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      A decade of progress in cancer research

      editorial
        1 , , 1
      BMC Cancer
      BioMed Central

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          Abstract

          BMC Cancer [1] was launched ten years ago at a time when open access publishing was in its infancy. Although initially looked upon with skepticism, the open access publishing model, which provides an unrestricted and free access to scientific and scholarly work, has become increasingly accepted as a viable model, with more than 7, 000 open access journals now operating worldwide [2]. In a decade, this model has moved from the fringe to the core of the publishing industry. BMC Cancer was one of the first journals to be open access and exclusively published online. The journal published 20 articles during its first year and has steadily grown since then with over 490 articles already published this year. BMC Cancer now boasts an impact factor of 3.15, which places it in the first quartile of the "oncology" category. To celebrate this first very successful decade for the journal, we present a special series of commissioned articles that not only highlight the most important advances in cancer research over the last ten years, but also discuss the new developments we might expect to see in the near future. One major challenge in the treatment of cancer is to diagnose the disease at an early stage in order to improve prognosis. While several screening programmes exist for common cancers such as colorectal and breast cancer, they only detect cancers of one particular type [3,4]. In his commentary, Ian Cree [5] discusses how technical improvements in tests to detect circulating tumor markers, and indeed the potential for some molecules to act as general tumor markers, raise the possibility of blood test-based general screening for multiple cancers - in effect, screening for who to screen. Recently, an increasing number of studies have suggested that micro-RNAs (miRs) represent a promising new class of biomarkers for human malignancies [6-8]. In their review, Fei-Fei Liu and colleagues [9] specifically focus on the potential role of micro-RNAs as diagnostic and prognostic biomarkers in human epithelial tumors. The last decade has also seen huge developments in sequencing technologies and several projects such as the Cancer Genome Atlas [10] and the International Cancer Genome Consortium [11] have aimed to provide a more complete picture of the mutational profile of cancer via large-scale analysis of cancer genomes. Hans Kristian Moen Vollan and Carlos Caldas [12] discuss how results of next generation sequencing hold the potential to refine molecular classification of breast cancer by integrating information from genomic signatures to existing knowledge derived from histopathological sub-classification. These advances could thus improve targeted cancer therapy and prognosis. It is becoming increasingly clear that a multi-drug approach to targeted cancer therapy is needed due to increasing drug resistance to individual therapeutic agents [13,14]. In particular, Joanna Pancewicz and Christophe Nicot [15] discuss how recent advances on the role of Notch signaling pathway in the pathogenesis of human leukemia suggest that multi-drug chemotherapy targeting Notch signaling might be a promising therapeutic strategy in various hematological disorders. In his commentary, Dirk Vordermark [16] discusses how the individualization of radiotherapy concepts and the combination of radiotherapy with molecular approaches are central to major developments in the field of radiation oncology, and he outlines the particular role of BMC Cancer as a platform for disseminating this research. Individualized and targeted therapy approaches hold great promise in oncology but resistance to therapy remains to be overcome. It is well-established that low tumor oxygenation can cause poor response to radiation therapy [17,18]. Kevin Bennewith and Shoukat Dedhar discuss in their review [19] how the clinical potential of hypoxic tumor cells extends beyond the treatment of primary tumors, and they elaborate on the promising role of hypoxic tumor cells as targets for the treatment and prevention of metastatic cancer. This special issue sets the stage for 'hot topics' we might expect to see in the coming decade, and BMC Cancer is poised to be at the forefront of disseminating this research in a rapid and freely-accessible manner. We would like to thank all our external academic editors and Editorial Board Members for their continuing support, and our Section Editors in particular for their contribution to this special anniversary issue. We hope you enjoy reading it. Pre-publication history The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1471-2407/11/498/prepub

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          Most cited references6

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          miR-21-mediated tumor growth.

          MicroRNAs (miRNAs) are approximately 22 nucleotide non-coding RNA molecules that regulate gene expression post-transcriptionally. Although aberrant expression of miRNAs in various human cancers suggests a role for miRNAs in tumorigenesis, it remains largely unclear as to whether knockdown of a specific miRNA affects tumor growth. In this study, we profiled miRNA expression in matched normal breast tissue and breast tumor tissues by TaqMan real-time polymerase chain reaction miRNA array methods. Consistent with previous findings, we found that miR-21 was highly overexpressed in breast tumors compared to the matched normal breast tissues among 157 human miRNAs analysed. To better evaluate the role of miR-21 in tumorigenesis, we transfected breast cancer MCF-7 cells with anti-miR-21 oligonucleotides and found that anti-miR-21 suppressed both cell growth in vitro and tumor growth in the xenograft mouse model. Furthermore, this anti-miR-21-mediated cell growth inhibition was associated with increased apoptosis and decreased cell proliferation, which could be in part owing to downregulation of the antiapoptotic Bcl-2 in anti-miR-21-treated tumor cells. Together, these results suggest that miR-21 functions as an oncogene and modulates tumorigenesis through regulation of genes such as bcl-2 and thus, it may serve as a novel therapeutic target.
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            Cytotoxic and hormonal treatment for metastatic breast cancer: a systematic review of published randomized trials involving 31,510 women.

