normal cellular function of the protein, which might play a role in the tumourigenesis and metastasis of OSCCs. © 2007 Springer-Verlag.

  • 165. Zhang, JT
    et al.
    Li, QX
    Wang, DW
    Zhu, ZL
    Yang, YH
    Cui, DS
    Wang, MW
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Up-regulation of PINCH in the stroma of oral squamous cell carcinoma predicts nodal metastasis2005In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 14, no 6, p. 1519-1522Article in journal (Refereed)
    Abstract [en]

    Particularly interesting new cysteine-histidine rich protein (PINCH), an adapter protein involved in integrin and growth factor signalling, is up-regulated in the stroma of colorectal, breast, prostate, lung and skin cancer. Strong stromal immunostaining for PINCH is an independent prognostic indicator for reduced survival in colorectal cancer, suggesting that PINCH is involved in the signalling that promotes tumour progression. Since no study on PINCH has been carried out in oral squamous cell carcinoma (OSCC), this study aimed to determine PINCH expression in OSCC and its clinicopathological significance. PINCH protein expression was examined by immunohistochemistry in 20 normal oral mucosa and in 57 OSCC specimens, The frequency of strong PINCH immunostaining was higher in tumour-associated stroma of OSCC (37%) as compared to normal oral mucosa (10%) (p=0.02). Strong PINCH stromal immunostaining predicted nodal metastasis: 19/26 (73%) OSCC cases with nodal metastasis had strong PINCH immunostaining compared to 9/31 (29%) cases without nodal metastasis (p=0.02). The PINCH expression in OSCC was more intense in stroma at the invasive edge than in intratumoural stroma. In conclusion, the up-regulation of PINCH protein in stroma may be involved in promoting invasion and metastasis in OSCC.

  • 166.
    Zhang, Wei
    et al.
    Sichuan University, Peoples R China .
    Li, Yuan
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Yang, Lie
    Sichuan University, Peoples R China .
    Zhou, Bin
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Chen, Ke-Ling
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Meng, Wen-Jian
    Sichuan University, Peoples R China .
    Liu, Yong
    Sichuan University, Peoples R China .
    Hu, Jian-Kun
    Sichuan University, Peoples R China .
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Zhou, Zong-Guang
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Knockdown of MMP-7 inhibits cell proliferation and enhances sensitivity to 5-fluorouracil and X-ray irradiation in colon cancer cells2014In: Clinical and Experimental Medicine (Testo stampato), ISSN 1591-8890, E-ISSN 1591-9528, Vol. 14, no 1, p. 99-106Article in journal (Refereed)
    Abstract [en]

    The role of matrix metalloproteinase-7 (MMP-7) in the pathogenesis of colon cancer is not understood thoroughly. Previous studies from our group have shown that the expression levels of MMP-7 were highly elevated in colorectal cancer patient specimens and were correlated with Dukes Staging, histological differentiation grade and CEA level. The goal of this study was to investigate the cellular impact of MMP-7 in colon cancer. In this study, we used the SW480 colon cancer cell lines of MMP-7 knockdown by lentivirus-mediated RNA interference as a model system to investigate the impact of MMP-7 on cell proliferation and sensitivity to 5-Fluorouracil (5-FU) and X-ray irradiation (IR). Cell proliferation and sensitivity to 5-FU and IR were measured by MTT assay and colony formation assay. Cell cycle was evaluated by flow cytometry. We showed that the down regulation of MMP-7 inhibits colon cancer cell proliferation and sensitizes tumour cells to 5-FU and IR (P less than 0.05). Decreased MMP-7 expression in SW480 cells by RNA interference triggered cell cycle arrest at G1 phase (P less than 0.05). Down regulation of MMP-7 may inhibit the cell proliferation of colon cancer cells and increase tumour cells sensitivity to radiotherapy and chemotherapy. RNAi-mediated silencing of MMP-7 may represent a powerful therapeutic approach for controlling human colorectal cancer growth.

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  • 167.
    Zhang, Xueli
    et al.
    Orebro Univ, Sweden; Soochow Univ, Peoples R China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Cao, Yang
    Orebro Univ, Sweden; Karolinska Inst, Sweden.
    Ye, Benchen
    Soochow Univ, Peoples R China.
    Peng, Qiliang
    Soochow Univ, Peoples R China.
    Liu, Xingyun
    Soochow Univ, Peoples R China.
    Shen, Bairong
    Soochow Univ, Peoples R China.
    Zhang, Hong
    Orebro Univ, Sweden.
    CBD: a biomarker database for colorectal cancer2018In: Database: The Journal of Biological Databases and Curation, E-ISSN 1758-0463, Vol. 2018, no 1 January 2018, article id bay046Article in journal (Refereed)
    Abstract [en]

