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  • 1.
    Bu, H.
    et al.
    Linköping University.
    Rosdahl, I.
    Linköping University.
    Sun, X-F.
    Linköping University.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Genotype <21CAs/≥21CAs and allele <21CAs of the MANBA gene in melanoma risk and progression in a Swedish population2009In: Molecular Medicine Reports, ISSN 1791-2997, E-ISSN 1791-3004, Vol. 2, no 2, p. 259-263Article in journal (Refereed)
    Abstract [en]

    Cutaneous melanoma is characterized by poor patient outcome in its later stages. The search for genetic markers is therefore crucial for the identification of populations at risk for melanoma. Highly polymorphic CA repeats in 3' proximity in the MANBA gene were examined by PCR-capillary electrophoresis in 185 Swedish melanoma patients and 441 tumor-free age- and gender-matched individuals. The associations of the polymorphisms with melanoma risk, the pigment phenotypes of the patients and tumor characteristics were analyzed. A significant difference in allelic distribution between melanoma patients and tumor-free individuals was observed. The frequency of the MANBA genotype <21CAs/≥21CAs was significantly higher in melanoma patients than in the controls. When comparing allele distribution in patients and their matched controls, the allele <21CAs was found to be associated with the female gender (39.8 vs. 31.2%, P=0.041, OR=1.46, 95% CI 1.02-2.10), but not with male gender (34.4 vs. 30.9%, P%0.39). Within the melanoma group, there were no differences in the distribution of the MANBA alleles associated with patient gender or age before or after 55 years at diagnosis, nor was there any association between the MANBA genotype and pigment phenotype or tumor sites. The MANBA allele <21CAs was, however, associated with thin melanomas at diagnosis (Breslow thickness ≤1.5 mm and Clark levels I and II). In conclusion, these data suggest that MANBA polymorphisms might be an indicator of tumor growth and progression and, together with other markers, could be used to identify individuals at increased risk of melanoma.

  • 2.
    Gao, Jingfang
    et al.
    Department of Oncology, Institute of Clinical and Experimental Medicine, Linköping University, 581 85 Linköping, Sweden.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Arbman, Gunnar
    Department of Surgery, Östergötland, Sweden.
    Sun, Xiao-Feng
    Department of Oncology, Institute of Clinical and Experimental Medicine, Linköping University, 581 85 Linköping, Sweden.
    RAD50/MRE11/NBS1 proteins in relation to tumour development and prognosis in patients with microsatellite stable colorectal cancer2008In: Histology and Histopathology, ISSN 0213-3911, E-ISSN 1699-5848, Vol. 23, no 12, p. 1495-1502Article in journal (Refereed)
    Abstract [en]

    RAD50/MRE11/NBS1 complex is essential for DNA double-strand break repair and for maintaining genomic integrity. In this study, we immunohistochemically examined MRE11, NBS1 and RAD50 expression in primary CRCs (n = 208), the corresponding distant (n= 41) and adjacent normal mucosa ( n= 130), and lymph node metastases ( n= 26), and investigated their clinicopathological significance in colorectal cancers ( CRCs). We found that the intensity and percentage of MRE11 and NBS1 in primary CRCs were positively correlated with each other and with RAD50 (P < 0.0001). Strong expression of MRE11, NBS1 or combined RAD50/MRE11/NBS1 was related to MSS, positive hMLH1 expression, earlier tumour stage (TNM stage I and II) and favourable survival (P < 0.05). A high percentage of MRE11 expression was associated with less local recurrence and high apoptotic activity (P < 0.05). In MSS CRCs, the expression of MRE11 and NBS1 was stronger than that in normal mucosa (P < 0.05), and strong expression of NBS1 in primary tumour was related to favourable survival of patients in TNM stage I and II (univariate analysis: P = 0.03; multivariate analysis: P = 0.07). In MSI CRCs, neither MRE11 nor NBS1 expression showed differences among normal mucosa, primary tumour and metastasis, or among clinicopathological variables. In conclusion, RAD50/MRE11/NBS1 proteins interacted with each other, which had different clinicopathological significance in MSS and MSI CRCs, and further, each component of the complex might have additional roles. NBS1 might be a prognostic factor for patients with MSS tumour in TNM stage I and II.

  • 3.
    Gnosa, Sebastian
    et al.
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, University of Linköping, Linköping, Sweden.
    Shen, Yang-Mei
    Department of Pathology, West China Second University Hospital, Sichuan University, Chengdu, People's Republic of China.
    Wang, Chao-Jie
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, University of Linköping, Linköping, Sweden.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Stratmann, Johannes
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, University of Linköping, Linköping, Sweden.
    Arbman, Gunnar
    Department of Surgery, Vrinnevi Hospital, Norrköping, Sweden.
    Sun, Xiao-Feng
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, University of Linköping, Linköping, Sweden / Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Country Council of Östergötland, University of Linköping, Linköping, Sweden.
    Expression of AEG-1 mRNA and protein in colorectal cancer patients and colon cancer cell lines2012In: Journal of Translational Medicine, ISSN 1479-5876, E-ISSN 1479-5876, Vol. 10, article id 109Article in journal (Refereed)
    Abstract [en]

