Kooperativer Bibliotheksverbund

In: Japanese Journal of Applied Physics, IOP Publishing, Vol. 34, No. 8S ( 1995-08-01), p. 4408-

Abstract: We have performed photoluminescence experiments on modulated barrier In 0.13 Ga 0.87 As/GaAs quantum wires in normal magnetic fields up to B = 10.5 T. By using high excitation powers we observed emission from several lateral subbands. In comparison to low excitation spectra the emission features are shifted to lower energies due to band gap renormalization. Calculated luminescence spectra are in excellent agreement with the experimental spectra and have been used to study many-particle effects in these wires. We have found clear indications for an enhancement of the renormalization in quantum wires as expected due to the increase of the Coulomb interaction.

Type of Medium: Online Resource

ISSN: 0021-4922 , 1347-4065

URL: Article

DOI: 10.1143/JJAP.34.4408

Language: Unknown

Publisher: IOP Publishing

Publication Date: 1995

detail.hit.zdb_id: 218223-3

detail.hit.zdb_id: 797294-5

detail.hit.zdb_id: 2006801-3

detail.hit.zdb_id: 797295-7

In: The Lancet Haematology, Elsevier BV, Vol. 10, No. 7 ( 2023-07), p. e495-e509

Type of Medium: Online Resource

ISSN: 2352-3026

URL: Article

DOI: 10.1016/S2352-3026(23)00089-3

Language: English

Publisher: Elsevier BV

Publication Date: 2023

In: Blood, American Society of Hematology, Vol. 104, No. 11 ( 2004-11-16), p. 1100-1100

Abstract: Introduction: Genomic aberrations represent important prognostic markers in many hematological cancers. In multiple myeloma (MM), chromosome 13q deletion (13q-) has emerged as one of the most important outcome predictors and indicates a dismal prognosis. Other chromosomal abnormalities have been discussed as prognostic markers in this disease but came not out as independent variables when they were tested in a multivariate fashion. However, the complexity of genomic rearrangements and the clinical heterogeneity seen in malignant plasma cell disorders argue against 13q- as the sole genomic change of prognostic relevance. Material and Methods: In a retrospective analysis, 109 patients (pts.) treated with one or two cycles of high-dose chemotherapy (HD-CTX) followed by autologous stem cell transplantation (ASCT) at a single center were analyzed by tri-color FISH and four DNA probes mapping to chromosome bands 1q21, 9q34, 11q25, and 13q14. The selection of DNA probes based upon previous data from a comprehensive molecular cytogenetic study that revealed a high incidence of chromosomal gains (+) and losses (−) involving these four loci. The Cox proportional hazards regression model was applied to correlate molecular cytogenetic markers with clinical data. Results: The most frequent chromosomal abnormalities in the present series were +9q (49%), +1q (48%), +11q (47%), and 13q- (42%). The median follow-up time was 30 months (m) and the median event free survival (EFS) and overall survival (OS) time (calculated from first ASCT) of the entire cohort was 30 m and 71 m, respectively. There were 52 events (31 deaths). In a multivariable analysis including the four most frequent chromosomal abnormalities, +9q (hazard ratio 2.49, 95% CI 1.20-5.18; p=.01) and 13q- (2.34, 1.17–4.68; p=.02) were statistically significant risk factors for shorter EFS. The median EFS in pts. lacking both genomic changes was 3.6 years , while it was 2.5 years in pts. with either +9q or 13q- and only 1.5 years in pts. that exhibited both chromosomal abnormalities. Of note, when other potential prognostic factors ß2-microglobulin, albumin, number of chemotherapy cycles prior to first ASCT) were included in the multivariable analysis, +9q and 13q- remained independent risk factors for shorter EFS (p=.008 and p=.03, respectively). Due to the diversity of salvage treatment protocols applied after relapse, OS was not analyzed in this study. Conclusions: +9q34 could represent a novel independent marker of adverse prognosis in MM pts. receiving HD-CTX with ASCT. The prognostic significance of +9q34 and other molecular cytogenetic aberrations is currently investigated within large multicenter trials on more homogenously treated cohorts of pts.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V104.11.1100.1100

Language: English

Publisher: American Society of Hematology

Publication Date: 2004

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Genes, Chromosomes and Cancer, Wiley, Vol. 42, No. 1 ( 2005-01), p. 78-81

