Annals of Oncology 2007 18(3):611; doi:10.1093/annonc/mdm054
© 2007 European Society for Medical Oncology
erratum |
Celecoxib reduces microvessel density in patients treated with nasopharyngeal carcinoma and induces changes in gene expression. Ann Oncol 2006; 17: 1625–1630
The publisher wishes to apologise to the authors of this article for the incorrect reproduction of one of the author names and for deleting two sections of text from the discussion section of the article.
The author W. L. Soon should have been printed as J. S. W. Low.
In the discussion section, on page 1628, in the middle of paragraph 2 and after the line ending with "... in control samples." the following text was deleted in error:
In addition, pre-clinical studies have also shown celecoxib to be an effective anti-angiogenic agent [14–16, 24]. Using the corneal micropocket assay, investigators have shown neovascularisation was inhibited by celecoxib [14, 15] and in a pancreatic cancer model, celecoxib reduced Sp1 transcription factor activity leading to reduced MVD [24].
In contrast to our findings, a decrease in COX-2 expression has been reported in a study of patients with cervical cancer [23]. In that study, computerised image analysis was used to assess COX-2 expression by immunohistochemistry in cervical tumors. In our study, a semi-quantitative assessment of COX- 2 by immunohistochemistry was used and the different findings may be due to the potentially different sensitivities of COX-2 assessment. Interestingly, in-vitro studies have found celecoxib and other non-steroidal anti-inflammatory drugs increased COX-2 expression [25, 26]. The effect of COX-2 inhibition on COX-2 expression should be further investigated.
A reduction in cell proliferation as measured by Ki-67 was not seen in our study. There are conflicting reports on the effect of celecoxib on cell proliferation in clinical studies. In one study reported by Ferrandina et al. [23], Ki-67 was reduced after ten days of celecoxib therapy whereas in a study of patients with oesophageal carcinoma receiving pre-operative celecoxib, no reduction in Ki-67 was seen [27]. As a down regulation of genes related to cell growth was observed (Table 2), it is possible further time was required to observe the histological effect down-stream to the transcriptional changes.
The plasma concentration of celecoxib achieved in our study was comparable to efficacious levels in animal models [15] and in a study of patients with cervical cancer. Similar to our results, a wide interindividual variation in plasma celecoxib concentration was also seen in patients with cervical cancer [23].
A number of the genes were differentially expressed in our microarray analysis.
In the same section, on page 1629, at the beginning of paragraph 3, the following text was deleted in error:
Absent from the up-regulated genes were apoptotic genes. This is consistent with the known lack of apoptotic activity of clinically achievable levels of celecoxib as compared to the levels required to induce tumor apoptosis in vitro, typically > 7.63 ug/mL [15, 23, 34] which is several fold higher than levels reported in our study.
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