    Colorectal cancer (CRC) biomarker database (CBD) was established based on 870 identified CRC biomarkers and their relevant information from 1115 original articles in PubMed published from 1986 to 2017. In this version of the CBD, CRC biomarker data were collected, sorted, displayed and analysed. The CBD with the credible contents as a powerful and time-saving tool provide more comprehensive and accurate information for further CRC biomarker research. The CBD was constructed under MySQL server. HTML, PHP and JavaScript languages have been used to implement the web interface. The Apache was selected as HTTP server. All of these web operations were implemented under the Windows system. The CBD could provide to users the multiple individual biomarker information and categorized into the biological category, source and application of biomarkers; the experiment methods, results, authors and publication resources; the research region, the average age of cohort, gender, race, the number of tumours, tumour location and stage. We only collect data from the articles with clear and credible results to prove the biomarkers are useful in the diagnosis, treatment or prognosis of CRC. The CBD can also provide a professional platform to researchers who are interested in CRC research to communicate, exchange their research ideas and further design high-quality research in CRC. They can submit their new findings to our database via the submission page and communicate with us in the CBD.

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  • 168.
    Zhang, Zhi Y
    et al.
    Tangshan Gongren Hospital, China.
    Tian, Yan F
    First Hospital of Hebei Medical University, Shijiazhuang, China .
    Wang, Yuan Y
    First Hospital of Hebei Medical University, Shijiazhuang, China .
    Zhang, Li J
    First Hospital of Hebei Medical University, Shijiazhuang, China .
    Zhao, Zeng R
    First Hospital of Hebei Medical University, Shijiazhuang, China .
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    PINCH mRNA Overexpression in Colorectal Carcinomas Correlated with VEGF and FAS mRNA Expression2011In: Anticancer Research, ISSN 0250-7005, E-ISSN 1791-7530, Vol. 31, no 12, p. 4127-4133Article in journal (Refereed)
    Abstract [en]

    BACKGROUND:

    Particularly interesting new cysteine-histidine-rich protein (PINCH) was found to be up-regulated in the stroma of colorectal carcinomas (CRCs) in our previous studies and was involved in angiogenesis through activation of fibroblasts in extracellular matrix (ECM) in response to tumors. Here, we examined PINCH mRNA expression in colorectal cancer and investigated its relationship with the clinicopathological features and proliferation cell nuclear antigen (PCNA), vascular endothelial growth factor (VEGF) and FAS.

    MATERIALS AND METHODS:

    The primary cancer tissues, adjacent noncancerous tissues and the proximal and distant margins of normal mucosa were collected from 81 colorectal cancer patients during surgery. PINCH, PCNA, VEGF and FAS mRNA expression was examined by reverse transcriptional PCR (RT-PCR).

    RESULTS:

    PINCH mRNA expression was significantly increased in primary tumors compared with that in adjacent noncancerous tissues, and the proximal and distant margins of normal mucosa (p<0.0001). Expression of PINCH mRNA in colon cancer tended to be higher than expression in rectal cancer (p=0.051). Tumors which had infiltrated through the wall of the colorectum trended to have higher PINCH mRNA expression (p=0.073). PINCH mRNA expression in primary tumors was positively related to the expression of PCNA mRNA (r=0.534, p=0.010), VEGF mRNA (r=0.431, p=0.022) and FAS mRNA (r=0.542, p=0.012).

    CONCLUSION:

    PINCH mRNA was overexpressed in colorectal cancer and associated with PCNA mRNA, VEGF mRNA and FAS mRNA expression. PINCH mRNA was involved in the development of colorectal cancer and might play a role in the epithelial mesenchymal transition in the rectum differently than in the colon, through the adenomatous polyposis coli (APC)/catenin pathway.

  • 169.
    Zhang, Zhiyong
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences.
    Zhang, Hong
    University of Skovde.
    Adell, Gunnar
    Karolinska University Hospital.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Endosialin expression in relation to clinicopathological and biological variables in rectal cancers with a Swedish clinical trial of preoperative radiotherapy2011In: BMC CANCER, ISSN 1471-2407, Vol. 11, no 89Article in journal (Refereed)
    Abstract [en]

