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BIOMARKER:

MYB-NFIB fusion

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Other names: MYB, MYB Proto-Oncogene, Transcription Factor, V-Myb Avian Myeloblastosis Viral Oncogene Homolog, Transcriptional Activator Myb, Proto-Oncogene C-Myb, Oncogene AMV, C-Myb_CDS, C-Myb, Cmyb, NFIB, Nuclear Factor I B, CCAAT-Box-Binding Transcription Factor, Nuclear Factor 1 B-Type, TGGCA-Binding Protein, Nuclear Factor I/B, Nuclear Factor 1/B, NFI-RED, NF-I/B, NF1-B, NFI-B, NFIB2, NFIB3, CTF, HMGIC/NFIB, MACID
Entrez ID:
Related biomarkers:
2ms
We report a lower rate of NFIB rearrangement and MYB- NFIB fusion than expected. In keeping with the other studies performed in this anatomical location, the prevalence of NFIB rearrangement and MYB-NFIB fusion seems to be lower in the vulva than elsewhere. Although MYB activation occurs in the majority of vulvar ACC, it is likely due to other mechanisms yet to be unravelled.
NFIB (Nuclear Factor I B)
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MYB-NFIB fusion
2ms
Six novel gene fusions other than MYB/MYBL1-NFIB were identified. The detection of novel fusion genes and investigation of the molecular mechanism will contribute to the development of novel molecular targeted therapies for this disease.
Journal • Next-generation sequencing
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NFIB (Nuclear Factor I B)
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MYB-NFIB fusion
2ms
However, this finding is sensible given that the MYB-NFIB fusion is not present in all ACC PDX models. Through our work, investigators will have a better understanding of the advantages and limitations of the utilization of the ACC PDX as a model for ACC research.
Clinical
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NFIB (Nuclear Factor I B)
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MYB-NFIB fusion
6ms
ACC is a genetically heterogenous disease with an immune-excluded microenvironment . NOTCH1 mutations were associated with worse, while MYB:NFIB fusion was not associated with prognosis . Our study shows that M2 macrophages and MYC are potential novel therapeutic targets in ACC.
TP53 (Tumor protein P53) • MYC (V-myc avian myelocytomatosis viral oncogene homolog) • NOTCH1 (Notch 1) • ARID1A (AT-rich interaction domain 1A) • KMT2C (Lysine Methyltransferase 2C) • KDM6A (Lysine Demethylase 6A) • MYB (MYB Proto-Oncogene, Transcription Factor) • EGF (Epidermal growth factor) • NFIB (Nuclear Factor I B)
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NOTCH1 mutation • MYC expression • NOTCH1 expression • MYB-NFIB fusion
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MI Tumor Seek™
6ms
Further, a rare case of a SS18-ZBTB7A rearranged low-grade adenocarcinoma previously described as potential spectrum of microsecretory adenocarcinoma, is reported. In addition, features of six cases within the spectrum of polymorphous adenocarcinoma / cribriform adenocarcinoma of salivary gland including PRKD1 p.E710D mutations and novel fusions involving PRKAR2A-PRKD1, SNX9-PRKD1 and ATL2-PRKD3, are described.
Journal • Next-generation sequencing
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RET (Ret Proto-Oncogene) • NTRK2 (Neurotrophic tyrosine kinase, receptor, type 2) • NR4A3 (Nuclear receptor subfamily 4 group A member 3) • NFIB (Nuclear Factor I B) • NTRK (Neurotrophic receptor tyrosine kinase) • SS18 (SS18 Subunit Of BAF Chromatin Remodeling Complex) • ZBTB7A (Zinc finger and BTB domain containing 7A) • MAML2 (Mastermind Like Transcriptional Coactivator 2)
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NTRK2 fusion • RET fusion • MYB-NFIB fusion
7ms
In this study, we displayed the morphologically and genetic featured PDXs which recapitulated the heterogeneity of original ACC tumors, indicating that the models could be used as a platform for drug screening for therapy response. The feasibility of combination treatment approaches for dual targets were confirmed, providing new regimens for personalized therapies in ACC.
Preclinical • Journal • Combination therapy
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PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NOTCH1 (Notch 1) • KMT2D (Lysine Methyltransferase 2D) • NOTCH2 (Notch 2) • KMT2C (Lysine Methyltransferase 2C) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • KDM6A (Lysine Demethylase 6A) • MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B)
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PIK3CA mutation • PIK3CA amplification • MYB-NFIB fusion
7ms
Further, chemotherapy (carboplatin/paclitaxel) was conducted on the PDX model. All three PDX models had histopathological features similar to those of the original tumors, and retained the MYB-NFIB fusion gene. We successfully established PDX models of adenoid cystic carcinoma, including an HGT model, which was characterized by detailed clinical and genomic information. Tumors that show HGT characteristics may be drug-sensitive, and can be used in the development of personalized cancer treatments.
Clinical
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • SOX10 (SRY-Box 10) • NFIB (Nuclear Factor I B) • TP63 (Tumor protein 63)
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MYB-NFIB fusion
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carboplatin • paclitaxel
7ms
Collectively, these findings provide a strong molecular rationale for exploring PRT543 as a potential therapeutic option for ACC tumors. PRT543 is currently under evaluation in a Phase I clinical trial in patients with advanced solid tumors and hematological malignancies (NCT03886831).
NOTCH1 (Notch 1) • MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B) • PRMT5 (Protein Arginine Methyltransferase 5) • FOXM1 (Forkhead Box M1) • GATA3 (GATA binding protein 3) • SOX4 (SRY-Box Transcription Factor 4)
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NOTCH1 mutation • NOTCH1 expression • MYB-NFIB fusion
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PRT543
8ms
Our data suggest that MYB expression by RNA ISH is sensitive and specific for AdCC, with an overall sensitivity of 87% and specificity of 91%. MYB RNA ISH assay can be applied in assisting the diagnosis of AdCC on cytology FNA samples. The significance of lower sensitivity in AdCCs from trachea and lung is uncertain, requiring future large series of studies to validate or explore further of our findings
MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B)
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MYB-NFIB fusion