Michael Hallek on Muck Rack

Michael Hallek

Cologne
As seen in: Blood Cancer Journal, Future Oncology, Color Research & Application, Nature, Wiley Online Library, PLOS, The New England Journal of Medicine, The Lancet, Annals of Internal Medicine, Kölner Stadt-Anzeiger, Blood, Future Medicine
Hematologist and oncologist, @UKKoeln & @UniCologne, Germany. Tweets are my own & no medical advice.
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Articles

Goals-of-care transition after an allogeneic hematopoietic stem-cell transplantation: A cross-sectional survey among hematologists on associated challenges

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By Anne Pralong, Steffen T. Simon, Marco Herling, Christoph Scheid, Michael Hallek, Jithmi Weliwitage, Martin Hellmich, Raymond Voltz, Udo Holtick, Alinda Reimer, Berenike Schoerger, Lisa Pusch
| Nature
To the editor Patients with hematological malignancies undergoing allogeneic hematopoietic stem-cell transplantation (allo-HSCT) face a (procedural) mortality of about 50% against the background of a real chance of cure [1]. Therefore, timely attention to end-of-life issues during the transplant trajectory is essential in cases of an unfavorable disease course, to prevent detrimental aggressive therapies at the end of life [2, 3].
Open in Who Shared Issue with article?

The spectrum of immunoglobulin heavy chain enhancer hijacking in chronic lymphocytic leukemia

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By Cristina Lopez , Cristina Sen López, Nnamdi Okeke, Christoph Wiegreffe, Susanne Bens, Emil Chteinberg, Barbara Eichhorst, Martin Dyer, Anja Fischer, Kirsten Fischer, Selina Glaser, Michael Hallek, Helene Kretzmer, Anja Mottok, Jan P. Meier-Kolthoff, Matthias Schlesner, Christof Schneider, Stefan Britsch, Ole Ammerpohl, Stephan Stilgenbauer, Eugen Tausch, Reiner Siebert, Cosima Drewes, Billy Jebaraj, Isabelle Kraus, Sina Hillebrecht, Amani Awada, Sarah Datismann, Dominick Pfaff, Karoline Schnitzler
| Nature
Abstract Activation of oncogenes by hijacking immunoglobulin gene loci (IG) enhancers via chromosomal translocation is a common pathogenetic mechanism in B-cell malignancies, affecting 5–10% of chronic lymphocytic leukemia (CLL). The oncogenic partners in many of these cases remain unidentified. Therefore, we conducted a comprehensive analysis of 144 CLL samples with IGH-translocation excluding IGH::BCL2, IGH::CCND1, IGH::BCL3 and IGH::MYC.
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Single-cell genomics highlight MYC-associated metabolic activation and altered cell interactions in T-prolymphocytic leukemia progression - Nature Communications

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By Linus Wahnschaffe, Tony Muller, Tea Pemovska, Alexander Pichler, Edith Julia, Sanna Timonen, Martin Böttcher, Qu Jiang, Julia Patricia Bischoff, Marek Franitza, Theodoros Georgomanolis, Kerstin Becker, Michael Hallek, Dimitrios Mougiakakos, Thorsten Zenz, Satu Mustjoki, Emmanuel Bachy, Charles Herbaux, Alexandra Schrader, Philipp B. Staber, Till Braun, Marco Herling, Dennis Jungherz, Stéphanie Poulain, David Beverungen, Natali Pflug
| Nature
Abstract T-prolymphocytic leukemia (T-PLL) typically presents with rapidly progressing tumor burden. However, 15–25% of cases are diagnosed at an indolent stage with asymptomatic and stable low-level blood lymphocytosis over up to 2-3 years before advancing to active-stage disease.
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See all 27 licensed articles (30 Total)

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