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Alectinib

Summary[edit]

Description
English: Figure 1. ALK-rearrangement-targeted cancer therapy in non-small cell lung cancer. EML4-ALK translocation activates PI3K-AKT, RAS, and JAK/STAT signaling cascades, thereby influencing tumor progression, survival, and growth. ALK inhibitors such as crizotinib, alectinib, and brigatinib act on mutated ALKs, such as ELM4-ALK, and suppress the production of ALK fusion protein resulting from ALK rearrangement. EML4-ALK, echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase; ALK, anaplastic lymphoma kinase; PI3K, phosphatidylinositol-3 kinase; mTOR, mammalian target of rapamycin; RAS, reticular activating system; MEK, mitogen-activated extracellular signal regulated kinase; ERK, extracellular signal-regulated kinase (ERK); JAK, Janus kinase; STAT, signal transducer and activator of transcription.
Date
Source https://www.mdpi.com/2072-6694/12/4/942
Author Ando, K.; Akimoto, K.; Sato, H.; Manabe, R.; Kishino, Y.; Homma, T.; Kusumoto, S.; Yamaoka, T.; Tanaka, A.; Ohmori, T.;Hironori Sagara

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current18:20, 21 March 2024Thumbnail for version as of 18:20, 21 March 2024550 × 312 (245 KB)Ozzie10aaaa (talk | contribs)Uploaded a work by Ando, K.; Akimoto, K.; Sato, H.; Manabe, R.; Kishino, Y.; Homma, T.; Kusumoto, S.; Yamaoka, T.; Tanaka, A.; Ohmori, T.;Hironori Sagara from https://www.mdpi.com/2072-6694/12/4/942 with UploadWizard

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