    Background: Astrocyte elevated gene 1 (AEG-1), an important oncogene, has been shown to be overexpressed in several types of cancers. In colorectal cancer (CRC), the protein level of AEG-1 is up-regulated in tumour tissue compared to normal mucosa, showing prognostic significance. Since little is known about the transcriptional level of AEG-1 expression and its biological pathway in CRC the aim of the present study was to examine the relationship of AEG-1 mRNA expression, the protein level and clinicopathological variables as well as its biology pathway in CRC. Material and methods: The mRNA expression of AEG-1 was analysed by qPCR in fresh frozen patient samples including 156 primary tumours, along with the corresponding normal mucosa, and in five colon cancer cell lines, SW480, SW620, KM12C, KM12SM and KM12L4a. AEG-1 protein expression was investigated by immunohistochemistry in paraffin-embedded materials from 74 distant normal mucosa, 107 adjacent mucosa, 158 primary tumour, 35 lymph node metastasis and 9 liver metastasis samples. In addition, the AEG-1 protein expression was elucidated in the cell lines by Western blot. Results: The lymph node metastatic cell line SW620 had a significantly higher AEG-1 mRNA (0.27 +/- 0.02) expression compared to the primary tumour cell line SW480 (0.17 +/- 0.04, p = 0.026). AEG-1 expression at the mRNA level and/or the protein level was significantly up-regulated gradually from normal mucosa to primary CRC, and then to lymph node metastasis and finally to liver metastasis (p < 0.05). There were significant associations of AEG-1 mRNA expression with tumour location (p = 0.047), as well as mRNA and protein expression with the tumour stage (p < 0.03). Furthermore AEG-1 protein expression was positively related to biological variables including NF-kappa B, p73, Rad50 and apoptosis (p < 0.05). Conclusion: AEG-1 is up-regulated, at the mRNA and the protein level, during CRC development and aggressiveness, and is related to tumour location and stage. It may play its role in CRC through the NF-kappa B signaling pathway.

  • 4.
    Hu, Chun
    et al.
    Xiamen Univ, Coll Med, Canc Res Ctr, Xiamen 361005, Peoples R China .
    Song, Gang
    Xiamen Univ, Coll Med, Canc Res Ctr, Xiamen 361005, Peoples R China .
    Zhang, Bing
    Xiamen Univ, Coll Med, Dept Basic Med, Xiamen 361005, Peoples R China.
    Liu, Zhongchen
    Xiamen Univ, Coll Med, Zhongshan Affiliated Hosp, Xiamen 361005, Peoples R China .
    Chen, Rong
    Wuhan Inst Technol, Minist Educ, Key Lab Green Chem Proc, Wuhan, Peoples R China and Wuhan Inst Technol, Minist Educ, Sch Chem Engn & Pharm, Wuhan, Peoples R China .
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Hu, Tianhui
    Xiamen Univ, Coll Med, Canc Res Ctr, Xiamen 361005, Peoples R China .
    Intestinal metabolite compound K of panaxoside inhibits the growth of gastric carcinoma by augmenting apoptosis via Bid-mediated mitochondrial pathway2012In: Journal of Cellular and Molecular Medicine (Print), ISSN 1582-1838, E-ISSN 1582-4934, Vol. 16, no 1, p. 96-106Article in journal (Refereed)
    Abstract [en]

    Compound K (20-O-beta-D-glucopyranosyl-20(S)-protopanaxadiol, CK), an intestinal bacterial metabolite of panaxoside, has been shown to inhibit tumour growth in a variety of tumours. However, the mechanisms involved are largely unknown. We use human gastric carcinoma cell lines BGC823, SGC7901 and human gastric carcinoma xenograft in nude mice as models to study the mechanisms of CK in gastric cancers. We found that CK significantly inhibits the viabilities of BGC823 and SGC7901 cells in dose- and time-dependent manners. CK-induced BGC823 and SGC7901 cells apoptosis and cell cycle arrest in G2 phase by up-regulation of p21 and down-regulation of cdc2 and cyclin B1. Further studies show that CK induces apoptosis in BGC823 and SGC7901 cells mainly through mitochondria-mediated internal pathway, and that CK induces the translocation of nuclear Bid to mitochondria. Finally, we found that CK effectively inhibited the tumour formation of SGC7901 cells in nude mice. Our studies show that CK can inhibit the viabilities and induce apoptosis of human gastric carcinoma cells via Bid-mediated mitochondrial pathway.

  • 5.
    Kertat, Khadija
    et al.
    Division of Dermatology, Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    Rosdahl, Inger
    Division of Dermatology, Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    Sun, Xiao-Feng
    Division of Oncology, Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    Synnerstad, Ingrid
    Division of Dermatology, Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    Zhang, Hong
    University of Skövde, School of Life Sciences. Division of Dermatology, Department of Experimental and Clinical Medicine, Linköping University, Linköping, Sweden.
    The Gln/Gln genotype of XPD codon 751 as a genetic marker for melanoma risk and Lys/Gln as an important predictor for melanoma progression: A case control study in the Swedish population2008In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 20, no 1, p. 179-183Article in journal (Refereed)
    Abstract [en]

    The Xeroderma pigmentosum complementation group D (XPD) is a critical protein in the nucleotide excision repair system for DNA damage. Genetic variations in XPD exert an important effect on the capacity of DNA repair. In this study, we examined Lys751Gln polymorphism at the XPD gene in 244 melanoma patients and 251 healthy individuals (as controls) from the south-eastern region of Sweden. The associations of polymorphism with melanoma risk, as well as with melanoma features and pigment phenotypes of the melanoma patients were analysed. DNA was extracted from the mononuclear cells of venous blood of the melanoma patients and controls. XPD codon 751 was genotyped by the PCR restriction fragment length polymorphism technique. Results showed that there was no difference in the distribution of the XPD codon 751 genotypes between the melanoma patients and healthy controls. However, the Gln/Gln genotype was found to be associated with melanoma risk in the male population. Furthermore, the frequency of the Gln/Gln genotype was significantly higher in the early stages of melanomas, whereas Lys/Gln was more frequent in the later stages and in the patients with melanoma located on intermittently UV-exposed areas. No correlations between the polymorphisms and phenotypes of the patients were found. In conclusion, Gln/Gln was a useful genetic marker for melanoma risk in the males, while Lys/Gln was an important predictor for melanoma progression.

