Identification of a novel crizotinib-sensitive BCL11A-ALK gene fusion in a nonsmall cell lung cancer patient

Tian, Qing; Deng, Wenjing; Li, Zongwei

doi:10.1183/13993003.02149-2016

Cited by 24 publications

(15 citation statements)

References 4 publications

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“…Rearrangements of the ALK gene with partner genes other than EML4 have been described, namely, KIF5B , KLC1 , TFG , TPR , HIP1 , STRN , DCTN1 , SQSTM1 , NPM1 , BCL11A , and BIRC6 (Table ) . Targeted therapeutic agents, including the TKI crizotinib, have shown clinical efficacy in treating NSCLC patients harboring EML4‐ALK gene fusion .…”

Section: Alk Rearrangement In Non‐small Cell Lung Cancer (Nsclc)mentioning

confidence: 99%

“…21,34,36 Rearrangements of the ALK gene with partner genes other than EML4 have been described, namely, KIF5B, KLC1, TFG, TPR, HIP1, STRN, DCTN1, SQSTM1, NPM1, BCL11A, and BIRC6 (Table 3). [37][38][39][40][41][42][43][44][45][46][47][48][49][50] Targeted therapeutic agents, including the TKI crizotinib, have shown clinical efficacy in treating NSCLC patients harboring EML4-ALK gene fusion. 34 Furthermore, a previous study demonstrated that crizotinib is also effective at treating tumors harboring ALK fused with other partner genes, including NPM1 and BCL11A.…”

Section: Types Of Oncogenesis In Alkmentioning

confidence: 99%

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ALK‐rearrangement in non‐small‐cell lung cancer (NSCLC)

et al. 2018

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The ALK gene encodes a transmembrane tyrosine kinase receptor. ALK is physiologically expressed in the nervous system during embryogenesis, but its expression decreases postnatally. ALK first emerged in the field of oncology in 1994 when it was identified to fuse to NPM1 in anaplastic large‐cell lymphoma. Since then, ALK has been associated with other types of cancers, including non‐small‐cell lung cancer (NSCLC). More than 19 different ALK fusion partners have been discovered in NSCLC, including EML4, KIF5B, KLC1, and TPR. Most of these ALK fusions in NSCLC patients respond well to the ALK inhibitor, crizotinib. In this paper, we reviewed fusion partner genes with ALK, detection methods for ALK‐rearrangement (ALK‐R), and the ALK‐tyrosine kinase inhibitor, crizotinib, used in NSCLC patients.

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Section: Alk Rearrangement In Non‐small Cell Lung Cancer (Nsclc)mentioning

confidence: 99%

Section: Types Of Oncogenesis In Alkmentioning

confidence: 99%

ALK‐rearrangement in non‐small‐cell lung cancer (NSCLC)

et al. 2018

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“…172,[175][176][177] It is thought that breakpoint clustering exists in both EML4 and ALK regions leading to the prevalence of these variants, but other fusion partners with similar mutagenesis have been identified in lung cancer including huntingtin-interacting protein 1 (HIP1), kinesin family member 5B (KIF5B), kinesin light chain 1 (KLC1), Trk-fused gene (TFG), translocated promotor region (TPR), striatin (STRN), dynactin 1 (DCTN1), α-2 macroglobulin (A2M), baculoviral IAP repeat containing 6 (BIRC6), sequestosome 1 (SQSTM1), B cell CLL/lymphoma 11A (BCL11A), myelin transcription factor 1 like (MYT1L), steroid 5 α-reductase 2 (SRD5A2), and sarcolemma-associated protein (SLMAP). 169,[178][179][180][181][182][183][184][185][186][187][188][189][190] It is likely that this list will continue to grow as various fusions may lead to oncogenic pairings of promoter regions with ALK's tyrosine kinase region. It should be noted that this discussion focuses on ALK rearrangements.…”

Section: Anaplastic Lymphoma Kinase Rearrangementsmentioning

confidence: 99%

Targeted Therapy for Non-Small Cell Lung Cancer

Noor

Cummings

Johnson

et al. 2020

Semin Respir Crit Care Med

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Lung cancer is a heterogeneous disease, and the availability of comprehensive genomic profiling has allowed for the characterization of its molecular subtypes. This has increased the ability to deliver “personalized medicines” by tailoring therapies to target driver mutations in a patient's cancer. The development of targeted therapies for non-small cell lung cancer (NSCLC) has helped define the era of precision medicine throughout oncology. This article aims to contextualize recent research and provide an updated summary of targeted therapies available for patients with NSCLC. With practitioners and clinical researchers in mind, we note standard of care therapies, important approvals, practice guidelines, and treatments in development. The first section discusses mutations in the epidermal growth factor receptor (EGFR) gene, and the second section examines rearrangements in the anaplastic lymphoma kinase (ALK) and ROS1 fusions. Finally, we explore the rarer molecular alterations in BRAF, RET, MET, HER2, and KRAS. Given the many available therapies, it is important to understand the molecular alterations in NSCLC, and how to target them.

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“…1 In recent years, other fusion types sensitive to crizotinib, such as DYS-F&ITGAV-ALK, BCL11A-ALK, and BIRC6-ALK, have been discovered by next-generation sequencing (NGS). [2][3][4][5][6] However, a WD (Trp-Asp) planar cell polarity (PCP) effector gene (WDPCP)-ALK fusion has not been previously published. Here, we report this novel WDPCP-ALK fusion, which is sensitive to crizotinib, in a patient with lung adenocarcinoma.…”

Section: Introductionmentioning

confidence: 99%

Next-generation Sequencing Identified a Novel WDPCP-ALK Fusion Sensitive to Crizotinib in Lung Adenocarcinoma

et al. 2019

Clinical Lung Cancer

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Identification of a novel crizotinib-sensitive BCL11A-ALK gene fusion in a nonsmall cell lung cancer patient

Cited by 24 publications

References 4 publications

ALK‐rearrangement in non‐small‐cell lung cancer (NSCLC)

ALK‐rearrangement in non‐small‐cell lung cancer (NSCLC)

Targeted Therapy for Non-Small Cell Lung Cancer

Next-generation Sequencing Identified a Novel WDPCP-ALK Fusion Sensitive to Crizotinib in Lung Adenocarcinoma

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