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  • 1
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    Hyperdiploidy Is Rare in Patients with AL Amyloidosis – Identification of Major Cytogenetic Groups in Early Monoclonal Plasma Cell Disorders.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 2823-2823
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 2823-2823
    Abstract: Abstract 2823 Poster Board II-799 AL amyloidosis (AL) is characterized by the deposition of amyloid fibrils in diverse tissues due to an underlying monoclonal plasma cell dyscrasia. In a previous study (Bochtler et al, Blood 2008) we have demonstrated that in AL cytogenetic aberrations were detectable in about 90% of patients (pts). Translocation t(11;14) proved to be the most frequent aberration in AL found in 45% of the pts. In this study we evaluated whether the concept of hyperdiploidy and non-hyperdiploidy as major pathogenetic pathways in monoclonal gammopathy of undetermined significance (MGUS) and multiple myeloma (MM) is also applicable to AL. Our study was based on the largest patient group tested for cytogenetics in AL thus far including 184 pts with AL - among them 21 pts with concomitant MM I. They were assessed for their ploidy status by interphase fluorescence in situ hybridization (FISH). 179 MGUS and MM I pts not requiring therapy served as controls. We used a well established score (Wuilleme et al, Leukemia 2005), which requires extra copies for at least two out of the three probes 5p15/5q35, 9q34 and 15q22 as criterion for hyperdiploidy. The hyperdiploidy frequency was very low in AL with 14% as compared to 32% in MGUS / MM I (p 〈 0.001). Among AL pts those with a concomitant MM I displayed a higher hyperdiploidy frequency than those without (43% versus 10%, p 〈 0.001) suggesting that chromosomal gains reflect progression of the monoclonal plasma cell clone. Addressing hyperdiploidy probes in detail, we could show that both in the 184 pts. with AL and 179 pts. with MGUS / MM I gains of 11q23, 17p13 and 19q13.3 closely clustered with the three hyperdiploidy defining probes 5p15/5q35, 9q34 and 15q22 (p'0.01 for all probes after adjusting for multiple testing). However, gain of 11q23 was also frequently detected in association with t(11;14). The group with gain of 11q23 subdivides into a t(11;14) positive and a hyperdiploidy positive subgroup in both the AL (p 〈 0.001) and the MGUS / MM I (p 〈 0.001) entities. As revealed by additional probes for 11p15 and 11cen, gain of 11q23 in hyperdiploid pts reflected a gain of the whole chromosome 11 in all tested pts (10 AL and 31 MGUS / MM I). On the contrary, gain of 11q23 in t(11;14) positive pts was merely due to the translocation involving chromosome 11 (with 25 out of 26 AL and 5 out of 7 MGUS / MM I pts displaying a normal diploid status for 11p15 and 11cen). Therefore, gain of 11q23 is a poor indicator of hyperdiploidy in AL, where t(11;14) frequencies are particularly high and hyperdiploidy frequencies are particularly low. Addressing the cytogenetic clustering of hyperdiploidy with other cytogenetic aberrations we observed a strong inverse association of hyperdiploidy with t(11;14) in both AL and MGUS / MM I (p 〈 0.001 in both entities). Accordingly, both aberrations were allocated to branches separating from each other already at the root in the oncogenetic tree model (see figure 1). Del13q14/t(4;14) and IgH translocations with an unknown partner also separated as distinct branches early from the root. These similar clustering patterns of both AL and MGUS / MM I with 4 major cytogenetic groups suggests common pathogenetic mechanisms in both entities despite their differing hyperdiploidy and t(11;14) frequencies. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.2823.2823
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 2
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    Inhibition of aurora kinases for tailored risk-adapted treatment of multiple myeloma
    American Society of Hematology ; 2009
    In:  Blood Vol. 113, No. 18 ( 2009-04-30), p. 4331-4340
    Details
    In: Blood, American Society of Hematology, Vol. 113, No. 18 ( 2009-04-30), p. 4331-4340
    Abstract: Genetic instability and cellular proliferation have been associated with aurora kinase expression in several cancer entities, including multiple myeloma. Therefore, the expression of aurora-A, -B, and -C was determined by Affymetrix DNA microarrays in 784 samples including 2 independent sets of 233 and 345 CD138-purified myeloma cells from previously untreated patients. Chromosomal aberrations were assessed by comprehensive interphase fluorescence in situ hybridization and proliferation of primary myeloma cells by propidium iodine staining. We found aurora-A and -B to be expressed at varying frequencies in primary myeloma cells of different patient cohorts, but aurora-C in testis cell samples only. Myeloma cell samples with detectable versus absent aurora-A expression show a significantly higher proliferation rate, but neither a higher absolute number of chromosomal aberrations (aneuploidy), nor of subclonal aberrations (chromosomal instability). The clinical aurora kinase inhibitor VX680 induced apoptosis in 20 of 20 myeloma cell lines and 5 of 5 primary myeloma cell samples. Presence of aurora-A expression delineates significantly inferior event-free and overall survival in 2 independent cohorts of patients undergoing high-dose chemotherapy, independent from conventional prognostic factors. Using gene expression profiling, aurora kinase inhibitors as a promising therapeutic option in myeloma can be tailoredly given to patients expressing aurora-A, who in turn have an adverse prognosis.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood-2008-09-178350
