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BIOMARKER:

MYB-NFIB fusion

i
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:
6d
Impact of NOTCH1 expression in primary breast adenoid cystic carcinoma. (PubMed, J Clin Pathol)
Our study demonstrates that in patients with breast AdCC, overexpression of NOTCH1 ≥20% is associated with larger tumour size and aggressive clinical outcomes. Importantly, NOTCH1 inhibitors may have potential therapeutic effect in patients with breast AdCC.
Journal
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NOTCH1 (Notch 1) • NFIB (Nuclear Factor I B)
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NOTCH1 expression • MYB-NFIB fusion • NOTCH1 overexpression
29d
Adenoid cystic carcinoma of the Bartholin's gland is underpinned by MYB- and MYBL1- rearrangements. (PubMed, Gynecol Oncol)
AdCC-BGs constitute a convergent phenotype, whereby activation of MYB or MYBL1 can be driven by the MYB::NFIB fusion gene or MYBL1 rearrangements. Our observations further support the notion that AdCCs, irrespective of organ site, constitute a genotypic-phenotypic correlation. Assessment of MYB or MYBL1 rearrangements may be used as an ancillary marker for the diagnosis of AdCC-BGs.
Journal • IO biomarker
|
BCL2 (B-cell CLL/lymphoma 2) • GNAQ (G Protein Subunit Alpha Q) • AKT1 (V-akt murine thymoma viral oncogene homolog 1) • EWSR1 (EWS RNA Binding Protein 1) • RAD51B (RAD51 Paralog B) • KDM6A (Lysine Demethylase 6A) • GNAS (GNAS Complex Locus) • NFIB (Nuclear Factor I B) • MYBL1 (MYB Proto-Oncogene Like 1)
|
MYB-NFIB fusion
2ms
Adenoid Cystic Carcinoma of the Vulva and Vagina: A Clinicopathologic, Immunohistochemical, and Molecular Characterization of Five Cases. (PubMed, Int J Gynecol Pathol)
There were no MYBL1 or NFIB rearrangements and no MYB::NFIB fusions. Our findings corroborate that the histologic, immunohistochemical, and oncogenic background is similar between ACCs of the lower female genital tract and ACCs elsewhere, although the canonical MYB::NFIB fusion seems to be a less common finding in this location.
Journal
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KIT (KIT proto-oncogene, receptor tyrosine kinase) • NFIB (Nuclear Factor I B) • ANO1 (Anoctamin 1) • MYBL1 (MYB Proto-Oncogene Like 1)
|
MYB-NFIB fusion
4ms
Molecular characterisation of tumours of the lacrimal apparatus. (PubMed, Histopathology)
Our study highlights the variety of molecular alterations associated with lacrimal system tumours and emphasises the importance of molecular testing in these tumours, which can reveal potentially targetable mutations. Our results also reinforce the hypothesis of a common physiopathology of all ACCs, regardless of their primary location.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • TP53 (Tumor protein P53) • FGFR2 (Fibroblast growth factor receptor 2) • ATM (ATM serine/threonine kinase) • NOTCH1 (Notch 1) • NFIB (Nuclear Factor I B) • MYBL1 (MYB Proto-Oncogene Like 1)
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TP53 mutation • HER-2 amplification • HER-2 mutation • ATM mutation • FGFR2 mutation • FGFR2 fusion • CIC mutation • MYB-NFIB fusion
6ms
The Role of Novel Immunohistochemical Markers for Special Types of Breast Carcinoma. (PubMed, Adv Anat Pathol)
Immunohistochemical antibodies have emerged that identify the underlying genetic alterations in these tumors and serve as useful diagnostic tools. This review will provide an update on the molecular features and diagnostic immunohistochemical markers that have become increasingly popular to aid in diagnosing these uncommon triple-negative breast tumors.
Journal
|
HER-2 (Human epidermal growth factor receptor 2) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • ETV6 (ETS Variant Transcription Factor 6) • MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B)
|
NTRK3 fusion • HER-2 expression • ETV6-NTRK3 fusion • MYB-NFIB fusion
7ms
Solid-basaloid adenoid cystic carcinoma of the breast: an aggressive subtype enriched for Notch pathway and chromatin-modifier mutations with MYB overexpression. (PubMed, Mod Pathol)
The data highlight the histopathologic spectrum of basaloid carcinomas including SB-AdCC and reveal shared genetics and MYB activation, which can be diagnostically useful. Aggressive behavior and poor treatment responses emphasize a need for additional treatment approaches.
Journal
|
TP53 (Tumor protein P53) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • NOTCH1 (Notch 1) • NOTCH2 (Notch 2) • CREBBP (CREB binding protein) • SOX10 (SRY-Box 10) • NFIB (Nuclear Factor I B) • TP63 (Tumor protein 63) • GATA3 (GATA binding protein 3)
|
TP53 mutation • MYB-NFIB fusion
8ms
A RARE CASE OF ADENOID CYSTIC CARCINOMA OF THE LUNG (CHEST 2023)
This case highlights a rare presentation of primary adenoid cystic carcinoma of the lung treated with curative robot assisted surgical resection.