    Background: The importance of changes in tumour-associated stroma for tumour initiation and progression has been established. Endosialin is expressed in fibroblasts and pericytes of blood vessels in several types of tumours, and is involved in the progression of colorectal cancer. In order to see whether endosialin was related to radiotherapy (RT) response, and clinicopathological and biological variables, we investigated endosialin expression in rectal cancers from the patients who participated in a Swedish clinical trial of preoperative RT. Methods: Endosialin was immunohistochemically examined in normal mucosa, including distant (n = 72) and adjacent (n = 112) normal mucosa, and primary tumours (n = 135). Seventy-three of 135 patients received surgery alone and 62 received additional preoperative RT. Results: Endosialin expression in the stroma increased from normal mucosa to tumour (p andlt; 0.0001) both in RT and non-RT group. In the RT group, endosialin expression in the stroma was positively associated with expression of cyclooxygenase-2 (Cox-2) (p = 0.03), p73 (p = 0.01) and phosphates of regenerating liver (PRL) (p = 0.002). Endosialin expression in the tumour cells of both in the RT group (p = 0.01) and the non-RT group (p = 0.06) was observed more often in tumours with an infiltrative growth pattern than in tumours with an expansive growth pattern. In the RT group, endosialin expression in tumour cells was positively related to PRL expression (p = 0.02), whereas in the non-RT group, endosialin expression in tumour cells was positively related to p73 expression (p = 0.01). Conclusions: Endosialin expression may be involved in the progression of rectal cancers, and was related to Cox-2, p73 and PRL expression. However, a direct relationship between endosialin expression and RT responses in patients was not found.

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  • 170.
    Zhang, Zhiyong
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology.
    Zhao, Zeng-Ren
    Adell, Gunnar
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Jarlsfelt, Ingvar
    Cui, Yong-Xing
    Kayed, Hany
    Kleeff, Jörg
    Wang, Ming-Wei
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Expression of MAC30 in rectal cancers with or without preoperative radiotherapy2007In: Oncology, ISSN 0890-9091, Vol. 71, no 3-4, p. 259-265Article in journal (Refereed)
    Abstract [en]

    Objective: Meningioma-associated protein (MAC30) is overexpressed in several types of cancers, but its therapeutic implication in the patients has not been studied. We examined the relationship of MAC30 with clinicopathological and biological factors in rectal cancer patients with or without radiotherapy (RT). Methods: MAC30 was immunohistochemically examined in 75 distant and 91 adjacent normal mucosa specimens, 132 primary tumours and 39 lymph node metastases from rectal cancer patients participating in a clinical trial of preoperative RT. Results: In the RT group, MAC30 was or tended to be positively correlated with infiltrated growth pattern (p = 0.02), PRL (phosphatase of regenerating liver, p = 0.01) and Ki-67 expression (p = 0.06). MAC30 at the invasive margin of the metastasis was related to poor survival (p = 0.02) in the whole group of patients. MAC30 in primary tumours was not related to recurrence and survival in the non-RT or RT group. Conclusions:MAC30 expression in metastasis was an indicator for poor survival. After RT, MAC30 seemed to be more related to aggressive morphological and biological factors, however, we did not find direct evidence that MAC30 expression was related to the outcome of patients with or without RT. Copyright © 2006 S. Karger AG.

  • 171. Zhang, Zhi-Yong
    et al.
    Zhao, Zeng-Ren
    Jiang, Li
    Li, Jia-Chen
    Gao, Yan-Min
    Cui, Dong-Sheng
    Wang, Che-Jiang
    Schneider, Jose
    Wang, Ming-Wei
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Nup88 expression in normal mucosa, adenoma, primary adenocarcinoma and lymph node metastasis in the colorectum2007In: Tumor Biology, ISSN 1010-4283, E-ISSN 1423-0380, Vol. 28, no 2, p. 93-99Article in journal (Refereed)
    Abstract [en]

    Objectives: It was the aim of this study to investigate Nup88 expression in normal colorectal mucosa, adenoma, adenocarcinoma and lymph node metastasis, as well as the relationship between Nup88 expression and clinicopathological features. Methods: Nup88 expression was examined by immunohistochemistry in 84 normal mucosa samples, 32 adenomas, 181 primary adenocarcinomas, and 18 lymph node metastases from colorectal tumour patients. Results: Nup88 expression was observed in normal epithelial and tumour cells. The frequency of strong Nup88 expression was increased from normal mucosa or adenoma to primary tumour and lymph node metastasis (p < 0.0001). There was no significant difference in the expression between normal mucosa and adenoma (p = 0.41). The frequency of strong Nup88 expression was higher in ulcerated tumours (40%) than in polypoid/large fungating tumours (23%, p = 0.048). The frequency of strong Nup88 expression was significantly different among tumours with good (21%), moderate (42%) and poor differentiation (48%, p = 0.01). Nup88 expression was not related to the patients' gender, age, tumour location, size, histological type, invasive depth, lymph node status and Dukes stage (p > 0.05). Conclusion: Our results suggest that Nup88 may play a role during the development, aggressiveness and differentiation of colorectal tumours. Copyright © 2007 S. Karger AG.

