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  • The American Association for Cancer Research (AACR)  (19)
  • Nature Publishing Group (NPG)  (5)
  • Wiley-Blackwell  (5)
  • American Institute of Physics (AIP)  (1)
  • Dordrecht :Springer Netherlands,  (1)
  • 1
    Schlagwort(e): Astrometry-Congresses. ; Astronomical spectroscopy-Congresses. ; Electronic books.
    Beschreibung / Inhaltsverzeichnis: Proceedings of the 111th Symposium of the International Astronomical Union held at Villa Olmo, Como, Italy, May 24-29, 1984.
    Materialart: Online-Ressource
    Seiten: 1 online resource (625 pages)
    Ausgabe: 1st ed.
    ISBN: 9789400954564
    Serie: International Astronomical Union Symposia Series ; v.111
    DDC: 522
    Sprache: Englisch
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    ISSN: 1077-3118
    Quelle: AIP Digital Archive
    Thema: Physik
    Notizen: A systematic study of the optical properties of strained InxGa1−xAs/AlyGa1−yAs (x=0.16, y=0.33) single quantum-well structures grown by molecular-beam epitaxy is presented. An optimized growth procedure is shown to produce quantum-well structures exhibiting 2 K photoluminescence linewidths as low as 2.6 meV, very close to those observed for corresponding InxGa1−xAs/GaAs control structures.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    Biotechnology and Bioengineering 24 (1982), S. 2297-2308 
    ISSN: 0006-3592
    Schlagwort(e): Chemistry ; Biochemistry and Biotechnology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Biologie , Werkstoffwissenschaften, Fertigungsverfahren, Fertigung
    Notizen: Various yeasts such as several strains of Saccharomyces diastaticus, S. cerevisiae, and Kluyveromyces fregilis were investigated for their ability to ferment the carbohydrates from Jerusalem artichokes to alcohol. Juice extracted of the carbohydrates. Fermentation was also carried out with raw artichokes without prior juice extraction. Result indicate that this row material has good potential for fuel alcohol production by fermentation.
    Zusätzliches Material: 11 Ill.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Digitale Medien
    Digitale Medien
    New York, NY [u.a.] : Wiley-Blackwell
    American Journal of Anatomy 182 (1988), S. 318-324 
    ISSN: 0002-9106
    Schlagwort(e): Life and Medical Sciences ; Cell & Developmental Biology
    Quelle: Wiley InterScience Backfile Collection 1832-2000
    Thema: Medizin
    Notizen: The purpose of this study was to determine histologically the distribution of microspheres (MSs) (14 μm), and hence the relative distribution of blood flow, in rat plantaris muscle relative to the fiber types (fast-twitch-oxidative-glycolytic [FOG], fast-twitch-glycolytic [FG], and slow-twitch-oxidative [SO]). Three conditions were investigated: (1) preexercise standing; (2) treadmill locomotion at 15 m/min (fast walking); and (3) treadmill locomotion at 60 m/min (moderate galloping). The MS suspension (containing 1 × 106 MSs) was infused into the ascending aorta via a catheter in the carotid artery under each of the 3 conditions so that MSs were distributed to the tissues in proportion to their respective blood flows. Sections (20 m̈m) of the plantaris muscle were cut and assayed for reduced nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) and myofibrillar adenosine triphosphatase (ATPase) activities so the fibers could be typed as SO, FOG, or FG. MSs were located in the NADH-TR sections, and the fibers next to the MSs were classified and counted. The observed numbers of fibers of each type in each condition that were adjacent to MSs were compared to the predicted number of adjacent fibers based on the assumption the MSs were randomly distributed in the tissue. This analysis demonstrated that MSs (and blood flows) were preferentially distributed to SO fibers during preexercise, to SO and FOG fibers during slow locomotion, and to FOG fibers during fast locomotion. The data support the contention that blood flow is distributed in muscles of conscious animals as functions of fiber type and exercise intensity.
