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Zhang, Hong
Publications (10 of 23) Show all publications
Lööf, J., Pfeifer, D., Ding, Z., Sun, X.-F. & Zhang, H. (2012). Effects of ΔNp73β on Cisplatin Treatment in Colon Cancer Cells. Molecular Carcinogenesis, 51(8), 628-635
Open this publication in new window or tab >>Effects of ΔNp73β on Cisplatin Treatment in Colon Cancer Cells
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2012 (English)In: Molecular Carcinogenesis, ISSN 0899-1987, E-ISSN 1098-2744, Vol. 51, no 8, p. 628-635Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2012
Keywords
cell death; HCT116 cells; HT29 cells; p73 protein; p53
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5813 (URN)10.1002/mc.20835 (DOI)000305962400004 ()2-s2.0-84863477921 (Scopus ID)
Available from: 2012-05-02 Created: 2012-05-02 Last updated: 2017-12-07Bibliographically approved
Gnosa, S., Shen, Y.-M., Wang, C.-J., Zhang, H., Stratmann, J., Arbman, G. & Sun, X.-F. (2012). Expression of AEG-1 mRNA and protein in colorectal cancer patients and colon cancer cell lines. Journal of Translational Medicine, 10, Article ID 109.
Open this publication in new window or tab >>Expression of AEG-1 mRNA and protein in colorectal cancer patients and colon cancer cell lines
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2012 (English)In: Journal of Translational Medicine, ISSN 1479-5876, E-ISSN 1479-5876, Vol. 10, article id 109Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
BioMed Central, 2012
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-6641 (URN)10.1186/1479-5876-10-109 (DOI)000307018200001 ()22643064 (PubMedID)2-s2.0-84861470722 (Scopus ID)
Available from: 2012-11-12 Created: 2012-11-09 Last updated: 2018-11-28Bibliographically approved
Hu, C., Song, G., Zhang, B., Liu, Z., Chen, R., Zhang, H. & Hu, T. (2012). Intestinal metabolite compound K of panaxoside inhibits the growth of gastric carcinoma by augmenting apoptosis via Bid-mediated mitochondrial pathway. Journal of Cellular and Molecular Medicine (Print), 16(1), 96-106
Open this publication in new window or tab >>Intestinal metabolite compound K of panaxoside inhibits the growth of gastric carcinoma by augmenting apoptosis via Bid-mediated mitochondrial pathway
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2012 (English)In: Journal of Cellular and Molecular Medicine (Print), ISSN 1582-1838, E-ISSN 1582-4934, Vol. 16, no 1, p. 96-106Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Wiley-Blackwell, 2012
Keywords
gastric carcinoma, compound K, Bid, apoptosis
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5459 (URN)10.1111/j.1582-4934.2011.01278.x (DOI)000298586600009 ()21323864 (PubMedID)2-s2.0-84855174764 (Scopus ID)
Available from: 2012-02-22 Created: 2012-02-22 Last updated: 2019-11-26Bibliographically approved
Lewander, A., Gao, J., Carstensen, J., Arbman, G., Zhang, H. & Sun, X.-F. (2012). NF-kappa B p65 phosphorylated at serine-536 is an independent prognostic factor in Swedish colorectal cancer patients. International Journal of Colorectal Disease, 27(4), 447-452
Open this publication in new window or tab >>NF-kappa B p65 phosphorylated at serine-536 is an independent prognostic factor in Swedish colorectal cancer patients
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2012 (English)In: International Journal of Colorectal Disease, ISSN 0179-1958, E-ISSN 1432-1262, Vol. 27, no 4, p. 447-452Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Springer, 2012
Keywords
NF-kappa B, Survival, Colorectal cancer, Immunohistochemistry
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5692 (URN)10.1007/s00384-011-1356-8 (DOI)000301777100004 ()22102084 (PubMedID)2-s2.0-84862986139 (Scopus ID)
Available from: 2012-04-13 Created: 2012-04-13 Last updated: 2017-12-07Bibliographically approved
Shen, Y.-M., Arbman, G., Sandström, P., Gullstrand, P., Wei, Y.-Q., Zhang, H., . . . Sun, X.-F. (2012). Novel gene hBiot2 is an independent prognostic factor in colorectal cancer patients. Oncology Reports, 27(2), 376-382
Open this publication in new window or tab >>Novel gene hBiot2 is an independent prognostic factor in colorectal cancer patients
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2012 (English)In: Oncology Reports, ISSN 1021-335X, E-ISSN 1791-2431, Vol. 27, no 2, p. 376-382Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Spandidos Publ Ltd, 2012
Keywords
human Biot2, colorectal cancer, prognosis, real-time PCR, in situ hybridization
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5455 (URN)10.3892/or.2011.1521 (DOI)000298825900011 ()22024937 (PubMedID)2-s2.0-84862919681 (Scopus ID)
Available from: 2012-02-23 Created: 2012-02-22 Last updated: 2017-12-07Bibliographically approved