  • 172.
    Zhao, Senlin
    et al.
    Shanghai Jiao Tong University, Peoples R China.
    Sun, Hongcheng
    Shanghai Jiao Tong University, Peoples R China.
    Jiang, Weiliang
    Shanghai Jiao Tong University, Peoples R China.
    Mi, Yushuai
    Shanghai Jiao Tong University, Peoples R China.
    Zhang, Dongyuan
    Shanghai Jiao Tong University, Peoples R China.
    Wen, Yugang
    Shanghai Jiao Tong University, Peoples R China.
    Cheng, Dantong
    Shanghai Jiao Tong University, Peoples R China.
    Tang, Huamei
    Shanghai Jiao Tong University, Peoples R China.
    Wu, Shaohan
    Jiaxing Coll, Peoples R China.
    Yu, Yang
    Shanghai Jiao Tong University, Peoples R China.
    Liu, Xisheng
    Shanghai Jiao Tong University, Peoples R China.
    Cui, Weiyingqi
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Zhang, Meng
    Fudan University, Peoples R China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Zhou, Zongguang
    Sichuan University, Peoples R China.
    Peng, Zhihai
    Shanghai Jiao Tong University, Peoples R China.
    Yan, Dongwang
    Shanghai Jiao Tong University, Peoples R China.
    miR-4775 promotes colorectal cancer invasion and metastasis via the Smad7/TGF beta-mediated epithelial to mesenchymal transition2017In: Molecular Cancer, E-ISSN 1476-4598, Vol. 16, article id 12Article in journal (Refereed)
    Abstract [en]

    Background: Despite advancements in the diagnosis and treatment of colorectal cancer (CRC), many patients die because of tumor metastasis or recurrence. Therefore, identifying new prognostic markers and elucidating the mechanisms of CRC metastasis and recurrence will help to improve the prognosis of the disease. As dysregulation of microRNAs is strongly related to cancer progression, the aim of this study was to identify the role of miR-4775 in the prognosis of CRC patients and the underling mechanisms involved in CRC progression. Methods: qPCR and in situ hybridization were used to evaluate the expression of miR-4775 in 544 pairs of paraffin-embedded normal and CRC tissues. Kaplan-Meier analysis with the log-rank test was used for survival analyses. Immunohistochemical staining was applied to investigate the expression of miR-4775-regulated Smad7/TGF beta pathway-associated markers. In vitro and in vivo invasion and metastasis assays were used to explore the function of miR-4775 in the progression of CRC. Results: miR-4775 was identified as a high-risk factor for CRC metastasis and recurrence, with high levels predicting poor survival among the 544 studied CRC patients. Furthermore, high miR-4775 expression promoted the invasion of CRC cells as well as metastasis and the epithelial to mesenchymal transition (EMT) via Smad7-mediated activation of TGF beta signaling both in vitro and in vivo. Downregulating miR-4775 or overexpressing Smad7 reversed the tumor-promoting roles of miR-4775/ Smad7/TGF beta in vitro and in vivo. Conclusion: miR-4775 promotes CRC metastasis and recurrence in a Smad7/TGF beta signaling-dependent manner, providing a new therapeutic target for inhibiting the metastasis or recurrence of the disease.

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  • 173.
    Zhao, Zeng-Ren
    et al.
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Zhang, Li-Jing
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    He, Xin-Qi
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Zhang, Zhi-Yong
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Zhang, Feng
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Li, Fang
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Pei, Yong-Bin
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Hu, Yue-Ming
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Wang, Ming-Wei
    Hebei Med Univ, Shijiazhuang, Peoples R China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    Significance of mRNA and Protein Expression of MAC30 in Progression of Colorectal Cancer2011In: Chemotherapy, ISSN 0009-3157, E-ISSN 1421-9794, Vol. 57, no 5, p. 394-401Article in journal (Refereed)
    Abstract [en]

    Background: Meningioma-associated protein (MAC30), first described to be overexpressed in meningiomas, exhibits altered expression in certain human tumors. The aim of our study was to investigate the expression of MAC30 mRNA and its correlation with clinicopathological variables in human colorectal cancer (CRC). Methods: MAC30 mRNA expression was first examined in 55 CRCs, along with the samples from the matched distant normal and adjacent noncancerous tissue by RT-PCR, further verified in 18 CRCs by quantitative RT-PCR. MAC30 protein expression was detected by Western blot in 10 CRCs, and DNA sequencing was performed in 1 case of the paired CRC and the matched noncancerous specimen. MAC30 mRNA expression in two colon cancer cell lines, HCT-116(p53-/-) and HCT-116(p53+/+), was detected by quantitative RT-PCR. Results: The mRNA expression of MAC30 was increased in CRC when compared with distant normal (p < 0.01) and adjacent noncancerous mucosa (p < 0.01). The mean value of MAC30 mRNA expression in the tumor located in the colon was higher than in the rectum (0.677 +/- 0.419 vs. 0.412 +/- 0.162, p = 0.005). As the tumor penetrated the wall of the colon/rectum, MAC30 mRNA expression notably increased in tumors with T3+T4 stage compared to tumors with T1+T2 stage (0.571 +/- 0.364 vs. 0.404 +/- 0.115, p = 0.014). MAC30 protein expression in CRCs was also remarkably elevated compared to the adjacent noncancerous mucosa. There was no mutation in the coding region of the MAC30 gene either in CRC or in the noncancerous mucosa. mRNA expression of p53 was notably decreased in HCT-116(p53-/-) compared to HCT-116(p53+/+), while MAC30 did not vary greatly. Conclusion: The overexpression of MAC30 might be involved in the development and aggressiveness of CRCs, especially in the colon.