    Zusätzliches Material: 2 Ill.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Publikationsdatum: 2018-12-04
    Beschreibung: Purpose: Common resistance mechanisms to endocrine therapy (ET) in estrogen receptor (ER)–positive metastatic breast cancers include, among others, ER loss and acquired activating mutations in the ligand-binding domain of the ER gene ( ESR1 LBD m ). ESR1 mutational mediated resistance may be overcome by selective ER degraders (SERD). During the first-in-human study of oral SERD AZD9496, early changes in circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) were explored as potential noninvasive tools, alongside paired tumor biopsies, to assess pharmacodynamics and early efficacy. Experimental Design: CTC were enumerated/phenotyped for ER and Ki67 using CellSearch in serial blood draws. ctDNA was assessed for the most common ESR1 LBD m by droplet digital PCR (BioRad). Results: Before starting AZD9496, 11 of 43 (25%) patients had ≥5 CTC/7.5 mL whole blood (WB), none of whom underwent reduction to 〈5 CTC/7.5 mL WB on C1D15. Five of 11 patients had baseline CTC-ER + , two of whom had CTC-ER + reduction. CTC-Ki67 status did not change appreciably. Patients with ≥5 CTC/7.5 mL WB before treatment had worse progression-free survival (PFS) than patients with 〈5 CTC ( P = 0.0003). Fourteen of 45 (31%) patients had ESR1 LBD m + ctDNA at baseline, five of whom had ≥2 unique mutations. Baseline ESR1 LBD m status was not prognostic. Patients with persistently elevated CTC and/or ESR1 LBD m + ctDNA at C1D15 had worse PFS than patients who did not ( P = 0.0007). Conclusions: Elevated CTC at baseline was a strong prognostic factor in this cohort. Early on-treatment changes were observed in CTC-ER + and ESR1 LBD m + ctDNA, but not in overall CTC number. Integrating multiple biomarkers in prospective trials may improve outcome prediction and ET resistance mechanisms' identification over a single biomarker.
    Print ISSN: 1078-0432
    Digitale ISSN: 1557-3265
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Publikationsdatum: 2013-11-21
    Beschreibung: Aims Prognostic benefit from CRT compared with controls is well established. Symptomatic response rates, however, are controversial and have never been systematically evaluated with standard subtraction of control rates to establish the incremental symptomatic response effect of CRT pacing. Methods and results First, we identified 150 consecutive CRT papers and assessed researchers' perceptions of the symptomatic response to CRT. The mean quoted response rate was 66%. Only 26 studies acknowledged the existence of response without the device. Secondly, we examined actual symptomatic response rates in the randomized trials (CARE-HF, COMPANION, CONTAK-CD, MIRACLE, MIRACLE-ICD, MIRACLE-ICD II, MUSTIC, and REVERSE) totalling 3904 patients. The NYHA status improved in 51% of those randomized to CRT vs. 35% of controls (incremental effect 16%). This incremental improvement was significantly greater in open studies (with no device for controls) than in blinded studies (control arm receiving a device but no CRT, such as a defibrillator or a CRT programmed off), 20% vs. 13%, P 〈 0.001. Conclusions Quoting CRT responder rates in isolation without recognizing spontaneous ‘response’ is common but unwise. The incremental symptomatic response rate from CRT pacing is ~16%, much lower than widely reported. This value is similar to that for drugs in heart failure and should not be considered disappointing: they both exert powerful prognostic benefits. For scientific purposes, e.g. to explore potential improvements, symptomatic benefit from CRT should be quantified, like all other effects, by comparison with a control.
