@article{EckardtStasikKrameretal.2021,
  author    = {Eckardt, Jan-Niklas and Stasik, Sebastian and Kramer, Michael and R{\"o}llig, Christoph and Kr{\"a}mer, Alwin and Scholl, Sebastian and Hochhaus, Andreas and Crysandt, Martina and Br{\"u}mmendorf, Tim H. and Naumann, Ralph and Steffen, Bj{\"o}rn and Kunzmann, Volker and Einsele, Hermann and Schaich, Markus and Burchert, Andreas and Neubauer, Andreas and Sch{\"a}fer-Eckart, Kerstin and Schliemann, Christoph and Krause, Stefan W. and Herbst, Regina and H{\"a}nel, Mathias and Frickhofen, Norbert and Noppeney, Richard and Kaiser, Ulrich and Baldus, Claudia D. and Kaufmann, Martin and R{\´a}cil, Zdenek and Platzbecker, Uwe and Berdel, Wolfgang E. and Mayer, Jiř{\´i} and Serve, Hubert and M{\"u}ller-Tidow, Carsten and Ehninger, Gerhard and St{\"o}lzel, Friedrich and Kroschinsky, Frank and Schetelig, Johannes and Bornh{\"a}user, Martin and Thiede, Christian and Middeke, Jan Moritz},
  title     = {Loss-of-function mutations of BCOR are an independent marker of adverse outcomes in intensively treated patients with acute myeloid leukemia},
  series = {Cancers},
  volume    = {13},
  journal   = {Cancers},
  number    = {9},
  issn      = {2072-6694},
  doi       = {10.3390/cancers13092095},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-236735},
  year      = {2021},
  abstract  = {Acute myeloid leukemia (AML) is characterized by recurrent genetic events. The BCL6 corepressor (BCOR) and its homolog, the BCL6 corepressor-like 1 (BCORL1), have been reported to be rare but recurrent mutations in AML. Previously, smaller studies have reported conflicting results regarding impacts on outcomes. Here, we retrospectively analyzed a large cohort of 1529 patients with newly diagnosed and intensively treated AML. BCOR and BCORL1 mutations were found in 71 (4.6\%) and 53 patients (3.5\%), respectively. Frequently co-mutated genes were DNTM3A, TET2 and RUNX1. Mutated BCORL1 and loss-of-function mutations of BCOR were significantly more common in the ELN2017 intermediate-risk group. Patients harboring loss-of-function mutations of BCOR had a significantly reduced median event-free survival (HR = 1.464 (95\%-Confidence Interval (CI): 1.005-2.134), p = 0.047), relapse-free survival (HR = 1.904 (95\%-CI: 1.163-3.117), p = 0.01), and trend for reduced overall survival (HR = 1.495 (95\%-CI: 0.990-2.258), p = 0.056) in multivariable analysis. Our study establishes a novel role for loss-of-function mutations of BCOR regarding risk stratification in AML, which may influence treatment allocation.},
  language  = {en}
}
@article{SausseleHehlmannFabariusetal.2018,
  author    = {Saussele, Susanne and Hehlmann, Ruediger and Fabarius, Alice and Jeromin, Sabine and Proetel, Ulrike and Rinaldetti, Sebastien and Kohlbrenner, Katharina and Einsele, Hermann and Falge, Christine and Kanz, Lothar and Neubauer, Andreas and Kneba, Michael and Stegelmann, Frank and Pfreundschuh, Michael and Waller, Cornelius F. and Oppliger Leibundgut, Elisabeth and Heim, Dominik and Krause, Stefan W. and Hofmann, Wolf-Karsten and Hasford, Joerg and Pfirrmann, Markus and M{\"u}ller, Martin C. and Hochhaus, Andreas and Lauseker, Michael},
  title     = {Defining therapy goals for major molecular remission in chronic myeloid leukemia: results of the randomized CML Study IV},
  series = {Leukemia},
  volume    = {32},
  journal   = {Leukemia},
  number    = {5},
  doi       = {10.1038/s41375-018-0055-7},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-227528},
  pages     = {1222-1228},
  year      = {2018},
  abstract  = {Major molecular remission (MMR) is an important therapy goal in chronic myeloid leukemia (CML). So far, MMR is not a failure criterion according to ELN management recommendation leading to uncertainties when to change therapy in CML patients not reaching MMR after 12 months. At monthly landmarks, for different molecular remission status Hazard ratios (HR) were estimated for patients registered to CML study IV who were divided in a learning and a validation sample. The minimum HR for MMR was found at 2.5 years with 0.28 (compared to patients without remission). In the validation sample, a significant advantage for progression-free survival (PFS) for patients in MMR could be detected (p-value 0.007). The optimal time to predict PFS in patients with MMR could be validated in an independent sample at 2.5 years. With our model we provide a suggestion when to define lack of MMR as therapy failure and thus treatment change should be considered. The optimal response time for 1\% BCR-ABL at about 12-15 months was confirmed and for deep molecular remission no specific time point was detected. Nevertheless, it was demonstrated that the earlier the MMR is achieved the higher is the chance to attain deep molecular response later.},
  language  = {en}
}
@article{SchofferSchueleinArandetal.2016,