Abstract: 14q32 translocations [t(14q)] represent critical but not universal events in multiple myeloma (MM). Gains of chromosome arms 1q, 9q, and 11q (+1q, +9q, and +11q) have recently been identified as frequent aberrations in this disease, but their pathogenetic significance remains unclear. We studied a series of 108 MM patients using fluorescence in situ hybridization and DNA probes mapping to chromosome bands 1q21, 9q34, 11q25, 13q14, and 14q32. Three subsets of tumors were defined: (1) MM+/+ (detection of +9q and +11q; 43.5% of cases), (2) MM+/− (+9q or +11q; 21.3%), and (3) MM−/− (neither +9q nor +11q; 35.2%). The incidence of t(14q) was significantly different in these subgroups: 23% in MM+/+, 56% in MM+/−, and 89% in MM−/−. Deletion of 13q (13q−) also was significantly less frequent in MM+/+ (23%) than in MM+/− and MM−/− (36% and 63%, respectively). The nonrandom distribution of chromosomal aberrations in the present series of MM tumors points to a novel, 14q32 translocation–independent pathogenetic pathway in plasma cell neoplasms. © 2005 Wiley‐Liss, Inc.

Type of Medium: Online Resource

ISSN: 1045-2257 , 1098-2264

URL: Issue

URL: Article

DOI: 10.1002/gcc.v42:1

DOI: 10.1002/gcc.20098

Language: English

Publisher: Wiley

Publication Date: 2005

detail.hit.zdb_id: 1018988-9

detail.hit.zdb_id: 1492641-6

SSG: 12

In: Blood, American Society of Hematology, Vol. 128, No. 22 ( 2016-12-02), p. 449-449

Abstract: Background: Internal tandem duplications (ITD) in the receptor tyrosine kinase FLT3 occur in roughly 25% of younger adult patients (pts) with acute myeloid leukemia (AML). The multi-targeted kinase inhibitor midostaurin combined with intensive chemotherapy has shown activity against AML with FLT3 mutations. However, toxicity and potential drug-drug interactions with strong CYP3A4 inhibitors such as posaconazole may necessitate dose reduction. Aims: To evaluate the impact of age and midostaurin dose-adaptation after intensive induction chemotherapy on response and outcome in AML with FLT3-ITD within the AMLSG 16-10 trial (NCT01477606). Methods: The study included adult pts (age 18-70 years (yrs)) with newly diagnosed FLT3-ITD positive AML enrolled in the ongoing single-arm phase-II AMLSG 16-10 trial. Pts with acute promyelocytic leukemia were not eligible. The presence of FLT3-ITD was analyzed within our diagnostic study AMLSG-BiO (NCT01252485) by Genescan-based DNA fragment-length analysis. Induction therapy consisted of daunorubicin (60 mg/m², d1-3) and cytarabine (200 mg/m², continuously, d1-7); midostaurin 50 mg bid was applied from day 8 until 48h before start of the next treatment cycle. A second cycle was allowed in case of partial remission (PR). For consolidation therapy, pts proceeded to allogeneic hematopoietic-cell transplantation (HCT) as first priority; if alloHCT was not feasible, pts received three cycles of age-adapted high-dose cytarabine (HDAC) in combination with midostaurin starting on day 6. In all pts one-year maintenance therapy with midostaurin was intended. The first patient entered the study in June 2012 and in April 2014, after recruitment of n=147 pts, the study was amended including a sample size increase to 284 pts and a dose reduction to 12.5% of the initial dose of midostaurin in case of co-medication with strong CYP3A4 inhibitors (e.g. posaconazole). This report focuses on age and the comparison between the first (n=147) and the second cohort (n=137) of the study in terms midostaurin dose-adaptation. Results: Patient characteristics were as follows: median age 54 yrs (range, 18-70; younger, 68% 〈 60 yrs; older, 32% ≥ 60 yrs); median white cell count 44.7G/l (range 1.1-1543 G/l); karyotype, n=161 normal, n=16 high-risk according to ELN recommendations; mutated NPM1 n=174 (59%). Data on response to first induction therapy were available in 277 pts; complete remission (CR) including CR with incomplete hematological recovery (CRi) 60%, PR 20%, refractory disease (RD) 15%, and death 5%. A second induction cycle was given in 54 pts. Overall response (CR/CRi) after induction therapy was 76% (76%, younger; 76%, older) and death 6% (4%, younger; 10% older). The dose of midostaurin during first induction therapy was reduced in 53% and 71% of patients in cohort-1 and cohort-2, respectively. Reasons for dose reduction were in 58% and 49% toxicity, and in 9% and 23% co-medication in cohort-1 and cohort-2, respectively. No difference in response to induction therapy was noted between cohorts (p=0.81). Median follow-up was 18 months. Overall 146 pts received an alloHCT, 128 in first CR (n=94 younger, n=34 older; n=92 from a matched unrelated and n=36 from a matched related donor). In pts receiving an alloHCT within the protocol in median two chemotherapy cycles were applied before transplant (range 1-4). The cumulative incidence of relapse (CIR) and death after transplant were 13% (SE 3.2%) and 16% (SE 3.5%) without differences (p=0.97, p=0.41, respectively) between younger and older patients. So far maintenance therapy was started in 86 pts, 61 pts after alloHCT and 25 pts after HDAC. Fifty-five adverse events 3°/4° were reported being attributed to midostaurin; cytopenias after alloHCT were the most frequent (29%). CIR in patients starting maintenance therapy was 20% one year after start of maintenance without difference between alloHCT and HiDAC (p=0.99). In addition, no difference in CIR was identified in patients after consolidation with alloHCT or HDAC according to dose reduction of midostaurin during first induction therapy (p=0.43, p=0.98, respectively). Median overall survival was 25 months (younger, 26 months; older 23 months; p=0.15). Conclusions: The addition of midostaurin to intensive induction therapy and as maintenance after alloHCT or HDAC is feasible and effective without an impact of age and dose adaptation on outcome. Disclosures Schlenk: Amgen: Research Funding; Pfizer: Honoraria, Research Funding. Fiedler:GSO: Other: Travel; Pfizer: Research Funding; Kolltan: Research Funding; Amgen: Consultancy, Other: Travel, Patents & Royalties, Research Funding; Gilead: Other: Travel; Ariad/Incyte: Consultancy; Novartis: Consultancy; Teva: Other: Travel. Lübbert:Celgene: Other: Travel Funding; Janssen-Cilag: Other: Travel Funding, Research Funding; Ratiopharm: Other: Study drug valproic acid. Greil:Janssen-Cilag: Honoraria; Genentech: Honoraria, Research Funding; Mundipharma: Honoraria, Research Funding; Merck: Honoraria; AstraZeneca: Honoraria; Boehringer-Ingelheim: Honoraria; GSK: Research Funding; Ratiopharm: Research Funding; Cephalon: Consultancy, Honoraria, Research Funding; Celgene: Consultancy, Honoraria, Research Funding; Novartis: Honoraria; Bristol-Myers-Squibb: Consultancy, Honoraria; Pfizer: Honoraria, Research Funding; Roche: Honoraria, Research Funding; Sanofi Aventis: Honoraria; Eisai: Honoraria; Amgen: Honoraria, Research Funding. Greiner:BMS: Research Funding. Paschka:ASTEX Pharmaceuticals: Consultancy; Novartis: Consultancy; Medupdate GmbH: Honoraria; Bristol-Myers Squibb: Honoraria; Pfizer Pharma GmbH: Honoraria; Celgene: Honoraria. Heuser:Bayer Pharma AG: Research Funding; Karyopharm Therapeutics Inc: Research Funding; Novartis: Consultancy, Research Funding; Celgene: Honoraria; Pfizer: Research Funding; BerGenBio: Research Funding; Tetralogic: Research Funding.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V128.22.449.449