    Print ISSN: 1388-9842
    Digitale ISSN: 1879-0844
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Publikationsdatum: 2013-04-04
    Beschreibung: Somatic mutations in the KEAP1 ubiquitin ligase or its substrate NRF2 (NFE2L2) commonly occur in human cancer, resulting in constitutive NRF2-mediated transcription of cytoprotective genes. However, many tumors display high NRF2 activity in the absence of mutation, supporting the hypothesis that alternative mechanisms of pathway activation exist. Previously, we and others discovered that via a competitive binding mechanism, the proteins WTX (AMER1), PALB2, and SQSTM1 bind KEAP1 to activate NRF2. Proteomic analysis of the KEAP1 protein interaction network revealed a significant enrichment of associated proteins containing an ETGE amino acid motif, which matches the KEAP1 interaction motif found in NRF2. Like WTX, PALB2, and SQSTM1, we found that the dipeptidyl peptidase 3 (DPP3) protein binds KEAP1 via an “ETGE” motif to displace NRF2, thus inhibiting NRF2 ubiquitination and driving NRF2-dependent transcription. Comparing the spectrum of KEAP1-interacting proteins with the genomic profile of 178 squamous cell lung carcinomas characterized by The Cancer Genome Atlas revealed amplification and mRNA overexpression of the DPP3 gene in tumors with high NRF2 activity but lacking NRF2 stabilizing mutations. We further show that tumor-derived mutations in KEAP1 are hypomorphic with respect to NRF2 inhibition and that DPP3 overexpression in the presence of these mutants further promotes NRF2 activation. Collectively, our findings further support the competition model of NRF2 activation and suggest that “ETGE”-containing proteins such as DPP3 contribute to NRF2 activity in cancer. Cancer Res; 73(7); 2199–210. ©2013 AACR.
    Print ISSN: 0008-5472
    Digitale ISSN: 1538-7445
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    Publikationsdatum: 2013-03-05
    Beschreibung: Although current breast cancer treatment guidelines limit the use of HER2-blocking agents to tumors with HER2 gene amplification, recent retrospective analyses suggest that a wider group of patients may benefit from this therapy. Using breast cancer cell lines, mouse xenograft models and matched human primary and metastatic tissues, we show that HER2 is selectively expressed in and regulates self-renewal of the cancer stem cell (CSC) population in estrogen receptor-positive (ER+), HER2− luminal breast cancers. Although trastuzumab had no effects on the growth of established luminal breast cancer mouse xenografts, administration after tumor inoculation blocked subsequent tumor growth. HER2 expression is increased in luminal tumors grown in mouse bone xenografts, as well as in bone metastases from patients with breast cancer as compared with matched primary tumors. Furthermore, this increase in HER2 protein expression was not due to gene amplification but rather was mediated by receptor activator of NF-κB (RANK)-ligand in the bone microenvironment. These studies suggest that the clinical efficacy of adjuvant trastuzumab may relate to the ability of this agent to target the CSC population in a process that does not require HER2 gene amplification. Furthermore, these studies support a CSC model in which maximal clinical benefit is achieved when CSC targeting agents are administered in the adjuvant setting. Cancer Res; 73(5); 1635–46. ©2012 AACR.
    Print ISSN: 0008-5472
    Digitale ISSN: 1538-7445
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
    Publikationsdatum: 2013-08-15
    Beschreibung: A comprehensive description of genomic alterations in lung squamous cell carcinoma (lung SCC) has recently been reported, enabling the identification of genomic events that contribute to the oncogenesis of this disease. In lung SCC, one of the most frequently altered receptor tyrosine kinase families is the fibroblast growth factor receptor (FGFR) family, with amplification or mutation observed in all four family members. Here, we describe the oncogenic nature of mutations observed in FGFR2 and FGFR3, each of which are observed in 3% of samples, for a mutation rate of 6% across both genes. Using cell culture and xenograft models, we show that several of these mutations drive cellular transformation. Transformation can be reversed by small-molecule FGFR inhibitors currently being developed for clinical use. We also show that mutations in the extracellular domains of FGFR2 lead to constitutive FGFR dimerization. In addition, we report a patient with an FGFR2-mutated oral SCC who responded to the multitargeted tyrosine kinase inhibitor pazopanib. These findings provide new insights into driving oncogenic events in a subset of lung squamous cancers, and recommend future clinical studies with FGFR inhibitors in patients with lung and head and neck SCC. Cancer Res; 73(16); 5195–205. ©2013 AACR.
    Print ISSN: 0008-5472
    Digitale ISSN: 1538-7445
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
    Publikationsdatum: 2017-05-12
    Beschreibung: Caspase-2-mediated cell death is required for deleting aneuploid cells Oncogene 36, 2704 (11 May 2017). doi:10.1038/onc.2016.423 Authors: S Dawar, Y Lim, J Puccini, M White, P Thomas, L Bouchier-Hayes, D R Green, L Dorstyn & S Kumar
    Print ISSN: 0950-9232
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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