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 3
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    Clinical Outcome of Patients with Follicular Lymphoma and Bulky Disease After Rituximab-CHOP Immunochemotherapy with and without Consolidating Radiotherapy.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 2722-2722
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 2722-2722
    Abstract: Abstract 2722 Poster Board II-698 Background: As the clinical management of patients with bulky disease remains challenging, many centres apply involved-field radiotherapy (IF-RT) after completion of immunochemotherapy. This strategy remains controversial. Patients and Methods: To evaluate the benefit of consolidating IF-RT in addition to immunochemotherapy, we retrospectively analyzed relapse patterns and survival of patients presenting with bulky follicular lymphoma (FL). Bulky disease was defined as abdominal/ mediastinal lymphoma mass 〉 7.5 cm and/ or peripheral lymphoma mass 〉 5 cm. All patients were treated within a prospective randomized trial on 126 patients with FL with six cycles of standard CHOP-chemotherapy in combination with 1, 3 or 6 cycles of Rituximab, followed by consolidating IF-RT in patients with bulky disease. 42 eligible patients with bulky disease were identified and form the foundation of this analysis, of which 26 were irradiated and 16 were not, violating the protocol. Results: With the exception of number of affected nodal regions, there was no significant difference between the irradiated and the non-irradiated group with regards to presenting characteristics (p 〉 .05). Among all patients, bulks were located below the diaphragm in 91%. A second tumour bulk was present in 9 patients (22%). Female to male ratio was 1.3:1, and the median age at diagnosis was 54 years (range 23–73). According to FLIPI, 10% were classified as low risk (0–1), 45% as intermediate risk (2), and 45% as high risk (3–5). B symptoms were absent in 69%. Eleven patients (26 %) had received one course of Rituximab, 17 (41%) three courses and 14 (33%) six courses. There was no significant difference between the irradiated and the non-irradiated group with regards to previous exposure to immunochemotherapy (p = .628). After a median follow-up of 60 months, a total of 21 patients (50%) had progressed or relapsed and 9 patients (21%) had died. With the exception of one patient who died from congestive heart failure following chemotherapy-related cardiomyopathy, the main cause of death was disease progression or relapse. Highly malignant transformation into diffuse large B-cell lymphoma was observed in 5 cases. In the irradiated group, relapse occurred in 12 of 26 patients. Half of these relapses were located within the original bulk or within the bulk plus a new location, and 50% at a new location altogether; 42% occurred within the previously irradiated area. In the non-irradiated group, 9 of 16 patients relapsed. The corresponding rates regarding relapse location were 67% for original plus new location and 33% for new location only. There was no statistically significant difference between exposure to radiotherapy after immunochemotherapy and the likelihood of a relapse per se (p = .751) or at a specific location (p = .66). At the last follow-up, 31% of irradiated patients had achieved CR and 23% PR. Among the non-irradiated group, the corresponding rates were 25% and 19%. There was no significant difference in remission rates at any staging examination throughout the clinical trial between the two treatment groups (p 〉 .05). 6-year progression-free- and overall survival rates were 52% and 80% after IF-RT and 48% and 73% without IF-RT (p = 1.00, p = .68 respectively). Conclusion: In this analysis, there was no difference in relapse rate, relapse location, PFS and OS between patients with bulky FL treated with and without consolidating IF-RT. Although patient numbers are limited, this is the first analysis of its kind conducted in the Rituximab era. Disclosures: No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.2722.2722
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 4
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    Rituximab Maintenenance Therapy in CD20+ B-Cell Non-Hodgkin-Lymphoma – Final Results of a Multicenter Prospective Randomised Phase II Study.