Language: English

Publisher: American Society of Hematology

Publication Date: 2016

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: Blood, American Society of Hematology, Vol. 106, No. 11 ( 2005-11-16), p. 1559-1559

Abstract: Introduction: Genomic aberrations represent important prognostic markers in many hematological cancers. In multiple myeloma (MM), chromosome 13q and 17p deletions (13q−, 17p−) have emerged as important outcome predictors that indicate a dismal prognosis. Other chromosomal abnormalities have been discussed as prognostic markers in this disease but came not out as independent variables when they were tested in a multivariable fashion. However, the complexity of genomic rearrangements and the clinical heterogeneity seen in malignant plasma cell disorders argue against 13q− and 17p− as the sole genomic change of prognostic relevance. The significance of chromosome arm 1q, 9q, and 11q extra copies - three frequent genomic imbalances in MM - is undetermined. Material and Methods: 90 patients (pts.) treated with one or two cycles of high-dose chemotherapy (HD-CTX) followed by autologous stem cell transplantation (ASCT) at a single center were analyzed by tri-color FISH and five DNA probes mapping to chromosome bands 1q21, 9q34, 11q25, 13q14, and 17p13. A multivariable analysis (Cox proportional hazards regression model) including genetic and clinical variables was performed. Results: The most frequent aberrations in the present series were (in order of decreasing prevalence): +1q (n=39/78, 50.0%), +9q (n=38/78, 48.7%), 13q− (n=42/90, 46.6%), and +11q (n=39/85, 45.9%). 17p− was identified in only 3 out of 88 patients (3.4%), while +17p were present in 13 out of 88 patients (14.8%). The median follow-up time was 37 months (m) and the median event free survival (EFS) and overall survival (OS) time from first ASCT of the entire cohort was 26 m and 71 m, respectively. Multivariable analysis including genetic aberrations, ß2-microblobulin, albumin, LDH, Salmon/Durie stage, and age at time of diagnosis revealed +9q and 13q− as the only independent predictors of EFS (p=0.003 and p=0.01, respectively). The mEFS in patients with 13q− was 19.0 m and 20.7 m in patients with +9q. In patients with concurrent +9q and 13q−, mEFS was only 12.2 m. In patients lacking these two abnormalities, mEFS was not reached. OS was not significantly influenced by any genetic or clinical variable in our series, most likely due to effective salvage treatment after relapse. Conclusions: +9q represents a novel and independent marker of adverse prognosis in MM. A single FISH experiment applying two DNA probes allows easy and rapid assessment of outcome in patients with malignant plasma cell disorders.

