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Preoperative Chemotherapy Plus Bevacizumab and Morbidity after Resection of Colorectal Cancer Liver Metastases
Pages 65-72
Mª José Safont, Jorge Aparicio, Alejandra Giménez Ortiz, José Mir, Eva Montalvá and Miriam Cantos Pallarés
DOI:
http://dx.doi.org/10.6000/1927-7229.2014.03.01.10
Published: 18 February 2014


Abstract: Aims and background: The addition of bevacizumab to preoperative chemotherapy is a common therapeutic practice in patients with colorectal liver metastases. The aim of the present study was to assess the effect of bevacizumab on postoperative complications after liver resection.

Methods:A retrospective analysis was performed including patients who underwent liver resection for colorectal liver metastases after receiving chemotherapy with or without bevacizumab in two hospitals. Univariate logistic regression models were used to identify predictors of postoperative morbidity in both groups of patients.

Results: A total of 76 patients were analyzed: 22 patients did not receive preoperative chemotherapy (control group), 21 patients received preoperative chemotherapy alone and 33 patients received preoperative chemotherapy in combination with bevacizumab. The median number of chemotherapy cycles received was 4 (range, 1-23) for the chemotherapy group and 7 (range, 2-36) for the chemotherapy plus bevacizumab group Morbidity rate was similar in the three groups of patients considered: 54.5 %, 47.6% and 39.4, respectively. The most common complications were infections and wound complications. The number of preoperative chemotherapy cycles received was the only clinical variable that was significantly correlated with postoperative comorbidity.

Conclusions: Our results support the evidence that the addition of bevacizumab to preoperative chemotherapy does not increase the risk of complications following surgery of colorectal liver metastases.

Keywords: Colorectal liver metastases, bevacizumab, postoperative complications, preoperative chemotherapy, surgery complications.
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The Role of Secreted Frizzled Related Protein 4 (sFRP-4) in Regulating Oestradiol-Induced Growth of the MCF-7 Breast Cancer Cell Line
Pages 1-10
Sally McLaren, Frank Arfuso, Nik Zeps and Arun Dharmarajan
DOI:
http://dx.doi.org/10.6000/1927-7229.2014.03.01.1
Published: 31 January 2014Open Access


Abstract: The Wnt signalling pathway is involved in regulating cellular proliferation and differentiation, and aberrant activation has been described in several cancers including breast. Oestradiol up regulates Wnt pathway gene expression, and thereby activates the Wnt signalling pathway. We used the oestrogen-responsive breast cancer cell line MCF-7 to examine the effects of secreted frizzled related protein 4 (sFRP-4) on oestradiol-induced growth, including gene expression of the Wnt signalling pathway genes Frizzled Receptor, Wnt-10b, and β-catenin. We demonstrate here that sFRP-4 inhibits oestradiol-induced cell growth in the MCF-7 cell line and also down regulates oestradiol-induced expression of selected Wnt signalling genes including β-catenin. We propose that sFRP-4 is a potent inhibitor of the Wnt signalling pathway and may negatively regulate oestradiol-mediated proliferation in human breast cancer cells.

Keywords: Breast cancer, sFRP4, Wnt signalling, oestradiol, β-catenin, cellular proliferation, growth inhibition.
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Correlations between Carcinoembryonic Antigen, Epidermal Growth Factor and Leptin in Patients with Non-Small-Cell Lung Cancer
Pages 11-17
Cuihong Song, Jie Liao, Zihui Deng, Jinying Zhang, Hui Xue, Yongming Li, Chen Liang, Ming Han, Jianhua Li and Guangtao Yan
DOI:
http://dx.doi.org/10.6000/1927-7229.2014.03.01.2
Published: 31 January 2014


Abstract: Objectives:Carcinoembryonic antigen (CEA), epidermal growth factor (EGF) and leptin have been reported to be intimately intertwined in lung carcinogenesis.However, few studies have simultaneously examined these proteins in lung cancer and whether a correlation exist among them remains unclear. Here, we compared the levels of CEA, EGF and leptin in non-small-cell lung cancer (NSCLC) patients and controls and evaluated the possible associations among them.

Methods:97 patients ranged from 30 to 83 years of age were studied. Serum CEA, EGF and leptin levels were determined following a standard protocol. The relationships between these proteins and clinicopathological factors were evaluated by Wilcoxon rank sum or Kruskal-Wallis H test. Spearman rank-correlation were used to determine the correlations among CEA, EGF and leptin. Co-expression of these proteins in NSCLC tissues was examined by immunofluorescence.

Results: Serum CEA and leptin levels in NSCLC patients were significantly higher compared to controls (both P = 0.000), but no statistically significant difference was found for EGF. CEA and EGF were not associated with the tumor-related factors, but leptin was strongly correlated with sex (P = 0.005). Significant correlations among these proteins were found when the patients were categorized into subgroups. Co-expresstion of these proteins was significantly enhanced with lung carcinogenesis.

Conclusions:CEA, EGF and leptin may interplay and play vital roles in the pathogenesis of NSCLC. Besides CEA, the leptin levels were also significantly higher in NSCLC patients than in controls. Determination of preoperative leptin levels may prove useful for screening and predicting NSCLC.

Keywords: Non-small-cell lung cancer, Carcinoembryonic antigen (CEA), Epidermal growth factor (EGF), Leptin,Immunofluorescence,Correlation.
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Secretory Kin17 is Correlated with Chemoresistance in Oral Squamous Cell Carcinoma
Pages 18-25
Xiaoyi Liu, Lijuan Deng, Haixia Zhang, Tao Zeng, Hua Wang and Yan Zhang
DOI:
http://dx.doi.org/10.6000/1927-7229.2014.03.01.3
Published: 31 January 2014


Abstract: Purpose: Kin17 is a conserved nuclear protein that participates in DNA damage repair, DNA replication and cell proliferation. Several reports have linked Kin17 to tumor progression. However, the role of Kin17 in oral squamous cell carcinoma (OSCC) has not yet been described. The aims of this study were to assess Kin17 transcript and protein expression in OSCC and to evaluate an association for this protein with chemoresistance.

Methods: Kin17 expression in OSCC tissues and OSCC cell lines was measured by standardized immunohistochemistry, western blotting and semi-quantitative RT-PCR. Secretory Kin17 protein was measured in serum samples and cell culture conditioned media. A recombinant Kin17 protein was purified and used in a chemoresistance assay.

Results: Kin17 was identified as an unconventional secretory protein, whose expression levels were correlated with chemotherapy and chemoresistance in OSCC. Kin17 protein expression was up-regulated in patients exhibiting chemoresistance. Serum Kin17 levels were significantly increased in patients receiving chemotherapy. We provide evidence that the secretory Kin17 protein plays a role in the DNA damage response in OSCC. Furthermore, we also show that the secretory Kin17 protein enhances the chemoresistance of OSCC cells and increases the expression of multidrug resistant genes.

Conclusion:To our knowledge, this is the first report of Kin17 being characterized as a secretory protein. This novel role for Kin17 may have implications for studying the chemoresistance process in OSCC. The effective inhibition of Kin17 secretion may improve or prolong chemotherapeutic effects, making it an attractive therapeutic target candidate for further study.

Keywords: Kin17, secretory protein, oral cancer, DNA damage, chemoresistance.
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