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  • American Association for Cancer Research (AACR)  (2)
  • 2010-2014  (2)
  • 1
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 20, No. 15 ( 2014-08-01), p. 3955-3961
    Abstract: Background: Patients with multiple myeloma may be susceptible to osteonecrosis of the jaw (ONJ) and stress fractures due to long-term aminobisphosphonate (aBP) therapy. However, it is unknown whether urinary N-telopeptide (NTX) or other bone biomarkers are predictive of skeletal-related events (SRE) or the impact of cessation of aBP therapy on bone remodeling. Methods: We studied markers of bone turnover over a 6-month period after a single dose of zoledronic acid in 29 patients with multiple myeloma in remission who previously received 8 to 12 doses of pamidronate or zoledronate (NCT00577642). Our primary objective was to determine the duration of time urinary NTX levels remain suppressed after a single dose of zoledronate. A secondary objective was to identify and correlate other markers of bone remodeling with NTX changes. Thirty cytokines, based on their possible role in bone remodeling, were tested using cytokine arrays. Candidates were confirmed by ELISA. Results: All patients had continued suppression of NTX levels, except 1 patient who had an increase in NTX levels associated with an SRE. GDF-15 and decorin were found to decrease, whereas bone-specific alkaline phosphatase (BSALP) increased. Although not significant in aggregate, osteopontin and osteoprotegerin levels increased in at least half of the patients. Conclusion: Our data show that NTX levels continue to be suppressed after aBP therapy, and suggest that suppressed NTX levels may be predictive of freedom from SRE in this patient population. Furthermore, osteoblast suppression by aBP may be reversible in myeloma. These data provide the basis for less frequent dosing of aBPs. Clin Cancer Res; 20(15); 3955–61. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
    Location Call Number Limitation Availability
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  • 2
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 2203-2203
    Abstract: A fundamental challenge in cancer genomics is to efficiently identify biologically relevant candidate oncogenes from the large amount of molecular information generated in human cancer studies from various high throughput modalities. METHODS. We developed the DELTA (Difference in Expression Lined to Amplification) measurement to systematically identify candidate oncogenes in human cancer cell lines. We applied this metric to a large, diverse collection of 365 cancer cell lines densely profiled at both the expression and genomic level using the Affymetrix U133X3P and 500K Mapping arrays. RESULTS. We first identified recurrent cancer-driving amplification events using a GISTIC-inspired approach. This algorithmic analysis revealed 170 amplicons across 18 different cancer types. The majority of these recurrent amplicons do not contain known oncogenes. We then used the DELTA metric to further prioritize candidate oncogenes within these recurrent amplicons. Systematic shRNA knock down of these candidates was then used to identify SOX2 and S100A8 as candidate oncogenes in esophageal and lung cancer cell lines, respectively. CONCLUSION. Differential gene expression analysis with the DELTA metric may be useful for the functional analysis of recurrent genomic amplicons across human cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Associa tion for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2203.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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