    American Society of Hematology ; 2009
    In:  Blood Vol. 114, No. 22 ( 2009-11-20), p. 1707-1707
    Details
    In: Blood, American Society of Hematology, Vol. 114, No. 22 ( 2009-11-20), p. 1707-1707
    Abstract: Abstract 1707 Poster Board I-733 Background Clinical and pharmacokinetic data suggest that the effect of rituximab could be improved by prolonged exposure to the drug. To test for this hypothesis we performed a prospective randomized trial of rituximab maintenance therapy in patients (pts) with CD20+ B-cell Non-Hodgkin-Lymphoma. Methods After completion of standard treatment pts with CD20+ B-cell lymphoma were randomized to either observation or maintenance therapy with rituximab (375 mg/m2) administered every 3 months for 2 years. Both pts after first line therapy and pts after relapse treatment were included in the study. Pts with aggressive lymphoma were enrolled if they had achieved a complete response (CR) after initial treatment. Pts with aggressive lymphoma with residual tumor mass underwent positron emission tomography (PET) and qualified for randomization if this examination showed no signs of tumor activity. Pts with indolent lymphoma were eligible for the study if at least a partial response (PR) was achieved. Primary endpoint of the study was event free survival (EFS), secondary endpoints were relapse rate (RR), relapse free survival (RFS) and overall survival (OS). EFS and OS were analysed using an asymptotic logrank test, RFS using a competing risk model and RR using Fisher's exact test. Results After recruitment of 171 pts the planned final analysis was performed on an intention to treat basis. Complete data sets of 163 pts were evaluable. 91 (62%) pts were male, median age was 58 years, 130 pts (80%) hat one previous therapy, 27 pts (17%) 2 previous therapies, 4 pts (2%) 3 previous therapies and 1 pt (1%) 4 previous therapies. At study entry, 120 pts (74%) were in CR, 2 pts (2%) in unconfirmed CR and 41 pts (25%) in PR. Histological subtypes included diffuse large cell lymphoma (67 pts), follicular lymphoma (35 pts), mantle cell lymphoma (18 pts), primary mediastinal lymphoma (16 pts), marginal zone lymphoma (7 pts), Burkitt's lymphoma (5 pts), and other lymphomas (15 pts). Age, sex, number of previous therapies, remission state and diagnoses were well balanced between the rituximab maintenance and the observation group (p 〉 0.05). After a median follow up of 28 months, EFS (HR 0.50, 95% CI 0.23-1.09, p=0.037,) and RFS (HR 2.52, 95% CI 1.11-5.70 p=0.03) were superior for the maintenance group. In regards to diagnostic subgroups, EFS was in particular prolonged in pts with mantle cell lymphoma (p=0.055, one sided logrank test) and to a lesser extent in pts with follicular lymphoma (p=0.16) and diffuse large cell B cell lymphoma (p=0.18). Relapse occurred more often in the observation group than in the treatment group, however this effect was not significant (relapse rate observation group/treatment group = 2.31, 95% CI 0.86-6.75, p=0.08). There was no difference in OS between the two groups (p=0.74). Maintenance therapy was generally well tolerated: in 5 pts a WHO Grade 3 toxicity event occurred, which were arrhythmia, neuropathy, leucopenia (n=1 each) and infections (n=2). In one pt two WHO Grade 3 toxicities were observed (pain and infection). Conclusion Rituximab maintenance therapy is feasible, safe and well tolerated and improves EFS in patients with CD20+ B-cell lymphoma. In this analysis, the benefit of rituximab maintenance was particularly striking in patients with mantle cell lymphoma. This study has been continued with an amendment including additional pts with mantle cell and diffuse large cell lymphoma. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V114.22.1707.1707
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2009
    detail.hit.zdb_id: 1468538-3
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  • 5
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    Inhibition of Aurora-Kinases for Tailored Risk-Adapted Treatment of Multiple Myeloma
    American Society of Hematology ; 2008
    In:  Blood Vol. 112, No. 11 ( 2008-11-16), p. 248-248
    Details
    In: Blood, American Society of Hematology, Vol. 112, No. 11 ( 2008-11-16), p. 248-248