  • 6.
    Lewander, Andreas
    et al.
    Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, SE-581 85 Linköping, Sweden.
    Gao, Jinfang
    Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, SE-581 85 Linköping, Sweden.
    Adell, Gunnar
    Department of Oncology, Karolinska University Hospital, Stockholm, Sweden.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Sun, Xiao-Feng
    Department of Oncology, Institute of Clinical and Experimental Medicine, University of Linköping, SE-581 85 Linköping, Sweden.
    Expression of NF-kappa B p65 phosphorylated at serine-536 in rectal cancer with or without preoperative radiotherapy2011In: Radiology and Oncology, ISSN 1318-2099, E-ISSN 1581-3207, Vol. 45, no 4, p. 279-284Article in journal (Refereed)
    Abstract [en]

    Background. In the present study, we investigated NF-kappa B p65 phosphorylated at Serine-536 (phosphor-Ser536-p65) in rectal cancer and its relationship to preoperative radiotherapy (RT), clinicopathological variables and biological factors. Patients and methods. Expression of phosphor-Ser536-p65 was examined by using immunohistochemistry in 141 primary rectal cancers, 149 normal mucosa specimens and 48 metastases in the lymph nodes, from rectal cancer patients who participated in a Swedish clinical trial of preoperative RT. Results. The expression of phosphor-Ser536-p65 in the cytoplasm increased from normal mucosa to primary tumour (p<0.0001, for both the group that did and the group that did not received RT). The expression did not further increase from primary tumour to metastasis in either group (p>0.05). Expression of phosphor-Ser536-p65 was positively related to, or tended to be related to, the expression of tumour endothelium marker 1 (TEM1, p=0.02), FXYD-3 (p=0.001), phosphatase of regenerating liver (PRL, p=0.02), p73 (p=0.048) and meningioma associated protein (MAC30, p=0.05) in the group that received RT but there were no such relationships in the group that did not received RT (p>0.05). The expression of phosphor-Ser536-p65 was not related to clinicopathological factors including survival (p>0.05). Conclusions. The increased expression of phosphor-Ser536-p65 may be involved in rectal cancer development. After RT, phosphor-Ser536-p65 seems to be positively related to the biological factors, which associated with more malignant features of tumours. However, phosphor-Ser536-p65 was not directly related to the response of RT based on recurrence and survival.

  • 7.
    Lewander, Andreas
    et al.
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Gao, Jinfang
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Carstensen, John
    Department of Health and Society, Faculty of Health Sciences, Linköping University, SE-581 85 Linköping, Sweden.
    Arbman, Gunnar
    Department of Surgery, Country Council of Östergötland, Norrköping, Sweden.
    Zhang, Hong
    University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    NF-kappa B p65 phosphorylated at serine-536 is an independent prognostic factor in Swedish colorectal cancer patients2012In: International Journal of Colorectal Disease, ISSN 0179-1958, E-ISSN 1432-1262, Vol. 27, no 4, p. 447-452Article in journal (Refereed)
    Abstract [en]

    The NF-kappa B transcription factor protein family has diverse cellular and biological functions, and posttranslational modification is important to regulate these functions. An important site of phosphorylation of NF-kappa B p65 subunit is at serine-536 (phospho-Ser536-p65), and this phosphorylation is involved in regulation of transcriptional activity, nuclear localization, and protein stability. In this study, we investigated expression of phospho-Ser536-p65 in colorectal cancers and its relationships with clinicopathological factors. The expression of phospho-Ser536-p65 was examined by immunohistochemistry in 203 primary colorectal cancers, 156 normal mucosa specimens, and 18 metastases in the lymph nodes. The expression of phospho-Ser536-p65 increased from normal mucosa to primary tumor (p < 0.0001). Further, the increased expression of phospho-Ser536-p65 in the cytoplasm of the primary tumors correlated with worse survival of the patients independently of gender, age, tumor location, stage, and differentiation (p = 0.04; hazard ratio, 1.89; 95% CI 1.03-3.47). The NF-kappa B p65 subunit phosphorylated at serine-536 is an independent prognostic factor in colorectal cancer patients.

  • 8.
    Lööf, Jasmine
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Pfeifer, Daniella
    Linköping University.
    Ding, Zhenyu
    Linköping University.
    Sun, Xiao-Feng
    Linköping University.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Effects of ΔNp73β on Cisplatin Treatment in Colon Cancer Cells2012In: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 51, no 8, p. 628-635Article in journal (Refereed)
    Abstract [en]

    p73 can activate transcription of p53-responsive genes, thereby inhibiting cell growth. An alternative promoter in the TP73 gene gives rise to an N-terminally truncated isoform of p73, DNp73, which lacks the transactivation domain of the full length TAp73 protein. TAp73 is considered pro-apoptotic, and DNp73 anti-apoptotic. In this study, we overexpressed DNp73β in p53 wild type and p53 mutant colon cancer cell lines and further exposed the cells to cancer therapeutic drug cisplatin. The results showed that cisplatin decreased the protein expression levels of DNp73β in a dose-dependent manner, and both TAp73 and p53 were upregulated after cisplatin treatment. Further, clonogenic potential and cell viability were decreased, and apoptotic cells increased, in p53 mutant and in p53 wild type cells. Cellular viability was significantly higher in DNp73β-cells than mock-transfected cells. However, DNp73β overexpression did not affect the cellular susceptibility to cisplatin. In conclusion, the overexpression of DNp73β increases viability in p53 wild type and p53 mutant colon cancer cells, and cisplatin induces the degradation of DNp73β in a dose-dependent manner.

