Following publication of the original article [1], the authors identified an error in Fig. 1f. The correct and incorrect figures are given below.
Incorrect Fig. 1:
×
Correct Fig. 1:
Fig. 1
shRNA-mediated knockdown of AURKA or AURKB decreases the transformed phenotype of KRAS-positive lung cells. Unless otherwise indicated, A549 and H358 stable cells with inducible expression of 2 different shRNAs targeting AURKA (shAKA#1 and shAKA#2), AURKB (shAKB#1 and shAKB#2) or a non-targeting shRNA (shCtrl) were either treated with 2 μg/mL doxycycline (DOX) for 5 days to induce shRNA expression or left untreated (MOCK). a Protein lysates of doxycycline-treated ( +) and untreated ( −) cells were submitted to western blotting with the indicated antibodies. TUBA) anti-α-tubulin. b Growth curve analysis of the indicated cells. All cells were treated with 2 μg/mL doxycycline (DOX) for the indicated times. c The indicated cells were plated for clonogenic assays as described in methods and treated for 21 days with 2 μg/mL doxycycline (DOX). Colonies formed were stained with crystal violet and counted. Images shown are representative of three independent experiments. d The indicated treated (DOX) or untreated (MOCK) cells were stained with BrdU and propidium iodide (PI) as described in methods, and cell cycle analysis was performed by flow cytometry. e Protein lysates of A549 and H358 stable cells with inducible expression of 2 different shRNAs targeting AURKA (shAKA#1 and #2), AURKB (shAKB#1 and #2) or a non-targeting shRNA (shCtrl), treated ( +) or not (-) with 2 μg/mL doxycycline (DOX) for 5 days, were submitted to western blotting with the indicated antibodies. C3) anti-caspase 3. f Anchorage-independent growth was evaluated by plating the indicated cells in soft agar as described in methods. Cells were then treated for 21 days with 2 μg/mL doxycycline (DOX) or left untreated (MOCK). Colonies formed were stained with MTT and counted. Images shown are representative of three independent experiments. In all cases, statistical significance was determined when appropriate by Student’s t-test (*p < 0.05, **p < 0.01) and the groups being compared are indicated by horizontal bars.
×
Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
Das Kombinationsregime BrECADD mit Brentuximab vedotin ermöglichte in der Studie HD21 beim fortgeschrittenen klassischen Hodgkin-Lymphom eine unerwartet hohe progressionsfreie Überlebensrate von 94,3% nach vier Jahren. Gleichzeitig war das Regime besser tolerabel als der bisherige Standard eBEACOPP.
Zwei Phase-3-Studien deuten auf erhebliche Vorteile des Antikörper-Wirkstoff-Konjugats Belantamab-Mafodotin bei vorbehandelten Personen mit Multiplem Myelom: Im Vergleich mit einer Standard-Tripeltherapie wurde das progressionsfreie Überleben teilweise mehr als verdoppelt.
Der Tyrosinkinasehemmer (TKI) Asciminib ist älteren Vertretern dieser Gruppe bei CML offenbar überlegen: Personen mit frisch diagnostizierter CML entwickelten damit in einer Phase-3-Studie häufiger eine gut molekulare Response, aber seltener ernste Nebenwirkungen.
Zurzeit untersuchen Forschende verschiedene neue Ansätze zur Prävention von Brustkrebs bei Personen mit hohem Risiko. Darunter Denosumab, die prophylaktische Bestrahlung der Brust – und Impfungen.
Update Onkologie
Bestellen Sie unseren Fach-Newsletterund bleiben Sie gut informiert.