  author    = {Schoffer, Olaf and Sch{\"u}lein, Stefanie and Arand, Gerlinde and Arnholdt, Hans and Baaske, Dieter and Bargou, Ralf C. and Becker, Nikolaus and Beckmann, Matthias W. and Bodack, Yves and B{\"o}hme, Beatrix and Bozkurt, Tayfun and Breitsprecher, Regine and Buchali, Andre and Burger, Elke and Burger, Ulrike and Dommisch, Klaus and Elsner, Gudrun and Fernschild, Karin and Flintzer, Ulrike and Funke, Uwe and Gerken, Michael and G{\"o}bel, Hubert and Grobe, Norbert and Gumpp, Vera and Heinzerling, Lucie and Kempfer, Lana Raffaela and Kiani, Alexander and Klinkhammer-Schalke, Monika and Kl{\"o}cking, Sabine and Kreibich, Ute and Knabner, Katrin and Kuhn, Peter and Lutze, Stine and M{\"a}der, Uwe and Maisel, Tanja and Maschke, Jan and Middeke, Martin and Neubauer, Andreas and Niedostatek, Antje and Opazo-Saez, Anabelle and Peters, Christoph and Schell, Beatrice and Schenkirsch, Gerhard and Schmalenberg, Harald and Schmidt, Peter and Schneider, Constanze and Schubotz, Birgit and Seide, Anika and Strecker, Paul and Taubenheim, Sabine and Wackes, Matthias and Weiß, Steffen and Welke, Claudia and Werner, Carmen and Wittekind, Christian and Wulff, J{\"o}rg and Zettl, Heike and Klug, Stefanie J.},
  title     = {Tumour stage distribution and survival of malignant melanoma in Germany 2002-2011},
  series = {BMC Cancer},
  volume    = {16},
  journal   = {BMC Cancer},
  number    = {936},
  doi       = {10.1186/s12885-016-2963-0},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-164544},
  year      = {2016},
  abstract  = {Background Over the past two decades, there has been a rising trend in malignant melanoma incidence worldwide. In 2008, Germany introduced a nationwide skin cancer screening program starting at age 35. The aims of this study were to analyse the distribution of malignant melanoma tumour stages over time, as well as demographic and regional differences in stage distribution and survival of melanoma patients. Methods Pooled data from 61 895 malignant melanoma patients diagnosed between 2002 and 2011 and documented in 28 German population-based and hospital-based clinical cancer registries were analysed using descriptive methods, joinpoint regression, logistic regression and relative survival. Results The number of annually documented cases increased by 53.2\% between 2002 (N = 4 779) and 2011 (N = 7 320). There was a statistically significant continuous positive trend in the proportion of stage UICC I cases diagnosed between 2002 and 2011, compared to a negative trend for stage UICC II. No trends were found for stages UICC III and IV respectively. Age (OR 0.97, 95\% CI 0.97-0.97), sex (OR 1.18, 95\% CI 1.11-1.25), date of diagnosis (OR 1.05, 95\% CI 1.04-1.06), 'diagnosis during screening' (OR 3.24, 95\% CI 2.50-4.19) and place of residence (OR 1.23, 95\% CI 1.16-1.30) had a statistically significant influence on the tumour stage at diagnosis. The overall 5-year relative survival for invasive cases was 83.4\% (95\% CI 82.8-83.9\%). Conclusions No distinct changes in the distribution of malignant melanoma tumour stages among those aged 35 and older were seen that could be directly attributed to the introduction of skin cancer screening in 2008. "},
  language  = {en}
}
@article{HanfsteinLausekerHehlmannetal.2014,
  author    = {Hanfstein, Benjamin and Lauseker, Michael and Hehlmann, R{\"u}diger and Saussele, Susanne and Erben, Philipp and Dietz, Christian and Fabarius, Alice and Proetel, Ulrike and Schnittger, Susanne and Haferlach, Claudia and Krause, Stefan W. and Schubert, J{\"o}rg and Einsele, Hermann and H{\"a}nel, Mathias and Dengler, Jolanta and Falge, Christiane and Kanz, Lothar and Neubauer, Andreas and Kneba, Michael and Stengelmann, Frank and Pfreundschuh, Michael and Waller, Cornelius F. and Spiekerman, Karsten and Baerlocher, Gabriela M. and Pfirrmann, Markus and Hasford, Joerg and Hofmann, Wolf-Karsten and Hochhaus, Andreas and M{\"u}ller, Martin C.},
  title     = {Distinct characteristics of e13a2 versus e14a2 BCR-ABL1 driven chronic myeloid leukemia under first-line therapy with imatinib},
  series = {Haematologica},
  volume    = {99},
  journal   = {Haematologica},
  number    = {9},
  issn      = {1592-8721},
  doi       = {10.3324/haematol.2013.096537},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-115476},
  pages     = {1441-1447},
  year      = {2014},
  abstract  = {The vast majority of chronic myeloid leukemia patients express a BCR-ABL1 fusion gene mRNA encoding a 210 kDa tyrosine kinase which promotes leukemic transformation. A possible differential impact of the corresponding BCR-ABL1 transcript variants e13a2 ("b2a2") and e14a2 ("b3a2") on disease phenotype and outcome is still a subject of debate. A total of 1105 newly diagnosed imatinib-treated patients were analyzed according to transcript type at diagnosis (e13a2, n=451; e14a2, n=496; e13a2+e14a2, n=158). No differences regarding age, sex, or Euro risk score were observed. A significant difference was found between e13a2 and e14a2 when comparing white blood cells (88 vs. 65 x 10(9)/L, respectively; P<0.001) and platelets (296 vs. 430 x 109/L, respectively; P<0.001) at diagnosis, indicating a distinct disease phenotype. No significant difference was observed regarding other hematologic features, including spleen size and hematologic adverse events, during imatinib-based therapies. Cumulative molecular response was inferior in e13a2 patients (P=0.002 for major molecular response; P<0.001 for MR4). No difference was observed with regard to cytogenetic response and overall survival. In conclusion, e13a2 and e14a2 chronic myeloid leukemia seem to represent distinct biological entities. However, clinical outcome under imatinib treatment was comparable and no risk prediction can be made according to e13a2 versus e14a2 BCR-ABL1 transcript type at diagnosis. (clinicaltrials.gov identifier: 00055874)},
  language  = {en}
}