  • 9.
    Lööf, Jasmine
    et al.
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Rosell, Johan
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Bratthäll, Charlotte
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Doré, Siv
    Department of Pathology, Linköping University, Linköping, Sweden.
    Starkhammar, Hans
    Department of Oncology, Linköping University Hospital, S-58185 Linköping, Sweden.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Department of Oncology, Linköping University, Linköping, Sweden.
    Impact of PINCH expression on survival in colorectal cancer patients2011In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. Artikelnr 103-Article in journal (Refereed)
    Abstract [en]

    Background: The adaptor protein PINCH is overexpressed in the stroma of several types of cancer, and is an independent prognostic marker in colorectal cancer. In this study we further investigate the relationship of PINCH and survival regarding the response to chemotherapy in colorectal cancer. Results: Paraffin-embedded tissue sections from 251 primary adenocarcinomas, 149 samples of adjacent normal mucosa, 57 samples of distant normal mucosa and 75 lymph node metastases were used for immunohistochemical staining. Stromal staining for PINCH increased from normal mucosa to primary tumour to metastasis. Strong staining in adjacent normal mucosa was related to worse survival independently of sex, age, tumour location, differentiation and stage (p = 0.044, HR, 1.60, 95% Cl, 1.01-2.52). PINCH staining at the invasive margin tended to be related to survival (p = 0.051). In poorly differentiated tumours PINCH staining at the invasive margin was related to survival independently of sex, age and stage (p = 0.013, HR, 1.90, 95% Cl, 1.14-3.16), while in better differentiated tumours it was not. In patients with weak staining, adjuvant chemotherapy was related to survival (p = 0.010, 0.013 and 0.013 in entire tumour area, invasive margin and inner tumour area, respectively), but not in patients with strong staining. However, in the multivariate analysis no such relationship was seen. Conclusions: PINCH staining in normal adjacent mucosa was related to survival. Further, PINCH staining at the tumour invasive margin was related to survival in poorly differentiated tumours but not in better differentiated tumours, indicating that the impact of PINCH on prognosis was dependent on differentiation status.

  • 10.
    Meng, N
    et al.
    Department of Surgery, The Forth Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China.
    Li, Y
    Department of Surgery, The Forth Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China.
    Zhang, Hong
    University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Department of Oncology, Institute of Clinical and Experimental Medicine, Linköping University, S-58185 Linköping, Sweden.
    RECK, a novel matrix metalloproteinase regulator2008In: Histology and Histopathology, ISSN 0213-3911, E-ISSN 1699-5848, Vol. 23, no 8, p. 1003-1010Article, review/survey (Refereed)
    Abstract [en]

    Extracellular matrix (ECM) macromolecules are important for creating the cellular environments required during development and morphogenesis of tissues. Matrix metalloproteinases (MMPs) are a family of Zn-dependent endopeptidases that collectively are capable of cleaving virtually all ECM substrates, and play an important role in some physiological and pathological processes. MMP activity can be inhibited by some natural and artificial inhibitors. A newly found membrane-anchored regulator of MMPs, the reversion-inducing-cysteine-rich protein with kazal motifs (RECK), is downregulated when the cells undergo a process of malignant transformation, and is currently the subject of considerable research activity because of its specific structure and function. In this review, we have chosen to concentrate our efforts on the structure, function, regulation, and future prospect of RECK in order to provide a new target for prevention and treatment of tumours

  • 11.
    Shen, Yang-Mei
    et al.
    Department of Oncology, Institute of Biomedicine and Surgery, University of Linköping, S-581 85 Linköping, Sweden / Department of Pathology, West China Second University Hospital, Sichuan University, Chengdu, P.R. China.
    Arbman, Gunnar
    Department of Surgery, Vrinnevi Hospital, Norrköping, Sweden.
    Sandström, Per
    Department of Surgery, Institute of Biomedicine and Surgery, University of Linköping, S-581 85 Linköping, Sweden.
    Gullstrand, Per
    Department of Surgery, Institute of Biomedicine and Surgery, University of Linköping, S-581 85 Linköping, Sweden.
    Wei, Yu-Quan
    State Key laboratory of Biotherapy of Human Diseases, West China University Hospital, Sichuan University, Chengdu, P.R. China.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Rosell, Johan
    Department of Oncology, Institute of Biomedicine and Surgery, University of Linköping, S-581 85 Linköping, Sweden.
    Olsson, Birgit
    Department of Oncology, Institute of Biomedicine and Surgery, University of Linköping, S-581 85 Linköping, Sweden.
    Peng, Feng
    State Key laboratory of Biotherapy of Human Diseases, West China University Hospital, Sichuan University, Chengdu, P.R. China.
    Yang, Han-Shuo
    State Key laboratory of Biotherapy of Human Diseases, West China University Hospital, Sichuan University, Chengdu, P.R. China.
    Wang, Chun-Ting
    State Key laboratory of Biotherapy of Human Diseases, West China University Hospital, Sichuan University, Chengdu, P.R. China.
    Sun, Xiao-Feng
    Department of Oncology, Institute of Biomedicine and Surgery, University of Linköping, S-581 85 Linköping, Sweden / Department of Gastrointestinal Surgery, West China Hospital, Sichuan University, Chengdu, P.R. China.
    Novel gene hBiot2 is an independent prognostic factor in colorectal cancer patients2012In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 27, no 2, p. 376-382Article in journal (Refereed)
    Abstract [en]

