The role of novel fusion genes in human GIST cell lines derived from imatinib-resistant GIST patients: A therapeutic potential of fusion gene

Cho, Woo Cheol; Shin, Young Kee; Na, Young Soon; Ryu, Min Hee; Ku, Ja Lok; Kang, Yoon Koo

doi:10.1016/j.bbrc.2020.05.174

Cited by 12 publications

(10 citation statements)

References 23 publications

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“…Describing the GIST metabolome thoroughly and continuing the research on its response to TKIs can support the ongoing research on treatment effectiveness problems in GIST patients. Although the genetic causes of primary or secondary tumour resistance are described in the literature, 53–55 metabolomic studies are necessary to find biochemical processes influenced by imatinib. By comparing a few mutational models, including imatinib-sensitive and resistant GISTs, specific metabolic pathways common for effective treatment may be recognised.…”

Section: Resultsmentioning

confidence: 99%

A multiplatform metabolomics approach for comprehensive analysis of GIST xenografts with various KIT mutations

Macioszek

Dudzik

Biesemans

et al. 2023

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Section: Resultsmentioning

confidence: 99%

A multiplatform metabolomics approach for comprehensive analysis of GIST xenografts with various KIT mutations

Macioszek

Dudzik

Biesemans

et al. 2023

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“…Further analysis of demographic and pathological data, and genomic profiling of qWT GISTs, can help to further clarify the largely undefined pathobiology of this GIST subtype. Additionally, this next-generation sequencing may reveal genomic alterations that are potentially targetable and therefore clinically relevant [5].…”

Section: Discussionmentioning

confidence: 99%

A Rare Case of Quadruple Negative GIST with an Unusual Presentation in a Young Female

Valasapalli¹,

Sathe²

2021

J Oncol Res Rev Rep

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Gastrointestinal stromal tumors (GISTs) are an uncommon malignancy, with origin in the interstitial cells of Cajal located in the myenteric plexus. The incidence is 5000 new cases every year in the US. It is important to determine genetic alterations in GIST. Approximately 90% of GISTs have a gain of function mutation in either the c-KIT protooncogene (which encodes for the receptor tyrosine kinase KIT) accounting for 75%, or the platelet derived growth factor receptor alpha (PDGFRA) protooncogene which accounts for 15%. Only 5-10% constitute Wild Type (WT) GISTs with mutations observed in BRAF, NF1, & SDH. While Imatinib, a Tyrosine Kinase Inhibitor (TKI), is used as adjuvant therapy for most KIT-positive tumors, it cannot be used in TKI-resistant tumors that harbor alternative genetic mutations. We present a rare case of quadruple negative (negative for all aforementioned genes) GIST with a mutation identified as ETV6-NTRK3 fusion. This mutation was first described in a case of rectal quadruple negative WT GIST.

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“…In addition, we have reported that patients with protein overexpression of actinin-4 had a worse prognosis than patients without overexpression in breast (4,12), pancreas (16,17), ovarian (13)(14)(15), thyroid (18), salivary gland (19), and tongue cancers (20). Moreover, involvement in malignant phenotypes for protein overexpression of actinin-4 was reported in brain tumors (21)(22)(23), head and neck cancer (24,25), lung cancer (26)(27)(28), breast cancer (29)(30)(31), esophageal cancer (32), gastric cancer (33), pancreatic cancer (34), gastrointestinal stromal tumor (GIST) (35), cervical cancer (36), ovarian cancer, bladder cancer (37), prostate cancer (38,39), melanoma (40,41), leukemia (42,43), and osteosarcoma (44,45) from not only our groups, but also other independent groups. In fact, use of an exogenous transfection technique to overexpress actinin-4 in cancer cells demonstrated that cancer cells overexpressing actinin-4 can form the protrusions that are involved in cell motility and cancer invasion and exhibit significantly increased invasive potential (6).…”

Section: Identification Of Actinin-4 That Is Associated With Cancer Invasion and Metastasismentioning

confidence: 99%

Development of Biomarkers to Predict Recurrence by Determining the Metastatic Ability of Cancer Cells

Honda

2022

J Nippon Med Sch

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Adjuvant chemotherapy has been carried out for patients with cancer who underwent curative resection, but it is basically not needed for patients without micro-metastatic lesions who undergo a perfectly curative surgical operation. The patients who need adjuvant chemotherapy are defined as those whose micrometastases cannot be detected by imaging modalities in the other sites of the resective areas, despite curative resection for the primary sites. If biomarkers to efficiently evaluate the metastatic potential of each patient could be developed, we may be able to provide personalized adjuvant chemotherapy in the clinical setting. Actinin-4 (ACTN4, gene name ACTN4) is an actin-bundling protein that we identified in 1998 as a novel molecule involved in cancer invasion and metastasis. Protein overexpression of actinin-4 in cancer cells leads to the invasive phenotype, and patients with gene amplification of ACTN4 have a worse prognosis than patients with a normal copy number in some cancers, including pancreas, lung, and salivary gland cancers. In this review, the biological roles of actinin-4 for cancer invasion and metastasis are summarized, and the potential usefulness of actinin-4 as a biomarker for evaluation of metastatic ability is examined.

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The role of novel fusion genes in human GIST cell lines derived from imatinib-resistant GIST patients: A therapeutic potential of fusion gene

Cited by 12 publications

References 23 publications

A multiplatform metabolomics approach for comprehensive analysis of GIST xenografts with various KIT mutations

A multiplatform metabolomics approach for comprehensive analysis of GIST xenografts with various KIT mutations

A Rare Case of Quadruple Negative GIST with an Unusual Presentation in a Young Female

Development of Biomarkers to Predict Recurrence by Determining the Metastatic Ability of Cancer Cells

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