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      Major clinical research advances in gynecologic cancer in 2011

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          Abstract

          The annual review of 2011 comprised 11 themes of major research achievements in gynecologic oncology including breast cancer. A potential paradigm shift in the management of ovarian cancer was reviewed through comprehensive genomic analyses and a tumor-specific new intraoperative fluorescence imaging technique using folate receptor-α targeted agent, which is expected to improve intraoperative staging and more radical cytoreduction. In addition, updates of bevacizumab and poly (ADP-ribose) polymerase inhibitors, risk-reducing salpingo-oophorectomy, and risk evaluation of pelvic mass were discussed. Regarding cervical cancer, this review covered new findings on human papillomavirus vaccines and human papillomavirus tests as well as the current status of clinical trials on locally advanced cervical cancer. The promising role of sentinel lymph node biopsy in the management of early stage endometrial cancer was followed by two notable clinical researches on: exemestane, an aromatase inhibitor, for the prevention of breast cancer and eribulin, a non-taxane microtubule dynamics inhibitor for the treatment of metastatic breast cancer. Lastly, in premenopausal women with breast cancer, the effect of gonadotropin-releasing hormone analogue on the occurrence of chemotherapy-induced early menopause was discussed.

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          Most cited references 145

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          MicroRNAs: genomics, biogenesis, mechanism, and function.

           David Bartel (2004)
          MicroRNAs (miRNAs) are endogenous approximately 22 nt RNAs that can play important regulatory roles in animals and plants by targeting mRNAs for cleavage or translational repression. Although they escaped notice until relatively recently, miRNAs comprise one of the more abundant classes of gene regulatory molecules in multicellular organisms and likely influence the output of many protein-coding genes.
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            Integrated Genomic Analyses of Ovarian Carcinoma

            Summary The Cancer Genome Atlas (TCGA) project has analyzed mRNA expression, miRNA expression, promoter methylation, and DNA copy number in 489 high-grade serous ovarian adenocarcinomas (HGS-OvCa) and the DNA sequences of exons from coding genes in 316 of these tumors. These results show that HGS-OvCa is characterized by TP53 mutations in almost all tumors (96%); low prevalence but statistically recurrent somatic mutations in 9 additional genes including NF1, BRCA1, BRCA2, RB1, and CDK12; 113 significant focal DNA copy number aberrations; and promoter methylation events involving 168 genes. Analyses delineated four ovarian cancer transcriptional subtypes, three miRNA subtypes, four promoter methylation subtypes, a transcriptional signature associated with survival duration and shed new light on the impact on survival of tumors with BRCA1/2 and CCNE1 aberrations. Pathway analyses suggested that homologous recombination is defective in about half of tumors, and that Notch and FOXM1 signaling are involved in serous ovarian cancer pathophysiology.
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              Trastuzumab emtansine for HER2-positive advanced breast cancer.

              Trastuzumab emtansine (T-DM1) is an antibody-drug conjugate incorporating the human epidermal growth factor receptor 2 (HER2)-targeted antitumor properties of trastuzumab with the cytotoxic activity of the microtubule-inhibitory agent DM1. The antibody and the cytotoxic agent are conjugated by means of a stable linker. We randomly assigned patients with HER2-positive advanced breast cancer, who had previously been treated with trastuzumab and a taxane, to T-DM1 or lapatinib plus capecitabine. The primary end points were progression-free survival (as assessed by independent review), overall survival, and safety. Secondary end points included progression-free survival (investigator-assessed), the objective response rate, and the time to symptom progression. Two interim analyses of overall survival were conducted. Among 991 randomly assigned patients, median progression-free survival as assessed by independent review was 9.6 months with T-DM1 versus 6.4 months with lapatinib plus capecitabine (hazard ratio for progression or death from any cause, 0.65; 95% confidence interval [CI], 0.55 to 0.77; P<0.001), and median overall survival at the second interim analysis crossed the stopping boundary for efficacy (30.9 months vs. 25.1 months; hazard ratio for death from any cause, 0.68; 95% CI, 0.55 to 0.85; P<0.001). The objective response rate was higher with T-DM1 (43.6%, vs. 30.8% with lapatinib plus capecitabine; P<0.001); results for all additional secondary end points favored T-DM1. Rates of grade 3 or 4 adverse events were higher with lapatinib plus capecitabine than with T-DM1 (57% vs. 41%). The incidences of thrombocytopenia and increased serum aminotransferase levels were higher with T-DM1, whereas the incidences of diarrhea, nausea, vomiting, and palmar-plantar erythrodysesthesia were higher with lapatinib plus capecitabine. T-DM1 significantly prolonged progression-free and overall survival with less toxicity than lapatinib plus capecitabine in patients with HER2-positive advanced breast cancer previously treated with trastuzumab and a taxane. (Funded by F. Hoffmann-La Roche/Genentech; EMILIA ClinicalTrials.gov number, NCT00829166.).
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                Author and article information

                Journal
                J Gynecol Oncol
                JGO
                Journal of Gynecologic Oncology
                Korean Society of Gynecologic Oncology and Colposcopy
                2005-0380
                2005-0399
                January 2012
                09 January 2012
                : 23
                : 1
                : 53-64
                Affiliations
                [1 ]Department of Obstetrics and Gynecology, Seoul National University College of Medicine, Seoul, Korea.
                [2 ]Department of Obstetrics and Gynecology, Seoul National University Bundang Hospital, Seongnam, Korea.
                Author notes
                Correspondence to Jae Weon Kim. Department of Obstetrics and Gynecology, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul 110-744, Korea. Tel: 82-2-2072-3511, Fax: 82-2-762-3599, kjwksh@ 123456snu.ac.kr
                10.3802/jgo.2012.23.1.53
                3280068
                22355468
                Copyright © 2012. Asian Society of Gynecologic Oncology, Korean Society of Gynecologic Oncology

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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