    The present study investigated the expression of the novel gene hBiot2 in colorectal cancer (CRC) and its relationships with clinicopathological variables in CRC patients. The expression of hBiot2 in 163 primary CRCs together with the corresponding normal mucosa, 36 liver metastases and 5 colon cancer cell lines was examined using real-time PCR. In situ hybridization (ISH) was performed to evaluate the localization of hBiot2 expression in CRC and normal mucosa. hBiot2 expression at the RNA level was localized in the nucleus of tumor cells and normal epithelial cells. The mean expression of hBiot2 in the CRCs (243.571 +/- 564.569) was higher compared to the normal mucosa (107.252 +/- 413.635, P<0.0001) and liver metastasis samples (42.002 +/- 40.809, P=0.0002). hBiot2 expression was increased from stages I + II to III (P=0.047), and no difference in the expression was found in stages III and IV (P=0.452). A high value of hBiot2 was associated with a poorer prognosis compared with a low value independently of gender, age, tumor site, stage and differentiation (P=0.007, RR 7.519, 95% Cl 1.729-32.704). Liver metastasis, smaller tumors, non-local recurrence and primary liver surgery alone were associated with a higher value of hBiot2 compared to larger tumors, local recurrence and repeated liver surgery (P=0.003, 0.044 and 0.026, respectively). An inverse relationship was found between hBiot2 expression and the metastatic potential of the colon cancer cell lines. Thus, increased expression of hBiot2 may be an early and interim event in the development of CRC. A higher expression of hBiot2 in primary CRC patients independently indicates a poorer prognosis.

  • 12.
    Song, Gang
    et al.
    Cancer Research Center, Medical College, Xiamen University, Xiamen 361005, China.
    Guo, Shiguang
    Cancer Research Center, Medical College, Xiamen University, Xiamen 361005, China.
    Wang, Weiwei
    Cancer Research Center, Medical College, Xiamen University, Xiamen 361005, China.
    Hu, Chun
    Cancer Research Center, Medical College, Xiamen University, Xiamen 361005, China.
    Mao, Yubing
    Department of Basic Medical Sciences, Medical College, Xiamen University, Xiamen 361005, China.
    Zhang, Bing
    Department of Basic Medical Sciences, Medical College, Xiamen University, Xiamen 361005, China.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre. Cancer Research Center, Medical College, Xiamen University, Xiamen 361005, China.
    Hu, Tianhui
    Cancer Research Center, Medical College, Xiamen University, Xiamen 361005, China.
    Intestinal Metabolite Compound K of Ginseng Saponin Potently Attenuates Metastatic Growth of Hepatocellular Carcinoma by Augmenting Apoptosis via a Bid-Mediated Mitochondrial Pathway2010In: Journal of Agricultural and Food Chemistry, ISSN 0021-8561, E-ISSN 1520-5118, Vol. 58, no 24, p. 12753-12760Article in journal (Refereed)
    Abstract [en]

    It was recently shown that compound K (CK), an intestinal bacterial metabolite of ginseng saponin, exhibits antihepatocellular carcinoma (HCC) activity, and Bid is a potential drug target for HCC therapy. This paper reports a novel mechanism of CK-induced apoptosis of HCC cells via Bid-mediated mitochondrial pathway. OK dramatically inhibited HCC cells growth in concentration- and time-dependent manners, and a high dose of OK could induce HCC cell apoptotic cell death. Furthermore, the effective dose of CK potently attenuated the subcutaneous tumor growth and spontaneous HOC metastasis in vivo. At the molecular level, immunohistochemical staining revealed that Bid expression in subcutaneous tumor and liver metastasis tissues decreased dramatically in OK-treated groups compared to untreated controls, which also implies that Bid may play a critical role in the growth and progression of HCC. Further study shows that translocation of full-length Bid to the mitochondria from nuclei during cytotoxic apoptosis was associated with the release of cytochrome c from mitochondria, indicating that full-length Bid is sufficient for the activation of mitochondrial cell death pathways in response to CK treatment in HCC cells. Taken together, the results not only reveal a Bid-mediated mitochondrial pathway in HCC cells induced by CK but also suggest that OK may become a potential cytotoxic drug targeting Bid in the prevention and treatment of HCC.

  • 13.
    Stratmann, Johannes
    et al.
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Wang, Chao-Jie
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Gnosa, Sebastian
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Wallin, Åsa
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Hinselwood, David
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Sun, Xiao-Feng
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-581 85, Linköping, Sweden.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Dicer and miRNA in relation to clinicopathological variables in colorectal cancer patients2011In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. 345-Article in journal (Refereed)
    Abstract [en]

    Background: Dicer is aberrantly expressed in several types of cancers. Applying real-time PCR, we detected the expression of Dicer mRNA in normal mucosa (n = 162), primary colorectal cancer (CRC) (n = 162) and liver metastasis (n = 37), and analysed the relationship between Dicer expression and clinicopathological features. We also correlated the expression of Dicer mRNA to the miRNA expression of miR-141, miR-200a, miR-200b, mir-200c and miR-429 in liver metastases.