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  • 174.
    Zhao, Zeng-Ren
    et al.
    Hebei Medical University, Peoples R China Hebei Medical University, Peoples R China .
    Zhang, Li-Jing
    Hebei Medical University, Peoples R China .
    Wang, Yuan-Yuan
    Hebei Medical University, Peoples R China .
    Li, Fang
    Hebei Medical University, Peoples R China .
    Wang, Ming-Wei
    Hebei Medical University, Peoples R China .
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    Increased serum level of Nup88 protein is associated with the development of colorectal cancer2012In: Medical Oncology, ISSN 1357-0560, E-ISSN 1559-131X, Vol. 29, no 3, p. 1789-1795Article in journal (Refereed)
    Abstract [en]

    Nucleoporin88 (Nup88) has been shown to be overexpressed in a wide variety of malignancies including colorectal cancer (CRC). However, no study about serum Nup88 in human CRC was reported. Therefore, in this study, we investigated the level of serum Nup88 protein and its relationships with clinicopathological variables in CRC. The serum concentration of Nup88 protein was determined by a quantitative sandwich enzyme-linked immunosorbent assay (ELISA) in 118 pre-operative serum samples, 66 post-operative and 96 healthy controls. Among the patients, the levels of CEA (n = 91) and CA19-9 (n = 87) in the pre-operative serum were measured, and DNA sequencing was performed in 12 CRCs and 2 samples from non-cancerous colon tissue. In the same patients, the level of pre-operative serum Nup88 was significantly higher than that of post-operative Nup88 (P = 0.021). Furthermore, the level of pre-operative Nup88 was positively related to the depth of tumor invasion (P = 0.002) and advanced stage (P = 0.001). The level of pre-operative Nup88 in the left colon tended to be higher than that in the right colon and the rectum (P = 0.063). DNA sequencing results showed that there were two single nucleotide polymorphisms, distributed in exon 6 (NM_002532.3:c.1044Gandgt;A (ACG-ACA, Thr -andgt; Thr) and exon 10 (NM_002532.3: c.1389Aandgt;T, CCA-CCT, Pro -andgt; Pro). Serum Nup88 might be a candidate for a new biomarker implicated in the development and aggressiveness of CRCs.

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  • 175. Zhao, Zeng-Ren
    et al.
    Zhang, Zhi-Yong
    Cui, Dong-Sheng
    Jiang, Li
    Zhang, Hui-Jun
    Wang, Ming-Wei
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Particularly interesting new cysteine-histidine rich protein expression in colorectal adenocarcinomas2006In: World Journal of Gastroenterology, ISSN 1007-9327, E-ISSN 2219-2840, Vol. 12, no 2, p. 298-301Article in journal (Refereed)
    Abstract [en]

    Aim: To study the relationship between particularly interesting new cysteine-histidine rich protein (PINCH) expression and clinicopathological factors in Chinese colorectal cancer patients. Methods: The expression of PINCH was examined by immumohistochemistry in 141 samples of primary colorectal adenocarcinoma and 92 normal samples of colorectal mucosa. Eighty of the cases had both primary tumour and normal mucosa from the same patients. Results: PINCH was expressed in the stroma of normal mucosa and tumours. PINCH expression in tumourassociated stroma was increased compared to normal mucosa in both unmatched cases (n = 141, X2 = 85.79, df = 3, P<0.0001) and matched cases (n = 80, X2 = 45.86, df = 3, P<0.0001). Among 135 tumours with visible invasive margin, 86 (64%) showed stronger PINCH expression at the invasive margin than in the intratumoural stroma. The frequency of PINCH strong expression in mucinous and signet-ring cell carcinomas was higher (52%) compared to non-mucinous carcinomas (29%, X2= 5.13, P= 0.02). We did not find that PINCH expression was related to patient's gender, age, tumour location, tumour size, gross status, histological type, differentiation, invasion depth, lymph node status and Dukes' stage (P>0.05). Conclusion: The expression of PINCH was upregulated in colorectal cancers, and especially at the margin of tumours, and further was related to mucinous and signet-ring cell carcinomas. The results suggest that expression of PINCH may be involved in the tumourigenesis and aggressiveness of colorectal cancers. © 2006 The WJG Press. All rights reserved.