Clinical
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NFIB (Nuclear Factor I B) • MYBL1 (MYB Proto-Oncogene Like 1)
|
MYB-NFIB fusion
12ms
Increased retinoic acid signaling decreases lung metastasis in salivary adenoid cystic carcinoma by inhibiting the noncanonical Notch1 pathway. (PubMed, Exp Mol Med)
Bioinformatic, RNA-seq, and immunohistochemical (IHC) analyses of primary tissues and metastatic lung tissues from patients with SACC suggested that RA system insufficiency partially promotes lung metastasis. These findings imply the value of the RA system in diagnosis and treatment.
Journal
|
NOTCH1 (Notch 1) • MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B)
|
NOTCH1 mutation • NOTCH1 expression • MYB-NFIB fusion
over1year
Rearrangements, Expression, and Clinical Significance of MYB and MYBL1 in Adenoid Cystic Carcinoma: A Multi-Institutional Study. (PubMed, Cancers (Basel))
We hypothesize that loss of the 3'-part of MYB results from an unbalanced t(6;9) leading to an MYB-NFIB fusion with concomitant loss of the segment distal to the MYB breakpoint in 6q23.3. Our study provides new knowledge about the prevalence and clinical significance of MYB/MYBL1 alterations and indicates the presence of genes with tumor suppressive functions in 6q23.3-qter that contribute to poor prognosis and short overall survival in ACC.
Clinical • Journal
|
MYB (MYB Proto-Oncogene, Transcription Factor) • NFIB (Nuclear Factor I B) • MYBL1 (MYB Proto-Oncogene Like 1)
|
MYB-NFIB fusion
over1year
MYB-NFIB fusion transcript in Adenoid Cystic Carcinoma: current state of knowledge and future directions. (PubMed, Crit Rev Oncol Hematol)
In vitro and in vivo studies have been conducted to understand the biological consequences of MYB-NFIB translocation, and such findings could contribute to improving the current inefficient therapeutic options for disseminated ACC. This review provides a discussion on relevant evidence in the context of ACC MYB-NFIB translocations to determine the current state of knowledge and discuss future directions.
Review • Journal
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NFIB (Nuclear Factor I B)
|
MYB-NFIB fusion
almost2years
Analysis of Human Papillomavirus (HPV) and Polyomaviruses (HPyVs) in Adenoid Cystic Carcinoma (AdCC) of the Head and Neck Region Reveals Three HPV-Positive Cases with Adenoid Cystic-like Features. (PubMed, Viruses)
We conclude that HPV and HPyV have no major role in AdCC. However, based on our data, we also suggest that HMSC should be considered as a basaloid variant of squamous cell carcinoma, and not its own entity, until better characterized.
Journal
|
KIT (KIT proto-oncogene, receptor tyrosine kinase) • NFIB (Nuclear Factor I B) • TP63 (Tumor protein 63)
|
MYB-NFIB fusion
almost2years
Development and Characterization of MYB-NFIB Fusion Expression in Adenoid Cystic Carcinoma. (PubMed, Cancers (Basel))
In vivo tumor formation analysis indicated the capacity of MYB-NFIB fusion cells to grow as implanted tumors, although there were no fusion-mediated growth advantages. This expression system may be useful not only in studies to determine the functional aspects of MYB-NFIB fusion but also in evaluating effective drug response in vitro and in vivo settings.
Journal
|
NFIB (Nuclear Factor I B)
|
MYB-NFIB fusion
almost2years
Fusion-Associated Carcinomas of the Breast: Diagnostic, Prognostic, and Therapeutic Significance. (PubMed, Genes Chromosomes Cancer)
Examples of the most significant recurrent gene fusions to date include (1) ESR1::CCDC170 gene fusions in luminal B and endocrine-resistant breast cancer that exert oncogenic function via modulating the HER2/HER3/SRC Proto-Oncogene (SRC) complex, (2) ESR1 exon 6 fusions in metastatic disease that drive estrogen-independent estrogen-receptor transcriptional activity, (3) BCL2L14::ETV6 fusions in a more aggressive form of the triple-negative subtype that prime epithelial-mesenchymal transition and endow paclitaxel resistance, (4) the ETV6::NTRK3 fusion in secretory breast carcinoma that constitutively activates NTRK3 kinase, (5) the oncogenic MYB-NFIB fusion as a genetic driver underpinning adenoid cystic carcinomas of the breast that activates MYB Proto-Oncogene (MYB) pathway, and (6) the NOTCH/microtubule-associated serine-threonine (MAST) kinase gene fusions that activate NOTCH and MAST signaling...Thus, these gene fusions could be utilized as genetic biomarkers to identify patients that require more intensive treatment and surveillance. In addition, kinase fusions are currently being evaluated in breast cancer clinical trials and on-going mechanistic investigation is exposing therapeutic vulnerabilities in patients with fusion positive disease.
