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Erratum: Non-small-cell lung cancers: a heterogeneous set of diseases

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TLDR
ADCs can be modelled by KrasG12D expression (long latency), KrasD expression and Trp53-null, and epidermal growth factor receptor (EGFR)T790M/L858R, among other genetic models, and they are thought to arise from more distal airway cells.
Abstract
Nature Reviews Cancer 14, 535–546 (2014) In the original version of this article, the word 'proximal' was incorrectly used twice instead of 'distal' in two sentences in the legend for Figure 2. The sentences should have stated “ADCs can be modelled by KrasG12D expression (long latency), KrasG12D expression and Trp53-null, and epidermal growth factor receptor (EGFR)T790M/L858R, among other genetic models, and they are thought to arise from more distal airway cells.

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Neutrophils dominate the immune cell composition in non-small cell lung cancer

TL;DR: The results show that the immune cell composition is fundamentally different in lung adenocarcinoma as compared with lung squamous cell carcinoma, and that neutrophils are the most prevalent immune cell type.
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HaloTag technology: a versatile platform for biomedical applications

TL;DR: All current applications of the HaloTag technology platform for biomedical applications, such as the study of protein isolation and purification, protein function, protein–protein and protein–DNA interactions, biological assays, in vitro cellular imaging, and in vivo molecular imaging are examined.
References
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Global cancer statistics

TL;DR: A substantial proportion of the worldwide burden of cancer could be prevented through the application of existing cancer control knowledge and by implementing programs for tobacco control, vaccination, and early detection and treatment, as well as public health campaigns promoting physical activity and a healthier dietary intake.
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Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib

TL;DR: A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib, and these mutations lead to increased growth factor signaling and confer susceptibility to the inhibitor.