Zhang, H., Wang, D.-W., Adell, G. & Sun, X.-F. (2012). WRAP53 is an independent prognostic factor in rectal cancer- a study of Swedish clinical trial of preoperative radiotherapy in rectal cancer patients. BMC Cancer, 12, 294
Open this publication in new window or tab >>WRAP53 is an independent prognostic factor in rectal cancer- a study of Swedish clinical trial of preoperative radiotherapy in rectal cancer patients
2012 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 12, p. 294-Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
BioMed Central, 2012
Keywords
WRAP53, Radiotherapy, Prognosis, Rectal cancer
National Category
Cancer and Oncology
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-7450 (URN)10.1186/1471-2407-12-294 (DOI)000311500000001 ()22805008 (PubMedID)2-s2.0-84870031289 (Scopus ID)
Available from: 2013-03-21 Created: 2013-03-21 Last updated: 2017-12-06Bibliographically approved
Yang, L., Zhang, H., Zhou, Z.-G., Yan, H., Adell, G. & Sun, X.-F. (2011). Biological Function and Prognostic Significance of Peroxisome Proliferator-Activated Receptor delta in Rectal Cancer. Clinical Cancer Research, 17(11), 3760-3770
Open this publication in new window or tab >>Biological Function and Prognostic Significance of Peroxisome Proliferator-Activated Receptor delta in Rectal Cancer
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2011 (English)In: Clinical Cancer Research, ISSN 1078-0432, E-ISSN 1557-3265, Vol. 17, no 11, p. 3760-3770Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
American Association for Cancer Research, 2011
National Category
Cancer and Oncology
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-5538 (URN)10.1158/1078-0432.CCR-10-2779 (DOI)000291200800027 ()21531809 (PubMedID)2-s2.0-79957887976 (Scopus ID)
Available from: 2012-03-19 Created: 2012-03-01 Last updated: 2017-12-07Bibliographically approved
Stratmann, J., Wang, C.-J., Gnosa, S., Wallin, Å., Hinselwood, D., Sun, X.-F. & Zhang, H. (2011). Dicer and miRNA in relation to clinicopathological variables in colorectal cancer patients. BMC Cancer, 11, 345
Open this publication in new window or tab >>Dicer and miRNA in relation to clinicopathological variables in colorectal cancer patients
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2011 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. 345-Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
BioMed Central, 2011
Keywords
CRC, Dicer, miRNAs, Prognosis, qPCR
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5814 (URN)10.1186/1471-2407-11-345 (DOI)000294408000001 ()21827717 (PubMedID)2-s2.0-81155158414 (Scopus ID)
Available from: 2012-05-02 Created: 2012-05-02 Last updated: 2017-12-07Bibliographically approved
Zhang, Z.-Y., Zhang, H., Adell, G. & Sun, X.-F. (2011). Endosialin expression in relation to clinicopathological and biological variables in rectal cancers with a Swedish clinical trial of preoperative radiotherapy. BMC Cancer, 11, Artikelnr 89
Open this publication in new window or tab >>Endosialin expression in relation to clinicopathological and biological variables in rectal cancers with a Swedish clinical trial of preoperative radiotherapy
2011 (English)In: BMC Cancer, ISSN 1471-2407, E-ISSN 1471-2407, Vol. 11, p. Artikelnr 89-Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
BioMed Central, 2011
National Category
Natural Sciences
Research subject
Natural sciences
Identifiers
urn:nbn:se:his:diva-5558 (URN)10.1186/1471-2407-11-89 (DOI)000288317700001 ()21362178 (PubMedID)2-s2.0-79952089288 (Scopus ID)
Available from: 2012-03-07 Created: 2012-03-01 Last updated: 2017-12-07Bibliographically approved
Lewander, A., Gao, J., Adell, G., Zhang, H. & Sun, X.-F. (2011). Expression of NF-kappa B p65 phosphorylated at serine-536 in rectal cancer with or without preoperative radiotherapy. Radiology and Oncology, 45(4), 279-284
Open this publication in new window or tab >>Expression of NF-kappa B p65 phosphorylated at serine-536 in rectal cancer with or without preoperative radiotherapy
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2011 (English)In: Radiology and Oncology, ISSN 1318-2099, E-ISSN 1581-3207, Vol. 45, no 4, p. 279-284Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Walter de Gruyter, 2011
Keywords
NF-kappa B, serine-536, radiotherapy, rectal cancer, immunohistochemistry, recurrence, prognosis
National Category
Cancer and Oncology
Research subject
Medical sciences
Identifiers
urn:nbn:se:his:diva-5510 (URN)10.2478/v10019-011-0030-7 (DOI)000297064900006 ()22933966 (PubMedID)2-s2.0-81755171096 (Scopus ID)
Available from: 2012-03-29 Created: 2012-03-01 Last updated: 2017-12-07Bibliographically approved
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