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Träfflista för sökning "L773:0007 0920 OR L773:1532 1827 srt2:(2010-2014)"

Sökning: L773:0007 0920 OR L773:1532 1827 > (2010-2014)

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141.
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142.
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143.
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144.
  • Lundin, Kristina, et al. (författare)
  • Androgen receptor genotypes predict response to endocrine treatment in breast cancer patients.
  • 2011
  • Ingår i: British Journal of Cancer. - Nature Publishing Group. - 1532-1827. ; 105:11, s. 1676-1683
  • Tidskriftsartikel (refereegranskat)abstract
    • Background:The androgen receptor (AR) is frequently expressed in breast cancers. The AR genotype may affect disease-free survival and response to endocrine therapy.Methods:In all, 634 women undergoing breast cancer surgery between 2002 and 2008 were followed until 30 June 2010. Six haplotype-tagging single-nucleotide polymorphisms in the AR, and the resulting AR diplotypes, were examined in relation to breast cancer patient characteristics, tumour characteristics, disease-free survival, and response to endocrine treatment.Results:Five common AR diplotypes were found. Seventeen rare variants were combined into a composite group. The resulting six AR diplotype groups were clustered into two subgroups, groups A (n=128) and B (n=499), with three diplotypes in each. Patients in group B had larger total breast volume (P=0.024), higher body mass index (BMI) (P=0.050), more axillary lymph node involvement (P(trend)=0.020), and higher histological grade (P(trend)=0.031). There were 59 breast cancer events in the 569 patients with invasive cancers and no preoperative treatment. Patients in group B also had shorter disease-free survival (P=0.037) than patients in group A. Among patients in group B with oestrogen receptor α positive tumours, tamoxifen (TAM) treatment was associated with longer disease-free survival (P=0.008), while treatment with aromatase inhibitors (AIs) was not (P=0.94). Response to endocrine treatment could not be predicted based on BMI, suggesting that the effect of AR diplotypes went beyond that of a higher BMI.Conclusion:A marker for a group of patients who responded to TAM, but not to AIs, was identified. If this finding is confirmed, AR genotyping may provide useful information for selection of endocrine treatment of breast cancer patients.British Journal of Cancer advance online publication, 27 October 2011; doi:10.1038/bjc.2011.441 www.bjcancer.com.
145.
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146.
  • Mehrara, Esmaeil, 1971-, et al. (författare)
  • Objective assessment of tumour response to therapy based on tumour growth kinetics.
  • 2011
  • Ingår i: British journal of cancer. - 1532-1827. ; 105:5, s. 682-6
  • Tidskriftsartikel (refereegranskat)abstract
    • Current standards for assessment of tumour response to therapy (a) categorise therapeutic efficacy values, inappropriate for patient-specific and deterministic studies, (b) neglect the natural growth characteristics of tumours, (c) are based on tumour shrinkage, inappropriate for cytostatic therapies, and (d) do not accommodate integration of functional/biological means of therapeutic efficacy assessed with, for example, positron emission tomography or magnetic resonance imaging, with data from anatomical changes in tumour.
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147.
  • Memon, A A, et al. (författare)
  • PET imaging of patients with non-small cell lung cancer employing an EGF receptor targeting drug as tracer
  • 2011
  • Ingår i: British Journal of Cancer. - Nature Publishing Group. - 1532-1827. ; 105:12, s. 5-1850
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: We have previously developed (11)C-erlotinib as a new positron emission tomography (PET) tracer and shown that it accumulates in epidermal growth factor receptor (EGFR)-positive lung cancer xenografts in mice. Here, we present a study in patients with non-small cell lung cancer (NSCLC) investigating the feasibility of (11)C-erlotinib PET as a potential method for the identification of lung tumours accumulating erlotinib.METHODS: Thirteen patients with NSCLC destined for erlotinib treatment were examined by contrast-enhanced computed tomography (CT), (11)C-erlotinib PET/low-dose CT and (18)F-fluoro-2-deoxy-D-glucose ((18)F-FDG) PET/low-dose CT before start of the erlotinib treatment. After 12 weeks treatment, they were examined by (18)F-FDG PET/contrast-enhanced CT for the assessment of clinical response.RESULTS: Of the 13 patients included, 4 accumulated (11)C-erlotinib in one or more of their lung tumours or lymph-node metastases. Moreover, (11)C-erlotinib PET/CT identified lesions that were not visible on (18)F-FDG PET/CT. Of the four patients with accumulation of (11)C-erlotinib, one died before follow-up, whereas the other three showed a positive response to erlotinib treatment. Three of the nine patients with no accumulation died before follow-up, four showed progressive disease while two had stable disease after 12 weeks of treatment.CONCLUSION: Our data show a potential for (11)C-erlotinib PET/CT for visualizing NSCLC lung tumours, including lymph nodes not identified by (18)F-FDG PET/CT. Large clinical studies are now needed to explore to which extent pre-treatment (11)C-erlotinib PET/CT can predict erlotinib treatment response.
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148.
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149.
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150.
  • Nishioka, T., et al. (författare)
  • Nicotine increases the resistance of lung cancer cells to cisplatin through enhancing Bcl-2 stability
  • 2014
  • Ingår i: British Journal of Cancer. - 0007-0920. ; 110:7, s. 1785-1792
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Nicotine is able to activate mitogenic signalling pathways, which promote cell growth or survival as well as increase chemoresistance of cancer cells. However, the underlying mechanisms are not fully understood. Methods: In this study, we used immunoblotting and immunoprecipitation methods to test the ubiquitination and degradation of Bcl-2 affected by nicotine in lung cancer cells. Apoptotic assay was also used to measure the antagonising effect of nicotine on cisplatin-mediated cytotoxicity. Results: We demonstrated that the addition of nicotine greatly attenuated Bcl-2 ubiquitination and degradation, which further desensitised lung cancer cells to cisplatin-induced cytotoxicity. In this process, Bcl-2 was persistently phosphorylated in the cells cotreated with nicotine and cisplatin. Furthermore, Akt was proven to be responsible for sustained activation of Bcl-2 by nicotine, which further antagonised cisplatin- mediated apoptotic signalling. Conclusions: Our study suggested that nicotine activates its downstream signalling to interfere with the ubiquitination process and prevent Bcl-2 from being degraded in lung cancer cells, resulting in the increase of chemoresistance.
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