    Methods: RT-PCR and qPCR were used to analyse the Dicer expression in normal mucosa, primary tumour and liver metastasis by using the High Capacity cDNA Reverse Transcription Kit and TaqMan™® Gene Expression assays for Dicer and GAPDH. RT-PCR and qPCR were used to detect miRNA expression in liver metastases by utilizing TaqMan® MicroRNA Reverse Transcription Kit and TaqMan® miRNA Assays. Statistical analyses were performed with STATISTICA.

    Results: Dicer expression in rectal cancer (3.146 ± 0.953) was higher than in colon cancer (2.703 ± 1.204, P = 0.018). Furthermore the Dicer expression was increased in primary tumours (3.146 ± 0.952) in comparison to that in normal mucosa from rectal cancer patients (2.816 ± 1.009, P = 0.034) but this is not evident in colon cancer patients. Dicer expression in liver metastases was decreased in comparison to that of either normal mucosa or primary tumour in both colon and rectal cancers (P < 0.05). Patients with a high Dicer expression in normal mucosa had a worse prognosis compared to those with a low Dicer expression, independently of gender, age, tumour site, stage and differentiation (P < 0.001, RR 3.682, 95% CI 1.749 - 7.750). In liver metastases, Dicer was positively related to miR-141 (R = 0.419, P = 0.015).

    Conclusion: Dicer is up-regulated in the early development of rectal cancers. An increased expression of Dicer mRNA in normal mucosa from CRC patients is significantly related to poor survival independently of gender, age, tumour site, stage and differentiation.

  • 14.
    Wang, Chao-Jie
    et al.
    Sichuan Univ, Inst Digest Surg, Dept Colorectal Surg, W China Hosp, Chengdu 610064, Peoples R China / Sichuan Univ, State Key Lab Biotherapy, W China Hosp, Chengdu 610064, Peoples R China.
    Zhou, Zong-Guang
    Sichuan Univ, Inst Digest Surg, Dept Colorectal Surg, W China Hosp, Chengdu 610064, Peoples R China / Sichuan Univ, State Key Lab Biotherapy, W China Hosp, Chengdu 610064, Peoples R China.
    Holmqvist, Annica
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, S-58185 Linkoping, Sweden .
    Zhang, Hong
    University of Skövde, School of Life Sciences.
    Li, Yuan
    Sichuan Univ, Inst Digest Surg, Dept Colorectal Surg, W China Hosp, Chengdu 610064, Peoples R China / Sichuan Univ, State Key Lab Biotherapy, W China Hosp, Chengdu 610064, Peoples R China.
    Adell, Gunnar
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Sun, Xiao-Feng
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, S-58185 Linkoping, Sweden .
    Survivin Expression Quantified by Image Pro-plus Compared With Visual Assessment2009In: Applied immunohistochemistry & molecular morphology (Print), ISSN 1541-2016, E-ISSN 1533-4058, Vol. 17, no 6, p. 530-535Article in journal (Refereed)
    Abstract [en]

    Over the past decades, immunohistochemistry has gained significance and already taken a crucial position in diagnosis of diseases and prognosis of patients. However, manual interpretation of immunohistochemistry and reproducibility of the scoring systems can be highly Subjective. In the article, the immunohistochemical staining of survivin in 98 rectal cancers was analyzed by using Image Pro-Plus (IPP) [3 parameters: density mean, area sum, and integrated optical density (IOD)] and the results were compared with visual assessment (2 parameters: intensity and percentage). The correlations between the 2 methods were examined, significant correlations were observed between density mean and staining intensity (Spearman correlation coefficient, r(s) = 0.806, P < 0.001) IOD and staining intensity (r(s) = 0.9147 P < 0.001) area sum and staining percentage (r(s) = 0.883, P < 0.001), IOD and staining percentage (r(s) = 0.884, P < 0.001). There was no significant difference between survivin expression and clinicopathologic variables (P > 0.05) by visual assessment. However, by IPP analysis, both the density mean and IOD were higher in better-differentiated cancers than in worse differentiated ones (P = 0.02 and 0.03). There was a substantial agreement between the 2 methods. Density mean and IOD of IPP were representative parameters to assess the immunostaining quantification, and increased sensitivity in scoring and provided a more reliable and reproducible analysis of protein expression, especially, more information of the protein expression in relation to clinicopathologic variables can be provided by IPP analysis.

  • 15.
    Widegren, Emma
    et al.
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Onnesjo, Sofia
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Arbman, Gunnar
    Vrinnevi Univ Hosp, Dept Surg, Norrkoping, Sweden .
    Kayed, Hany
    Univ Heidelberg, Inst Clin Radiol & Nucl Med, Univ Hosp Mannheim, Heidelberg, Germany .
    Zentgraf, Hanswalter
    German Canc Res Ctr, D-6900 Heidelberg, Germany .
    Kleeff, Joerg
    Tech Univ Munich, Dept Surg, Munich, Germany.
    Zhang, Hong
    University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Expression of FXYD3 Protein in Relation to Biological and Clinicopathological Variables in Colorectal Cancers2009In: Chemotherapy, ISSN 0009-3157, E-ISSN 1421-9794, Vol. 55, no 6, p. 407-413Article in journal (Refereed)
    Abstract [en]