  • 176.
    Zhao, Zeng-Ren
    et al.
    Hebei Medical University.
    Zhang, Zhi-Yong
    Tangshan Gongren Hospital.
    He, Xin-Qi
    Hebei Medical University.
    Hu, Yue-Ming
    Tangshan Gongren Hospital.
    Tian, Yan-Feng
    Hebei Medical University.
    Zhang, Li-Jing
    Hebei Medical University.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    Nup88 mRNA overexpression in colorectal cancers and relationship with p532010In: CANCER BIOMARKERS, ISSN 1574-0153, Vol. 8, no 2, p. 73-80Article in journal (Refereed)
    Abstract [en]

    Objectives: We measured nucleoporin 88 (Nup88) mRNA expression in primary colorectal cancers to investigate its relationship with clinicopathological features and p53. Methods: The primary cancer tissues, adjacent noncancerous tissues and the proximal and distant margins of normal mucosa were collected from 73 colorectal cancer patients during surgery. Nup88 mRNA expression was measured on these fresh specimens and on colon cell lines HCT-116 (P53+/+) and HCT-116 (P53-/-) by RT-PCR while p53 mRNA and beta-actin as controls. Nup88 and p53 protein expression were then immunohistochemistrically examined in other 25 colorectal cancers specimens paraffin embedded and formalin fixed. Results: Nup88 expression was higher in primary cancer tissues than in adjacent noncancerous tissues, and in the proximal and distant margins of normal mucosa. Overexpression of Nup88 mRNA was statistically associated with TNM stage (P = 0.044), lymphatic metastasis (P = 0.022), and cancer location (P = 0.036), while not related to gender, age of patients and histological type, infiltration depth, and differentiation of cancers. The expression of Nup88 mRNA in the HCT-116 (P53-/-) cell line was not significantly different from expression in the HCT-116 (P53+/+) cell line. And there was no correlation between Nup88 and p53 protein expression (r = 0.632, P = 0.368). Conclusions: Nup88 mRNA was overexpressed in colorectal cancers and the overexpression was associated with cancer development and aggressiveness. Nup88 might be regard as essential contributor to nodal metastagenicity of colorectal cancer.

  • 177.
    Zhao, Zeng-Ren
    et al.
    Department of General Surgery Hebei Medical University, Shijiazhuang 050031, P.R. China.
    Zhang, Zhiyong
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology .
    Zhang, Hong
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Dermatology and Venerology .
    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
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Overexpression of Id-1 protein is a marker in colorectal cancer progression2008In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 19, no 2, p. 419-424Article in journal (Refereed)
    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.

  • 178.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    PNAS-4 expression and its relationship to p53 in colorectal cancer2012In: Molecular Biology Reports, ISSN 0301-4851, E-ISSN 1573-4978, Vol. 39, no 1, p. 243-249Article in journal (Refereed)
    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.

  • 179.
    Zhou, Jin
    et al.
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Yang, Lie
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Li, Yuan
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Arbman, Gunnar
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Surgery in Norrköping.
    Chen, Ke-Ling
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Zhou, Bin
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Yu, Yong-Yang
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Wang, Cun
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Mo, Xian-Ming
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Lu, You
    Sichuan University, Peoples R China .
    Zhou, Zong-Guang
    Sichuan University, Peoples R China Sichuan University, Peoples R China .
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    The prognostic significance of peroxisome proliferator-activated receptor beta expression in the vascular endothelial cells of colorectal cancer2014In: Journal of gastroenterology, ISSN 0944-1174, E-ISSN 1435-5922, Vol. 49, no 3, p. 436-445Article in journal (Refereed)
    Abstract [en]

    Currently, little is known regarding the role of peroxisome proliferator-activated receptor-beta (PPAR beta) in the vascular endothelial cells (VECs) of colorectal cancers (CRCs). The aim of this study was to investigate the relationship of PPAR beta expression in the VECs of CRCs in terms of the prognosis and clinicopathological features of CRC patients. The expression and localization of PPAR beta in the primary cancers and the matched normal mucosal samples of 141 Swedish CRC patients were analyzed in terms of its correlation with clinicopathological features and the expression of angiogenesis-related genes. This study also included 92 Chinese CRC patients. PPAR beta was predominantly localized in the cytoplasm and was significantly downregulated in the VECs of CRC compared to that of the normal mucosa. The low expression levels of PPAR beta in the VECs of CRC were statistically correlated with enhanced differentiation, early staging and favorable overall survival and were associated with the increased expression of VEGF and D2-40. The patients exhibiting elevated expression of PPAR beta in CRC cells but reduced expression in VECs exhibited more favorable survival compared with the other patients, whereas the patients with reduced expression of PPAR beta in CRC cells but increased expression in VECs exhibited less favorable prognosis. PPAR beta might play a tumor suppressor role in CRC cells in contrast to a tumor promoter role in the VECs of CRCs.