Type of Medium: Online Resource

ISSN: 0006-4971 , 1528-0020

URL: Article

DOI: 10.1182/blood.V106.11.1559.1559

Language: English

Publisher: American Society of Hematology

Publication Date: 2005

detail.hit.zdb_id: 1468538-3

detail.hit.zdb_id: 80069-7

In: wwt Wasserwirtschaft Wassertechnik, VDI Verlag GmbH, Vol. 70, No. 10 ( 2021), p. 42-44

Type of Medium: Online Resource

ISSN: 1438-5716

URL: Issue

URL: Article

DOI: 10.51202/1438-5716-2021-10

DOI: 10.51202/1438-5716-2021-10-042

Language: Unknown

Publisher: VDI Verlag GmbH

Publication Date: 2021

detail.hit.zdb_id: 1458303-3

detail.hit.zdb_id: 202611-9

detail.hit.zdb_id: 2857366-3

In: Hematological Oncology, Wiley, Vol. 34, No. 4 ( 2016-12), p. 200-207

Abstract: Therapeutic options in heavily pretreated relapsed/refractory multiple myeloma patients are often very limited because of impaired bone marrow function. Bendamustine is effective in multiple myeloma and has a favourable toxicity profile. We hypothesized that dose‐intensified bendamustine (180 mg/m 2 , day 1 and 2) followed by autologous blood stem cell support (ASCS) would improve bone marrow function with low post‐transplant toxicity in patients with severely impaired haematopoiesis. We analyzed 28 consecutive myeloma patients, with a median of three prior lines of therapy (range 2–7), who had relapsed from the last treatment with very limited bone marrow function and were therefore ineligible for conventional chemotherapy, novel agents or trial enrolment. Dose‐intensified bendamustine with ASCS improved haematopoiesis as reflected by increased platelet counts (median 40/nl vs 94/nl, p  = 0.0004) and white blood cell counts (3.0/nl vs 4.8/nl, p  = 0.02) at day +100. The median time until engraftment of platelets ( 〉 50/nl) was 11 days (0–24 days) and of white cell counts ( 〉 1.0/nl) 0 days (0–24 days). At least, a minimal response was achieved in 36% of patients. The disease stabilization rate was 50% while the median progression‐free survival rate was limited to 2.14 months. Most importantly, patients were once again eligible for alternative treatments including enrolment into clinical trials. We conclude that dose‐intensified bendamustine followed by ASCS is safe and feasible for multiple myeloma patients with very limited bone marrow reserve. Copyright © 2015 John Wiley & Sons, Ltd.

Type of Medium: Online Resource

ISSN: 0278-0232 , 1099-1069

URL: Issue

URL: Article

DOI: 10.1002/hon.v34.4

DOI: 10.1002/hon.2199

Language: English

Publisher: Wiley

Publication Date: 2016

detail.hit.zdb_id: 2001443-0

In: PAMM, Wiley, Vol. 7, No. 1 ( 2007-12), p. 1030301-1030302

Abstract: Global properties play an important role in real life applications of time‐delayed feedback control of chaos. The success of control is not only determined by the change of the local stability of some unstable periodic state embedded in the chaotic attractor, but also related to a basin of attraction large enough to capture the chaotic trajectory within a reasonable time. We report on electronic circuit experiments where the control performance is essentially affected by the type of bifurcations limiting the control regime and their respective global properties. (© 2008 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim)

Type of Medium: Online Resource

ISSN: 1617-7061 , 1617-7061

URL: Issue

URL: Article

DOI: 10.1002/pamm.v7:1

DOI: 10.1002/pamm.200700088

Language: English

Publisher: Wiley

Publication Date: 2007

detail.hit.zdb_id: 2078931-2

In: Genes, Chromosomes and Cancer, Wiley, Vol. 44, No. 2 ( 2005-10), p. 194-203

Type of Medium: Online Resource

ISSN: 1045-2257 , 1098-2264

URL: Issue

URL: Journal

URL: Article

DOI: 10.1002/gcc.v44:2

DOI: 10.1002/(ISSN)1098-2264

DOI: 10.1002/gcc.20231

Language: English

Publisher: Wiley

Publication Date: 2005

detail.hit.zdb_id: 1018988-9

detail.hit.zdb_id: 1492641-6

SSG: 12