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      A Human Head and Neck Squamous Cell Carcinoma Cell Line with Acquired cis-Diamminedichloroplatinum-Resistance Shows Remarkable Upregulation of BRCA1 and Hypersensitivity to Taxane

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          Abstract

          Recently, an inverse relationship between resistance to platinum-based chemotherapeutic agents and taxanes has been implicated in breast and ovarian cancers, and a possible pivotal role for BRCA1 has also been suggested. Because cis-diamminedichloroplatinum (CDDP) and taxanes are the most active antitumor agents against head and neck squamous cell carcinoma (HNSCC), we analyzed the sensitivity of nine HNSCC cell lines and their previously established derived CDDP-resistant cell lines to two representative taxanes: docetaxel and paclitaxel. None of the nine original cell lines showed any cross resistance between CDDP and taxanes, but one of the CDDP-resistant cell lines, RPMI2650CR, demonstrated hypersensitivity to both taxanes when compared to the parental cell line, RPMI2650. Furthermore, RPMI2650CR exhibited increased expression of BRCA1. These data suggest that (i) taxanes are a good candidate for a second-line therapeutic drug for HNSCC patients with acquired CDDP resistance and (ii) BRCA1 can be a candidate marker for predicting an inverse CDDP/taxane sensitivity phenotype in HNSCC.

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          A systematic review of platinum and taxane resistance from bench to clinic: an inverse relationship.

          We undertook a systematic review of the pre-clinical and clinical literature for studies investigating the relationship between platinum and taxane resistance. Medline was searched for (1) cell models of acquired drug resistance reporting platinum and taxane sensitivities and (2) clinical trials of platinum or taxane salvage therapy in ovarian cancer. One hundred and thirty-seven models of acquired drug resistance were identified. 68.1% of cisplatin-resistant cells were sensitive to paclitaxel and 66.7% of paclitaxel-resistant cells were sensitive to cisplatin. A similar inverse pattern was observed for cisplatin vs. docetaxel, carboplatin vs. paclitaxel and carboplatin vs. docetaxel. These associations were independent of cancer type, agents used to develop resistance and reported mechanisms of resistance. Sixty-five eligible clinical trials of paclitaxel-based salvage after platinum therapy were identified. Studies of single agent paclitaxel in platinum-resistant ovarian cancer where patients had previously recieved paclitaxel had a pooled response rate of 35.3%, n=232, compared to 22% in paclitaxel naïve patients n=1918 (p<0.01, Chi-squared). Suggesting that pre-treatment with paclitaxel may improve the response of salvage paclitaxel therapy. The response rate to paclitaxel/platinum combination regimens in platinum-sensitive ovarian cancer was 79.5%, n=88 compared to 49.4%, n=85 for paclitaxel combined with other agents (p<0.001, Chi-squared), suggesting a positive interaction between taxanes and platinum. Therefore, the inverse relationship between platinum and taxanes resistance seen in cell models is mirrored in the clinical response to these agents in ovarian cancer. An understanding of the cellular and molecular mechanisms responsible would be valuable in predicting response to salvage chemotherapy and may identify new therapeutic targets.
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            A systematic review of genes involved in the inverse resistance relationship between cisplatin and paclitaxel chemotherapy: role of BRCA1.

            A systematic review of cell models of acquired drug resistance not involving genetic manipulation showed that 80% of cell models had an inverse resistance relationship between cisplatin and paclitaxel. Here we systematically review genetically modified cell lines in which the inverse cisplatin/paclitaxel resistance phenotype has resulted. This will form a short list of genes which may play a role in the mechanism of the inverse resistance relationship as well as act as potential markers for monitoring the development of resistance in the clinical treatment of cancer. The literature search revealed 91 genetically modified cell lines which report toxicity or viability/apoptosis data for cisplatin and paclitaxel relative to their parental cell lines. This resulted in 26 genes being associated with the inverse cisplatin/paclitaxel phenotype. The gene with the highest number of genetically modified cell lines associated with the inverse resistance relationship was BRCA1 and this gene is discussed in detail with reference to chemotherapy response in cell lines and in the clinical treatment of breast, ovarian and lung cancer. Other genes associated with the inverse resistance phenotype included dihydrodiol dehydrogenase (DDH) and P-glycoprotein. Genes which caused cross resistance or cross sensitivity between cisplatin and paclitaxel were also examined, the majority of these genes were apoptosis associated genes which may be useful for predicting cross resistance. We propose that BRCA1 should be the first of a panel of cellular markers to predict the inverse cisplatin/paclitaxel resistance phenotype.
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              Chemotherapy in the treatment of locally advanced head and neck cancer.

              Three decades of collaborative research have led to the integration of platinum-based chemotherapy into the curative management of squamous cell carcinoma of the head and neck and gains in local-regional control, organ preservation and survival endpoints. Concomitant cisplatin-based chemotherapy and radiotherapy is the strategy that has proven most effective for organ preservation for larynx and oropharynx cancers, the treatment of unresectable disease, nasopharyngeal cancer and the post-operative adjuvant treatment of patients at high risk of recurrence. The evolution of current indications for this multimodality approach is reviewed and current areas of investigation discussed. Nearly all patients with locally advanced head and neck cancer receive chemotherapy as part of initial curative treatment. The focus of future trials should be on survival improvement, toxicity reduction and risk stratification for treatment decision making. Copyright (c) 2008 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Int J Otolaryngol
                IJOL
                International Journal of Otolaryngology
                Hindawi Publishing Corporation
                1687-9201
                1687-921X
                2011
                20 October 2011
                : 2011
                : 521852
                Affiliations
                1Department of Molecular Pathology, Tohoku University School of Medicine, Sendai, Miyagi 980-8575, Japan
                2Department of Otolaryngology-Head and Neck Surgery, Tohoku University School of Medicine, Sendai, Miyagi 980-8574, Japan
                3Department of Digestive Tract Surgery and Transplantation Surgery, Tokyo Medical University Hachioji Medical Center, Hachioji, Tokyo 193-0998, Japan
                Author notes

                Academic Editor: Leonard P. Rybak

                Article
                10.1155/2011/521852
                3199181
                22046189
                7f3ddf40-489e-45aa-89f0-3a53fc3e1d7d
                Copyright © 2011 Yuriko Saiki et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 7 July 2011
                : 20 August 2011
                Categories
                Research Article

                Otolaryngology
                Otolaryngology

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