  • 180.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Zhou, Z.
    Sichuan University.
    Down-regulation of tumor necrosis factor-associated factor 6 is associated with progression of acute pancreatitis complicating lung injury in mice2009In: Tohoku Journal of Experimental Medicine, ISSN 0040-8727, Vol. 217, no 4, p. 279-285Article in journal (Refereed)
    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.

  • 181.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Li, Yuan
    Sichuan University.
    TRAF6 as the Key Adaptor of TLR4 Signaling Pathway Is Involved in Acute Pancreatitis2010In: PANCREAS, ISSN 0885-3177, Vol. 39, no 3, p. 359-366Article in journal (Refereed)
    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.

  • 182. Zhou, Xiao-Lei
    et al.
    Eriksson, Ulrika
    Werelius, Barbro
    Kressner, Ulf
    Sun, Xiao-Feng
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Oncology. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Lindblom, Annika
    Definition of candidate low risk APC alleles in a Swedish population2004In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 110, no 4, p. 550-557Article in journal (Refereed)
    Abstract [en]

    Many families experience an apparently inherited increased risk of colorectal cancer (CRC) similar to the known syndromes familial adenomatous polyposis (FAP) and hereditary nonpolyposis colorectal cancer (HNPCC). Besides these high-risk syndromes, approximately 10% of all CRC cases come from families with 2 affected 1st-degree relatives, and even 1st-degree relatives to a single case of CRC are at increased risk. Risk subjects from these families frequently show polyps at colonoscopy, which suggests the APC gene as a good candidate susceptibility gene for these attenuated polypotic syndromes. We used the sensitive DHPLC technique to search for possible predisposing germline mutations in the entire APC gene in 91 risk subjects from these high- and low-risk syndromes with unknown predisposing genes. Most exons were also screened for mutations in 96 normal controls and 96 colorectal cancer cases. In our study we probably have identified the most common APC variants in a Swedish population. Among 30 germline variants identified, 1 clearly pathogenic nonsense mutation and 11 putative pathogenic variants (10 missense and one 3′ UTR) were found in 20 index patients (22%). Twelve silent as well as 5 intronic variants were considered nonpathogenic. Two of the missense variants found here, E1317Q and D1822V, have previously been related to a difference in risk of colorectal cancer. One variant, 8636C>A, located within the 3′ UTR region of the APC gene, was suggested to constitute an additional low risk allele with a similar relative risk as the Jewish 11307K mutation (OR = 1.8, 9S% CI, 0.96-3.40). The question of whether all the other variants confer an increased colorectal cancer risk warrants future large association studies. © 2004 Wiley-Liss, Inc.

  • 183.
    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
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Oncology . Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    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 cancer2005In: Genetic Testing, ISSN 1090-6576, E-ISSN 1557-7473, Vol. 9, no 2, p. 147-151Article in journal (Refereed)
    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.

  • 184.
    Zhou, Yin
    et al.
    Sichuan University, Peoples R China.
    Li, Yibo
    Sichuan University, Peoples R China.
    Zhou, Bin
    Sichuan University, Peoples R China.
    Chen, Keling
    Sichuan University, Peoples R China.
    Lyv, Zhaoying
    Sichuan University, Peoples R China.
    Huang, Dongmei
    Sichuan University, Peoples R China.
    Liu, Bin
    Sichuan University, Peoples R China.
    Xu, Zhicheng
    Sichuan University, Peoples R China.
    Xiang, Bo
    Sichuan University, Peoples R China.
    Jin, Shuguang
    Sichuan University, Peoples R China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Surgery, Orthopedics and Oncology. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Li, Yuan
    Sichuan University, Peoples R China.
    Inflammation and Apoptosis: Dual Mediator Role for Toll-like Receptor 4 in the Development of Necrotizing Enterocolitis2017In: Inflammatory Bowel Diseases, ISSN 1078-0998, E-ISSN 1536-4844, Vol. 23, no 1, p. 44-56Article in journal (Refereed)
    Abstract [en]

