LMO1 Synergizes with MYCN to Promote Neuroblastoma Initiation and Metastasis

Zhu, Shizhen; Zhang, Xiaoling; Weichert-Leahey, Nina; Dong, Zhiwei; Zhang, Cheng; Lopez, Gonzalo; Tao, Ting; He, Shuning; Wood, Andrew C.; Oldridge, Derek A.; Ung, Choong Yong; Ree, Janine H. van; Khan, Adam Z.; Salazar, Brittany M.; Rocha, Edroaldo Lummertz da; Zimmerman, Mark W.; Guo, Feng; Cao, Hong; Hou, Xiaonan; Weroha, S. John; Perez‐Atayde, Antonio R.; Neuberg, Donna; Meves, Alexander; McNiven, Mark A.; Deursen, Jan M. van; Li, Hu; Maris, John M.; Look, A. Thomas

doi:10.1016/j.ccell.2017.08.002

Cited by 82 publications

(88 citation statements)

References 58 publications

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“…MYCN is involved in cell proliferation, apoptosis, survival and differentiation (62). Neuroblastoma models in which MYCN is overexpressed in the neural crest lead to neuroblastoma tumor development, that is accelerated by cooperation with other oncogenes and tumor suppressor genes, such as ALK, NF1, TP53, LIN28B and LMO1, driving increased penetrance and earlier onset of neuroblastoma (63)(64)(65)(66)(67)(68). Other factors, which also contribute to neuroblastoma tumorigenesis, are loss of heterozygosity (LOH) for chromosome 14 (14q), loss of NF1 and CDKN2A, amplification of DDX1 and MDM2, aberrant expression of neurotrophin receptors, ganglioside GD2, polycomb complex protein Bmi-1, micro RNAs (miR-10b, miR-29a/b, miR-335), as well as mutations in PHOX2B, ATRX, CHEK2 and BARD1 (53,(69)(70)(71)(72)(73)(74)(75)(76)(77).…”

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confidence: 99%

Targeting anaplastic lymphoma kinase in neuroblastoma

Umapathy

Mendoza-García

Hållberg

et al. 2019

APMIS

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Over the last decade, anaplastic lymphoma kinase (ALK), a receptor tyrosine kinase (RTK), has been identified as a fusion partner in a diverse variety of translocation events resulting in oncogenic signaling in many different cancer types. In tumors where the full‐length ALK RTK itself is mutated, such as neuroblastoma, the picture regarding the role of ALK as an oncogenic driver is less clear. Neuroblastoma is a complex and heterogeneous tumor that arises from the neural crest derived peripheral nervous system. Although high‐risk neuroblastoma is rare, it often relapses and becomes refractory to treatment. Thus, neuroblastoma accounts for 10–15% of all childhood cancer deaths. Since most cases are in children under the age of 2, understanding the role and regulation of ALK during neural crest development is an important goal in addressing neuroblastoma tumorigenesis. An impressive array of tyrosine kinase inhibitors (TKIs) that act to inhibit ALK have been FDA approved for use in ALK‐driven cancers. ALK TKIs bind differently within the ATP‐binding pocket of the ALK kinase domain and have been associated with different resistance mutations within ALK itself that arise in response to therapeutic use, particularly in ALK‐fusion positive non‐small cell lung cancer (NSCLC). This patient population has highlighted the importance of considering the relevant ALK TKI to be used for a given ALK mutant variant. In this review, we discuss ALK in neuroblastoma, as well as the use of ALK TKIs and other strategies to inhibit tumor growth. Current efforts combining novel approaches and increasing our understanding of the oncogenic role of ALK in neuroblastoma are aimed at improving the efficacy of ALK TKIs as precision medicine options in the clinic.

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mentioning

confidence: 99%

Targeting anaplastic lymphoma kinase in neuroblastoma

Umapathy

Mendoza-García

Hållberg

et al. 2019

APMIS

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“…Similarly, in the prostate adenocarcinoma model initiated by Pten mutation, further loss of Rb1 leads to metastasis formation (Ku et al, 2017). Using a genome-wide association study (GWAS) approach, Zhu et al (2017) found that expression of LIM-domain-only gene ( LMO1 ) in a zebrafish model promoted metastatic neuroblastoma driven by the MYCN oncogene. Together, these studies suggest that cooperation of multiple genomic variations could promote the metastatic abilities of tumor cells.…”

Section: Genetics and Genomics Of Metastatic Tumor Cellsmentioning

confidence: 99%

Metastatic tumor cells – genotypes and phenotypes

Gao

Mittal

et al. 2018

Front. Biol.

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BACKGROUND: Metastasis is the primary cause of mortality in cancer patients. Therefore, elucidating the genetics and epigenetics of metastatic tumor cells and the mechanisms by which tumor cells acquire metastatic properties constitute significant challenges in cancer research. OBJECTIVE: To summarize the current understandings of the specific genotype and phenotype of the metastatic tumor cells. METHOD and RESULT: In-depth genetic analysis of tumor cells, especially with advances in the next-generation sequencing, have revealed insights of the genotypes of metastatic tumor cells. Also, studies have shown that the cancer stem cell (CSC) and epithelial to mesenchymal transition (EMT) phenotypes are associated with the metastatic cascade. CONCLUSION: In this review, we will discuss recent advances in the field by focusing on the genomic instability and phenotypic dynamics of metastatic tumor cells.

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“…Delloye-Bourgeois et al highlight the considerable power of the chick embryo model for neuroblastoma. Zhu and colleagues have also shown that they can model metastasis in zebrafish, where overexpressing the transcriptional regulators LMO1 and MYCN led to metastatic spread (Zhu et al, 2017). These non-mammalian vertebrate models are already improving our understanding of metastatic neuroblastoma, and have potential to identify candidate targets for future clinical trials.…”

Section: Previewmentioning

confidence: 99%