    Background: FXYD3 is up-/down-regulated in different types of cancers. We examined FXYD3 expression in colorectal cancers and its relationship to biological and clinicopathological variables. Patients and Methods: Expression of FXYD3 protein was immunohistochemically examined in distant normal mucosa (n = 34), adjacent normal mucosa (n = 72), primary tumour (n = 150) and lymph node metastasis (n = 35) from colorectal cancer patients. Results: FXYD3 was highly expressed in primary tumour compared to adjacent normal mucosa (p = 0.02). FXYD3 was or tended to be positively related to the expression of ras (p = 0.02), p53 (p = 0.06), legumain (p = 0.02) and proliferating cell nuclear antigen (p = 0.03). Moreover, there was a higher frequency of strong FXYD3 expression in Dukes A-C tumours than in D tumours (p = 0.04). The strong FXYD3 expression tended to predict worse survival in the patients with Dukes A + B tumour (p = 0.07), while there was no such tendency in the patients with Dukes C + D tumour (p = 0.94). The tumours located in the colon had a higher degree of FXYD3 expression than the tumours located in the rectum (p = 0.05). Conclusion: The FXYD3 was associated with certain biological variables and may be involved in the development of the relative earlier stages of colorectal cancers. Copyright (C) 2009 S. Karger AG, Basel

  • 16.
    Yan, Bao-Yong
    et al.
    Hebei Medical University, Shijiazhuang.
    Wang, Da-Wei
    Hebei Medical University, Shijiazhuang.
    Zhu, Zhen-Long
    Hebei Medical University, Shijiazhuang.
    Yang, Yan-Hong
    Hebei Medical University, Shijiazhuang.
    Wang, Ming-Wei
    Hebei Medical University, Shijiazhuang.
    Cui, Dong-Sheng
    Hebei Medical University, Shijiazhuang.
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    University of Linköping.
    Overexpression of MAC30 in the Cytoplasm of Oral Squamous Cell Carcinoma Predicts Nodal Metastasis and Poor Differentiation2010In: Chemotherapy, ISSN 0009-3157, E-ISSN 1421-9794, Vol. 56, no 6, p. 424-428Article in journal (Refereed)
    Abstract [en]

    Background: Expression of the meningioma-associated protein (MAC30) was increased in several types of tumors, including esophageal, gastric and colon tumors, compared to normal tissue. MAC30 expression levels gradually increased from normal colorectal mucosa to primary colorectal cancer and colorectal cancer spreading to the lymph nodes. MAC30 expression was related to survival in patients with colorectal cancer. However, there is no study on MAC30 in oral squamous cell carcinoma (OSCC). Methods: Therefore, MAC30 expression in OSCC was investigated and possible associations of MAC30 expression with clinicopathological variables in OSCC have been analyzed. MAC30 expression was immunohistochemically examined in 20 normal oral mucosa and 43 OSCC specimens. Results: Expression levels of MAC30 in the cytoplasm markedly increased from normal oral epithelial cells to primary OSCC. Strong cytoplasmic staining was significantly higher in primary OSCC compared to normal oral mucosa samples (51 vs. 20%, p = 0.019). Furthermore, MAC30 expression levels in primary tumors of patients with lymph node metastasis exceeded levels in those without metastasis (65 vs. 35%, p = 0.048), and MAC30 expression in poorly differentiated tumors was higher than in well-differentiated ones (90 vs. 39%, p = 0.005). Conclusion: Overexpression of MAC30 in the cytoplasm of OSCC may predict nodal metastasis and poor differentiation.

  • 17.
    Yang, L.
    et al.
    Linköping University.
    Olsson, B.
    Linköping University.
    Pfeifer, D.
    Linköping University.
    Jönsson, J.-I.
    Linköping University.
    Zhou, Z.-G.
    Sichuan University.
    Jiang, X.
    Sichuan University.
    Fredriksson, B.-A.
    Linköping University.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Sun, X.-F.
    Linköping University.
    Knockdown of peroxisome proliferator-activated receptor-β induces less differentiation and enhances cell-fibronectinadhesion of colon cancer cells2010In: Oncogene, ISSN 0950-9232, E-ISSN 1476-5594, Vol. 29, no 4, p. 516-526Article in journal (Refereed)
    Abstract [en]

    The role of peroxisome proliferator-activated receptor-/ (PPAR-/) in the pathogenesis of colon cancer remains highly controversial. This study specifically silenced the PPAR- expression in three colon cancer cell lines with different metastatic potentials. Although PPAR-knockdown resulted in more malignant morphological changes, bigger colony sizes and lower carcinoembryonic antigen (CEA) secretion, and enhanced the cell-fibronectin adhesion, cell invasion and migration were unaffected. These effects were stronger in poorly metastatic cell lines compared with highly metastatic ones. Simultaneously, PPAR-knockdown decreased the mRNAs encoding adipocyte differentiation-related protein and liver fatty acid binding protein, and increased the mRNA of ILK, whereas the mRNAs encoding integrin-1 and angiopoietin-like 4 were unchanged. Using immunohistochemistry, we determined that the intensity of PPAR- expression was stronger in rectal cancers with better differentiation than in those with poor differentiation, and was stronger in early-stage tumors than in advanced ones. Together, these findings consistently indicate that PPAR- may facilitate differentiation and inhibit the cell-fibronectin adhesion of colon cancer, having a role as an inhibitor in the carcinogenesis and progression of colorectal cancer. Interestingly PPAR- seems to have a more important role in poorly metastatic cells than in highly metastatic ones.