Review • Journal
|
HER-2 (Human epidermal growth factor receptor 2) • ER (Estrogen receptor) • NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • ERBB3 (V-erb-b2 avian erythroblastic leukemia viral oncogene homolog 3) • ETV6 (ETS Variant Transcription Factor 6) • SRC (SRC Proto-Oncogene) • CCDC170(Coiled-Coil Domain Containing 170) • NFIB (Nuclear Factor I B)
|
NTRK3 fusion • ER-CCDC170 fusion • MYB-NFIB fusion
|
paclitaxel
2years
The evolving role of molecular pathology in the diagnosis of salivary gland tumours with potential pitfalls. (PubMed, Eur Arch Otorhinolaryngol)
This includes CRTC1-MAML2 and CRTC-MAML2 in mucoepidermoid carcinoma, MYBNFIB and MYBL1-NFIB fusions in adenoid cystic carcinoma, PLAG1 and HMGA2 in pleomorphic adenoma, ETV6-NTRK3 in secretory carcinoma, NR4A3 rearrangements in acinic cell carcinoma, PRKD1 mutations in polymorphous adenocarcinoma and EWSR1-ATF1 in clear cell carcinoma. This review is a lens for progress made till date in the molecular pathology of salivary gland tumours with a special focus on their role as diagnostic tools and implications on clinical management of the patient as prognostic and predictive markers.
Review • Journal
|
NTRK3 (Neurotrophic tyrosine kinase, receptor, type 3) • ETV6 (ETS Variant Transcription Factor 6) • EWSR1 (EWS RNA Binding Protein 1) • NR4A3 (Nuclear receptor subfamily 4 group A member 3) • HMGA2 (High mobility group AT-hook 2) • NFIB (Nuclear Factor I B) • ATF1 (Activating Transcription Factor 1) • PLAG1 (PLAG1 Zinc Finger) • CRTC1 (CREB Regulated Transcription Coactivator 1) • MAML2 (Mastermind Like Transcriptional Coactivator 2) • MYBL1 (MYB Proto-Oncogene Like 1) • PRKD1 (Protein Kinase D1)
|
MYB-NFIB fusion
over2years
Detection of novel fusion genes by next-generation sequencing-based targeted RNA sequencing analysis in adenoid cystic carcinoma of head and neck. (PubMed, Oral Surg Oral Med Oral Pathol Oral Radiol)
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)
|
MYB-NFIB fusion
over2years
[VIRTUAL] Characterization of the Transcriptome of the Adenoid Cystic Carcinoma Patient- derived Xenograft (AHNS 2021)
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
|
NFIB (Nuclear Factor I B)
|
MYB-NFIB fusion
almost3years
[VIRTUAL] Comprehensive genomic profiling and immune characterization of adenoid cystic carcinoma. (ASCO 2021)
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) • ARID1A (AT-rich interaction domain 1A) • NOTCH1 (Notch 1) • KMT2C (Lysine Methyltransferase 2C) • KDM6A (Lysine Demethylase 6A) • MYB (MYB Proto-Oncogene, Transcription Factor) • EGF (Epidermal growth factor) • NFIB (Nuclear Factor I B)
|
NOTCH1 mutation • MYC expression • NOTCH1 expression • MYB-NFIB fusion
|
MI Tumor Seek™
almost3years
SalvGlandDx - a comprehensive salivary gland neoplasm specific next generation sequencing panel to facilitate diagnosis and identify therapeutic targets. (PubMed, Neoplasia)
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)
|
NTRK2 fusion • RET fusion • MYB-NFIB fusion
almost3years
Establishment of patient-derived xenograft models of adenoid cystic carcinoma to assess pre-clinical efficacy of combination therapy of a PI3K inhibitor and retinoic acid. (PubMed, Am J Cancer Res)
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
|
PIK3CA (Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) • NOTCH1 (Notch 1) • KMT2D (Lysine Methyltransferase 2D) • SMARCA4 (SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily A, member 4) • KMT2C (Lysine Methyltransferase 2C) • NOTCH2 (Notch 2) • 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
3years
[VIRTUAL] Establishment of clinically and genetically well-annotated patient-derived xenografts of adenoid cystic carcinoma with high-grade transformation (AACR 2021)
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
|
KIT (KIT proto-oncogene, receptor tyrosine kinase) • SOX10 (SRY-Box 10) • NFIB (Nuclear Factor I B) • TP63 (Tumor protein 63)
|
MYB-NFIB fusion
|
carboplatin • paclitaxel