    Abstract: BACKGROUND. At the time of diagnosis, myeloma cells are characterized by a low proliferation rate that increases in relapse. Presence of proliferation correlates with adverse prognosis. At the same time, myeloma cells harbor a high median number of chromosomal aberrations, often associated with genetic instability. Cellular proliferation and genetic instability in turn have been associated with Aurora-kinase expression in several cancer entities, including multiple myeloma. PATIENTS AND METHODS. Expression of Aurora-A, -B and -C was assessed using Affymetrix DNA-microarrays in 784 samples including two independent sets of 233 and 345 CD138-purified myeloma cells from previously untreated patients. Chromosomal aberrations were assessed by comprehensive iFISH using a set of probes for the chromosomal regions 1q21, 6q21, 8p21, 9q34, 11q23, 11q13, 13q14.3, 14q32, 15q22, 17p13, 19q13, 22q11, as well as the translocations t(4;14)(p16.3;q32.3) and t(11;14) (q13;q32.3). Proliferation of primary myeloma cells (n=67) was determined by propidium iodine staining. The effect of the clinical Aurora-kinase inhibitor VX680 on proliferation of 20 human myeloma cell lines and survival of 5 primary myeloma cell-samples was tested. RESULTS. We found Aurora-A and -B to be expressed at varying frequencies in primary myeloma cells of different patient-cohorts, including 23% for Aurora A in our first cohort of patients treated with high dose therapy (see figure shown below). Aurora-C expression was found in testis-samples only. Myeloma cell-samples with detectable Aurora-A expression show a significantly higher proliferation rate, whereas the number of chromosomal aberrations (aneuploidy) is not higher compared to myeloma-cells with absent Aurora-A expression. The same holds true for subclonal aberrations (i.e. genetic instability). The Aurora-kinase inhibitor VX680 induces apoptosis in all myeloma cell lines and primary myeloma cell-samples tested. Presence of Aurora-A expression delineates significantly inferior event-free and overall survival in two independent cohorts of patients undergoing high-dose chemotherapy and autologous stem cell transplantation. This observation is independent of conventional prognostic factors, i.e. serum-ß2-microglobulin or ISS-stage. CONCLUSION. Aurora-kinase inhibitors (including VX680 tested here) are very active on myeloma cell lines as well as primary myeloma cells and represent a promising weapon in the therapeutic arsenal against multiple myeloma. Gene expression profiling allows the assessment of Aurora-kinase expression and thus in turn a tailoring of treatment to patients expressing Aurora-A associated with adverse prognosis. Figure Figure
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    URL: Article
    DOI: 10.1182/blood.V112.11.248.248
    RVK:
    XA 33000
    RVK:
    XA 10000
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2008
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 6
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    Genomic and Protein Expression Profiling Identifies CDK6 As Novel Independent Prognostic Marker in Medulloblastoma
    American Society of Clinical Oncology (ASCO) ; 2005
    In:  Journal of Clinical Oncology Vol. 23, No. 34 ( 2005-12-01), p. 8853-8862
    Details
    In: Journal of Clinical Oncology, American Society of Clinical Oncology (ASCO), Vol. 23, No. 34 ( 2005-12-01), p. 8853-8862
    Abstract: Medulloblastoma is the most common malignant brain tumor in children. Despite multimodal aggressive treatment, nearly half of the patients die as a result of this tumor. Identification of molecular markers for prognosis and development of novel pathogenesis-based therapies depends crucially on a better understanding of medulloblastoma pathomechanisms. Patients and Methods We performed genome-wide analysis of DNA copy number imbalances in 47 medulloblastomas using comparative genomic hybridization to large insert DNA microarrays (matrix-CGH). The expression of selected candidate genes identified by matrix-CGH was analyzed immunohistochemically on tissue microarrays representing medulloblastomas from 189 clinically well-documented patients. To identify novel prognostic markers, genomic findings and protein expression data were correlated to patient survival. Results Matrix-CGH analysis revealed frequent DNA copy number alterations of several novel candidate regions. Among these, gains at 17q23.2-qter (P 〈 .01) and losses at 17p13.1 to 17p13.3 (P = .04) were significantly correlated to poor prognosis. Within 17q23.2-qter and 7q21.2, two of the most frequently gained chromosomal regions, confined amplicons were identified that contained the PPM1D and CDK6 genes, respectively. Immunohistochemistry revealed strong expression of PPM1D in 148 (88%) of 168 and CDK6 in 50 (30%) of 169 medulloblastomas. Overexpression of CDK6 correlated significantly with poor prognosis (P 〈 .01) and represented an independent prognostic marker of overall survival on multivariate analysis (P = .02). Conclusion We identified CDK6 as a novel molecular marker that can be determined by immunohistochemistry on routinely processed tissue specimens and may facilitate the prognostic assessment of medulloblastoma patients. Furthermore, increased protein-levels of PPM1D and CDK6 may link the TP53 and RB1 tumor suppressor pathways to medulloblastoma pathomechanisms.