  • 18.
    Yang, Lie
    et al.
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China / Linkoping Univ, Dept Oncol & Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Zhang, Hong
    University of Skövde, The Systems Biology Research Centre. University of Skövde, School of Life Sciences.
    Zhou, Zong-Guang
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China .
    Yan, Hui
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China .
    Adell, Gunnar
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Sun, Xiao-Feng
    Sichuan Univ, W China Hosp, Inst Digest Surg, Chengdu 610064, Sichuan Prov, Peoples R China / Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Chengdu 610064, Sichuan Prov, Peoples R China / Linkoping Univ, Dept Oncol & Clin & Expt Med, SE-58185 Linkoping, Sweden .
    Biological Function and Prognostic Significance of Peroxisome Proliferator-Activated Receptor delta in Rectal Cancer2011In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 17, no 11, p. 3760-3770Article in journal (Refereed)
    Abstract [en]

    Purpose: To investigate the expression significance of PPAR beta/delta in relation to radiotherapy (RT), clinicopathologic, and prognostic variables of rectal cancer patients. Experimental Design: We included 141 primary rectal cancer patients who participated in a Swedish clinical trial of preoperative RT. Tissue microarray samples from the excised rectal cancers and the adjacent or distant normal mucosa and lymph node metastases were stained with PPAR delta antibody. Survival probability was computed by the Kaplan-Meier method and Cox regression model. The proliferation of colon cancer cell lines KM12C, KM12SM, and KM12L4a was assayed after PPAR delta knockdown. Results: PPAR delta was increased from adjacent or distant normal mucosa to primary cancers, whereas it decreased from primary cancers to lymph node metastases. After RT, PPAR delta was increased in normal mucosa, whereas it decreased in primary cancers and lymph node metastases. In primary cancers, the high expression of PPAR delta was related to higher frequency of stage I cases, lower lymph node metastasis rate, and low expression of Ki-67 in the unirradiated cases, and related to favorable survival in the cases either with or without RT. The proliferation of the KM12C, KM12SM, or KM12L4a cells was significantly accelerated after PPAR delta knockdown. Conclusions: RT decreases the PPAR delta expression in primary rectal cancers and lymph node metastases. PPAR delta is related to the early development of rectal cancer and inhibits the proliferation of colorectal cancer cells. Increase of PPAR delta predicts favorable survival in the rectal cancer patients either with or without preoperative RT. Clin Cancer Res; 17(11); 3760-70. (C)2011 AACR.

  • 19.
    Zhang, Hong
    et al.
    University of Skövde, School of Life Sciences.
    Sun, Xiao-Feng
    Department of Biomedicine and Surgery, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Synnerstad, Ingrid
    Division of Dermatology, Department of Clinical and Experimental Medicine, Linköping University, Sweden.
    Rosdahl, Inger
    Division of Dermatology, Department of Clinical and Experimental Medicine, Linköping University, Sweden.
    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 Analysis2007In: The Cancer Journal, ISSN 1528-9117, E-ISSN 1540-336X, 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.

  • 20.
    Zhang, Hong
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Wang, Da-Wei
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre. Department of Stomatology, The Third Hospital of Hebei Medical University, Hebei, China.
    Adell, Gunnar
    Department of Oncology, Karolinska University Hospital, Karolinska, Sweden.
    Sun, Xiao-Feng
    Division of Oncology, Department of Clinical and Experimental Medicine, Faculty of Heath Science, Linköping University, Sweden .
    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, p. 294-Article in journal (Refereed)
    Abstract [en]

    Background: Expression of WRAP53 protein has oncogenic properties and it is up regulated in several types of tumors. Methods: 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. Results: Frequency of WRAP53 protein expression was increased in primary rectal cancer compared to the normal mucosa (p < 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). Conclusion: WRAP53 may be a new biomarker used to predict prognosis and to select suitable patients for preoperative radiotherapy.

  • 21.
    Zhang, Hong
    et al.
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Widegren, Emma
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, Linkoping, Sweden .
    Wang, Da-Wei
    Hebei Med Univ, Hosp 3, Dept Stomatol, Shijiazhuang, Peoples R China.
    Sun, Xiao-Feng
    Linkoping Univ, Dept Oncol, Inst Clin & Expt Med, Linkoping, Sweden .
    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.

  • 22.
    Zhang, Zhi-Yong
    et al.
    Linkoping Univ, Inst Clin & Expt Med, Dept Oncol, S-58185 Linkoping, Sweden / Tangshan Gongren Hosp, Dept Pathol, Tangshan, Peoples R China / Hebei Med Univ, Hosp 1, Lab Ctr, Shijiazhuang, Peoples R China.
    Zhang, Hong
    University of Skövde, School of Life Sciences. University of Skövde, The Systems Biology Research Centre.
    Adell, Gunnar
    Karolinska Univ Hosp, Dept Oncol, Stockholm, Sweden.
    Sun, Xiao-Feng
    Linkoping Univ, Inst Clin & Expt Med, Dept Oncol, S-58185 Linkoping, Sweden.
    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, E-ISSN 1471-2407, Vol. 11, p. Artikelnr 89-Article 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 < 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.

  • 23.
    Zhao, Zeng-Ren
    et al.
    Department of General Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
    Zhang, Zhi-Yong
    Department of Oncology, Institute of Biomedicine and Surgery, Linköping University, Linköping, Sweden / Department of Pathology, Tangshan Gongren Hospital, Tangshan, P.R. China.
    Zhang, Hong
    Department of Dermatology, Institute of Biomedicine and Surgery, Linköping University, Linköping, Sweden.
    Jiang, Li
    Department of Pathology, Tangshan Gongren Hospital, Tangshan, P.R. China.
    Wang, Ming-Wei
    Laboratory Centre, The First Hospital of Hebei Medical University, Shijiazhuang, P.R. China.
    Sun, Xiao-Feng
    Department of Oncology, Institute of Biomedicine and Surgery, Linköping University, Linköping, Sweden.
    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]

    Abstract: 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.

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