HIP1–ALK, a Novel Fusion Protein Identified in Lung Adenocarcinoma

Hong, Mineui; Kim, Ryong Nam; Song, Ji-Young; Choi, Seong Hee; Oh, Ensel; Lira, Maruja E.; Mao, Mao; Takeuchi, Kengo; Han, Joungho; Kim, Young Tae; Choi, Yoon–La

doi:10.1097/jto.0000000000000061

Cited by 58 publications

(46 citation statements)

References 14 publications

(13 reference statements)

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“…Several non-EML4 ALK fusion partners are known [13][14][15][16], and the transforming potential of both KIF5B-ALK and KSC1-ALK has been confirmed by preclinical modeling. We further report three novel fusion partners for ALK, including validation that the in vitro crizotinibsensitive transforming activity of the PRKAR1A-ALK fusion was consistent with an in vivo response to crizotinib in the corresponding clinical case.…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Genomic Profiling Identifies a Subset of Crizotinib-Responsive ALK-Rearranged Non-Small Cell Lung Cancer Not Detected by Fluorescence In Situ Hybridization

Ali¹,

Hensing

Schrock³

et al. 2016

The Oncologist

111

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Introduction. For patients with non-small cell lung cancer (NSCLC) tobenefitfromALKinhibitors,sensitiveandspecificdetectionofALK genomic rearrangements is needed. ALK break-apart fluorescence in situ hybridization (FISH) is the U.S. Food and Drug Administration approved and standard-of-care diagnostic assay, but identification of ALK rearrangements by other methods reported in NSCLC cases that tested negative for ALK rearrangements by FISH suggests a significant false-negative rate. We report here a large series of NSCLC cases assayed by hybrid-capture-based comprehensive genomic profiling (CGP) in the course of clinical care. Materials and Methods. Hybrid-capture-based CGP using nextgenerationsequencingwasperformedinthe course ofclinicalcare of 1,070 patients with advanced lung cancer. Each tumor sample was evaluated for all classes of genomic alterations, including base-pair substitutions, insertions/deletions, copy number alterations and rearrangements, as well as fusions/rearrangements.

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Section: Discussionmentioning

confidence: 99%

Comprehensive Genomic Profiling Identifies a Subset of Crizotinib-Responsive ALK-Rearranged Non-Small Cell Lung Cancer Not Detected by Fluorescence In Situ Hybridization

Ali¹,

Hensing

Schrock³

et al. 2016

The Oncologist

111

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“…Some novel fusion genes of ALK rearrangement have recently been published but their clinical relevance is not yet clear [3,4]. The coexpression of different ALK splicing isoforms were presented in NSCLC and the results indicate that the response to crizotinib may also depend on the ALK splicing type [5].…”

Section: Discussionmentioning

confidence: 95%

Identification of atypical ATRNL1 insertion to EML4-ALK fusion gene in NSCLC

et al. 2015

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“…26 The EML4-ALK fusion protein has oncogenic signaling capabilities similar to activated EGFR because the fusion protein aberrantly dimerizes in the cell cytoplasm and subsequently constitutively activates the mitogen-activated protein kinase (MAPK) pathway. Additional ALK fusion genes are described, [27][28][29] but they are infrequent ( Table 1).…”

mentioning

confidence: 97%