    Background: Necrotizing enterocolitis (NEC) is the leading cause of neonatal gastrointestinal mortality; effective interventions are lacking with limited understanding of the pathogenesis of NEC. The importance of Toll-like receptor 4 (TLR4) signaling in NEC is well documented; however, the potential mechanisms that regulate enterocyte inflammation and apoptosis remain unclear. The aim of this study was to characterize the role of TLR4-mediated inflammation and apoptosis in the development of NEC and to determine the major apoptotic pathways and regulators in the process. Methods: TLR4-deficient C57BL/10ScNJ mice and lentivirus-mediated stable TLR4-silent cell line (IEC-6) were used. NEC was induced by formula gavage, cold, hypoxia, combined with lipopolysaccharide in vivo or lipopolysaccharide stimulation in vitro. Enterocyte apoptosis was evaluated by TUNEL or Annexin analysis. The expression of TLR4, caspase3, caspase8, caspase9, Bip, Bax, Bcl-2, and RIP was detected by Western blot and immunofluorescence. Inflammatory factors such as tumor necrosis factor-a and interleukin-2 were examined by Luminex. Results: Defect of TLR4 led to suppressed enterocytes apoptosis both in vitro and in vivo; the expression of caspase3, caspase8, Bip, and Bax was decreased; and caspase9 and Bcl-2 were increased. NEC severity was attenuated in TLR4-deficient mice compared with wild-type counterparts, and enterocytes apoptosis was correlated with NEC severity. RIP and cytokine level of tumor necrosis factor-a and interleukin-2 were also decreased. Conclusions: TLR4-induced inflammation and apoptosis play a critical role in the pathogenesis of NEC. TLR4 inhibition, combined with extrinsic (caspase8) and/or endoplasmic reticulum stress (Bip) apoptosis signaling blockade could serve as a potential effective treating strategy for NEC.

  • 185.
    Zhu, Zhen-Long
    et al.
    Hebei Medical University, Shijiazhuang, China.
    Yan, Bao-Yong
    Hebei Medical University, Shijiazhuang, China.
    Zhang, Yu
    Hebei Medical University, Shijiazhuang, China.
    Yang, Yan-Hong
    Hebei Medical University, Shijiazhuang, China.
    Wang, Ming-Wei
    Hebei Medical University, Shijiazhuang, China.
    Zentgraf, Hanswalter
    Heidelberg University, Germany.
    Zhang, Xiang-Hong
    Hebei Medical University, Shijiazhuang, China.
    Sun, Xiao-Feng
    Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology.
    Overexpression of FXYD-3 is involved in the tumorigenesis and development of esophageal squamous cell carcinoma2013In: Disease Markers, ISSN 0278-0240, E-ISSN 1875-8630, Vol. 35, no 3, p. 195-202Article in journal (Refereed)
    Abstract [en]

    Objective: To investigate the association of FXYD-3 expression with clinicopathological variables and PINCH in patients with ESCC.

    Patients and methods: Expression of FXYD-3 protein was immunohistochemically examined in normal esophageal mucous (n = 20) and ESCC (n = 64).  

    Results: Expression of FXYD-3 in the cytoplasm markedly increased from normal esophageal epithelial cells to primary ESCC ( p = 0.001). The expression of FXYD-3 was correlated with TNM stages and depth of tumour invasion. Furthermore, the cases with lymph node metastasis tended to show a higher frequency of positive expression than those without metastasis ( p = 0.086), and FXYD-3 expression tended to be positively related to the expression of PINCH (p = 0.063). Moreover, the cases positive for both proteins had the highest frequency of lymph node metastasis (p = 0.001). However, FXYD-3 expression was not correlated with patient,s gender (p = 0.847), age (p = 0.876), tumour location (p = 0.279), size (p = 0.771) , grade of differentiation (p = 0.279), and survival (p = 0.113).

    Conclusion: overexpression of FXYD-3 in the cytoplasm may play an important role in the tumourigenesis and development in the human ESCC, particularly in combination with PINCH expression.

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  • 186.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    Cytoplasmic expression of p33(ING1b) is correlated with tumorigenesis and progression of human esophageal squamous cell carcinoma.2013In: Oncology letters, ISSN 1792-1074, Vol. 5, no 1, p. 161-166Article in journal (Refereed)
    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.

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  • 187.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre for Surgery, Orthopaedics and Cancer Treatment, Department of Oncology UHL.
    PINCH expression and its clinicopathological significance in gastric adenocarcinoma2012In: Disease Markers, ISSN 0278-0240, E-ISSN 1875-8630, Vol. 33, no 4, p. 171-178Article in journal (Refereed)
    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.

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  • 188.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology. Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    PINCH expression and its significance in esophageal squamous cell carcinoma2008In: Disease Markers, ISSN 0278-0240, E-ISSN 1875-8630, Vol. 25, no 2, p. 75-80Article in journal (Refereed)
    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.

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  • 189.
    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
    Linköping University, Department of Clinical and Experimental Medicine, Oncology . Linköping University, Faculty of Health Sciences. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Oncology UHL.
    Expression and significance of FXYD-3 protein in gastric adenocarcinoma2010In: DISEASE MARKERS, ISSN 0278-0240, Vol. 28, no 2, p. 63-69Article in journal (Refereed)
    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.

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