NFIB
Overview
NFIB (nuclear factor I/B) is a transcription factor involved in neural progenitor self-renewal and glial differentiation. In oligodendroglioma, NFIB is expressed as part of the stem/progenitor transcriptional program that characterizes the rare cycling subpopulation at the apex of the tumor’s developmental hierarchy.
Alterations observed in the corpus
- NFIB is a component of the stem/progenitor gene program in grade II oligodendroglioma (IDH-mutant, 1p/19q codeleted), co-expressed with SOX2, SOX4, SOX11, ASCL1, CHD7, CD24, BOC, TCF4, and CCND2 in the rare proliferating subpopulation (1.5–8% of all cells) PMID:27806376.
- NFIB amplification in mouse SCLC; copy number gain observed in 3 human SCLC samples (CLCGP, 29 tumors) PMID:22941188
- NFIB copy-number amplification confirmed as a recurrent alteration in SCLC (JHU WES/WGS, 36 tumors) PMID:22941189
- Candidate oncogenic driver on 9p in OSCC; high-level amplification detected in 3/38 tumors despite background 9p loss in other tumors, suggesting positive selection for NFIB gain (40-tumor MD Anderson OSCC cohort) PMID:23619168
- MYB-NFIB fusion (t(6;9)) identified as the dominant structural lesion in adenoid cystic carcinoma (ACC); NFIB also bears independent truncating CTF/NFI mutations (Y249*, P390fs) and 4 homozygous deletions in 57 ACC cases PMID:23685749
- NFIB is the translocation partner of MYB in 19/24 ACC cases (t(6;9)); SNP6 copy-number breakpoints at the NFIB locus confirmed in MYB-activated cases PMID:23778141
- Recipient fusion partner in canonical MYB::NFIB (49/88, 57%) and MYBL1::NFIB (9/88, 10%) fusions in sinonasal adenoid cystic carcinoma; FISH detected an additional NFIB rearrangement in one fusion-negative case PMID:24418857
- Identified as 3′ fusion partner in MYB-NFIB chimeric transcripts (NFIB exon 8c or 9 fused to MYB exon 14) in 83% (10/12) of breast adenoid cystic carcinomas (AdCC). PMID:26095796
- 5’ end (exons 1-2) fuses with diverse partners (MYB, MYBL1, XRCC4, PTPRD, NKAIN2, AIG1) in adenoid cystic carcinoma; breakpoints in MYBL1-NFIB cluster in intron 10; present as fusion partner in ~53% (MYB-NFIB) and ~14% (MYBL1-NFIB) of 102-tumor ACC cohort PMID:26631609
- Partner locus in NFIB–MYB rearrangements (12/20 ACC tumors: 6 with 3′UTR loss, 6 with retained 3′UTR); hosts super-enhancers that translocate to MYB driving overexpression PMID:26829750
- Translocation target in 15/25 ACC tumors (60%) with five distinct fusion partners (MYB, MAP3K5, MYBL1, RIMS1, MYO6, RPS6KA2); overexpressed vs. normal (p=0.002) independent of fusion status (p=0.91), implicating a fusion-independent oncogenic role PMID:26862087
Cancer types (linked)
- ODG — NFIB marks the neural stem/progenitor-like subpopulation in oligodendroglioma; this proliferating fraction is the likely driver of tumor growth PMID:27806376.
Co-occurrence and mutual exclusivity
Therapeutic relevance
- NFIB-expressing stem/progenitor cells represent a plausible therapeutic target in oligodendroglioma; the differentiated compartment is non-proliferating and may be less sensitive to standard cytotoxic therapies PMID:27806376.
Open questions
- The upstream regulators of NFIB in the oligodendroglioma stem/progenitor context, and whether NFIB is required for tumor self-renewal, are not addressed PMID:27806376.
Sources
This page was processed by crosslinker on 2026-05-14. - PMID:22941188
This page was processed by crosslinker on 2026-05-14. - PMID:22941189
This page was processed by crosslinker on 2026-05-14. - PMID:23619168
This page was processed by crosslinker on 2026-05-14. - PMID:23685749
This page was processed by crosslinker on 2026-05-14. - PMID:23778141
This page was processed by crosslinker on 2026-05-14. - PMID:24418857
This page was processed by crosslinker on 2026-05-14. - PMID:26095796
This page was processed by crosslinker on 2026-05-14. - PMID:26631609
This page was processed by crosslinker on 2026-05-14. - PMID:26829750
This page was processed by wiki-cli on 2026-05-14. - PMID:26862087
This page was processed by wiki-cli on 2026-05-14.