    Type of Medium: Online Resource
    ISSN: 0732-183X , 1527-7755
    URL: Article
    DOI: 10.1200/JCO.2005.02.8589
    RVK:
    XA 52760
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    XA 10000
    Language: English
    Publisher: American Society of Clinical Oncology (ASCO)
    Publication Date: 2005
    detail.hit.zdb_id: 2005181-5
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  • 7
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    Early Pliocene change of deposition style in the Cape Basin, southeastern Atlantic
    Geological Society of America ; 2007
    In:  Geological Society of America Bulletin Vol. 119, No. 7-8 ( 2007-07-01), p. 1004-1013
    Details
    In: Geological Society of America Bulletin, Geological Society of America, Vol. 119, No. 7-8 ( 2007-07-01), p. 1004-1013
    Type of Medium: Online Resource
    ISSN: 0016-7606 , 1943-2674
    URL: Article
    DOI: 10.1130/B26110.1
    Language: English
    Publisher: Geological Society of America
    Publication Date: 2007
    detail.hit.zdb_id: 2028776-8
    detail.hit.zdb_id: 2008165-0
    detail.hit.zdb_id: 449720-X
    detail.hit.zdb_id: 1351-1
    SSG: 13
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  • 8
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    Deposition of amyloid proteins in the epicardial coronary arteries of 58 patients with primary systemic amyloidosis
    Elsevier BV ; 2007
    In:  Cardiovascular Pathology Vol. 16, No. 2 ( 2007-3), p. 75-78
    Details
    In: Cardiovascular Pathology, Elsevier BV, Vol. 16, No. 2 ( 2007-3), p. 75-78
    Type of Medium: Online Resource
    ISSN: 1054-8807
    URL: Article
    DOI: 10.1016/j.carpath.2006.09.011
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 1499916-X
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  • 9
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    Radiotherapy for Extramedullary Plasmacytoma of the Head and Neck
    Elsevier BV ; 2009
    In:  International Journal of Radiation Oncology*Biology*Physics Vol. 73, No. 3 ( 2009-3), p. 789-794
    Details
    In: International Journal of Radiation Oncology*Biology*Physics, Elsevier BV, Vol. 73, No. 3 ( 2009-3), p. 789-794
    Type of Medium: Online Resource
    ISSN: 0360-3016
    URL: Article
    DOI: 10.1016/j.ijrobp.2008.04.077
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 1500486-7
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  • 10
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    Microarray‐based gene expression profiling of benign, atypical and anaplastic meningiomas identifies novel genes associated with meningioma progression
    Wiley ; 2005
    In:  International Journal of Cancer Vol. 114, No. 2 ( 2005-03-20), p. 249-256
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    In: International Journal of Cancer, Wiley, Vol. 114, No. 2 ( 2005-03-20), p. 249-256
    Abstract: To identify gene expression profiles associated with human meningiomas of different World Health Organization (WHO) malignancy grades, we analyzed 30 tumors (13 benign meningiomas, WHO grade I; 12 atypical meningiomas, WHO grade II; 5 anaplastic meningiomas, WHO grade III) for the expression of 2,600 genes using cDNA‐microarray technology. Receiver operator curve (ROC) analysis with a cutoff value of 45% selection probability identified 37 genes with decreased and 27 genes with increased expression in atypical and anaplastic meningiomas, compared to benign meningiomas. Supervised classification of the tumors did not reveal specific expression patterns representative of each WHO grade. However, anaplastic meningiomas could be distinguished from benign meningiomas by differential expression of a distinct set of genes, including several ones associated with cell cycle regulation and proliferation. Investigation of potential correlations between microarray expression data and genomic aberrations, detected by comparative genomic hybridization (CGH), demonstrated that losses on chromosomes 10 and 14 were associated with distinct expression profiles, including increased expression of several genes related to the insulin‐like growth factor (IGF) ( IGF2 , IGFBP3 and AKT3 ) or wingless (WNT) ( CTNNB1 , CDK5R1 , ENC1 and CCND1 ) pathways. Taken together, our microarray‐based expression profiling revealed interesting novel candidate genes and pathways that may contribute to meningioma progression. © 2004 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v114:2
    DOI: 10.1002/ijc.20733
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    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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