            A systematic review of randomized clinical trials (RCTs) was undertaken to assess the effectiveness of medical treatment for metastatic breast cancer. RCTs published between 1975 and 1997 have been classified according to 12 therapeutic comparisons: (1) polychemotherapy (PCHT) agents versus single agent; (2) PCHT regimens with anthracycline versus PCHT without anthracycline; (3) other PCHT versus cyclophosphamide, methotrexate, and fluorouracil (CMF); (4) chemotherapy (CHT) with epirubicin versus CHT with doxorubicin; (5) CHT versus same CHT delivered with less intensive schedules; (6) other endocrine therapy (OET) versus tamoxifen; (7) OET plus tamoxifen versus tamoxifen alone; (8) OET versus medroxyprogesterone; (9) OET versus aromatase inhibitors; (10) OET versus megestrol; (11) endocrine therapy (ET) versus same ET at lower doses; and (12) CHT plus ET versus CHT. Tumor response rates, mortality hazards ratio (HR) and frequency of severe side effects were the outcome measures. A total of 189 eligible trials (31,510 patients) were identified. All provided response rates and 133 (70%) data or survival curves needed for calculation of the HR. In eight of 12 comparisons, statistically significant differences for response emerged (1, 2, 3, 5, 7, 8, 11, 12); all but no. 8 favored the first term of the comparison. Overall survival analysis showed better results of (a) PCHT versus single-agent CHT (HR=0.82; 95% confidence interval [CI], 0.75 to 0.90); (b) CHT with doxorubicin versus CHT with epirubicin (HR=1.13; 95% CI, 1.00 to 1.27); (c) CHT versus the same CHT delivered with less intensive schedules (HR=0.90; 95% CI, 0.83 to 0.97); (d) ET versus the same ET at lower doses (HR=0.86; 95% CI, 0.77 to 0.97). Quality of life was measured in only 2,995 of 31,510 patients (9.5%). Despite some evidence of effectiveness of specific regimens, the relevance of these findings is limited by the modest survival benefit and the lack of evaluation of the quality-of-life impact of these treatments.
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              Stool DNA and occult blood testing for screen detection of colorectal neoplasia.

              Stool DNA testing is a new approach to colorectal cancer detection. Few data are available from the screening setting. To compare stool DNA and fecal blood testing for detection of screen-relevant neoplasia (curable-stage cancer, high-grade dysplasia, or adenomas >1 cm). Blinded, multicenter, cross-sectional study. Communities surrounding 22 participating academic and regional health care systems in the United States. 4482 average-risk adults. Fecal blood and DNA markers. Participants collected 3 stools, smeared fecal blood test cards and used same-day shipment to a central facility. Fecal blood cards (Hemoccult and HemoccultSensa, Beckman Coulter, Fullerton, California) were tested on 3 stools and DNA assays on 1 stool per patient. Stool DNA test 1 (SDT-1) was a precommercial 23-marker assay, and a novel test (SDT-2) targeted 3 broadly informative markers. The criterion standard was colonoscopy. Sensitivity for screen-relevant neoplasms was 20% by SDT-1, 11% by Hemoccult (P = 0.020), 21% by HemoccultSensa (P = 0.80); sensitivity for cancer plus high-grade dysplasia did not differ among tests. Specificity was 96% by SDT-1, compared with 98% by Hemoccult (P < 0.001) and 97% by HemoccultSensa (P = 0.20). Stool DNA test 2 detected 46% of screen-relevant neoplasms, compared with 16% by Hemoccult (P < 0.001) and 24% by HemoccultSensa (P < 0.001). Stool DNA test 2 detected 46% of adenomas 1 cm or larger, compared with 10% by Hemoccult (P < 0.001) and 17% by HemoccultSensa (P < 0.001). Among colonoscopically normal patients, the positivity rate was 16% with SDT-2, compared with 4% with Hemoccult (P = 0.010) and 5% with HemoccultSensa (P = 0.030). Stool DNA test 2 was not performed on all subsets of patients without screen-relevant neoplasms. Stools were collected without preservative, which reduced detection of some DNA markers. Stool DNA test 1 provides no improvement over HemoccultSensa for detection of screen-relevant neoplasms. Stool DNA test 2 detects significantly more neoplasms than does Hemoccult or HemoccultSensa, but with more positive results in colonoscopically normal patients. Higher sensitivity of SDT-2 was particularly apparent for adenomas.
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                Author and article information

                Journal
                BMC Cancer
                BMC Cancer
                BioMed Central
                1471-2407
                2011
                30 November 2011
                : 11
                : 498
                Affiliations
                [1 ]BMC Cancer, BioMed Central, Gray's Inn Road, London, WC1 8HB, UK
                Article
                1471-2407-11-498
                10.1186/1471-2407-11-498
                3276491
                22128753
                e2633958-5a9a-4b1c-91d8-bb6cd545c28f
                Copyright ©2011 Chap and Patel; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 23 November 2011
                : 30 November 2011
                Categories
                Editorial

                Oncology & Radiotherapy
                Oncology & Radiotherapy

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