Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
IGF2/IGF1R Signaling as a Therapeutic Target in MYB-Positive Adenoid Cystic Carcinomas and Other Fusion Gene-Driven Tumors.
|
31426421 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We observed tumor inhibition using a novel MYB peptidomimetic in both human and murine tumor models.
|
31606723 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The aim of this meta-analysis is to evaluate myeloblastosis (MYB) as a prognostic marker for patients with adenoid cystic carcinoma (ACC) with respect to MYB gene fusion, MYB protein expression, and tumor sites.
|
30759319 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Analysis of the DNase1 gene regulatory network identified dense interconnectivity among PLAG1, MYB, and 13 other transcription factors associated with balanced chromosomal translocations and salivary gland tumors.
|
30392435 |
2019 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The protein is frequently overexpressed in human leukemias, breast cancers, and other solid tumors suggesting that it is a bona fide oncogene. c-MYB is often overexpressed by translocation in human tumors with t(6;7)(q23;q34) resulting in c-MYB-TCRβ in T cell ALL, t(X;6)(p11;q23) with c-MYB-GATA1 in acute basophilic leukemia, and t(6;9)(q22-23;p23-24) with c-MYB-NF1B in adenoid cystic carcinoma.
|
30599775 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RNA-seq analysis revealed that ARQ531 constrained tumor cell proliferation and survival through Bruton's tyrosine kinase and transcriptional program dysregulation, with proteasome-mediated MYB degradation and depletion of short-lived proteins that are crucial for tumor growth and survival, including ERK, MYC and MCL1.
|
31624110 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumor angiogenesis was evaluated by blood vessel (CD31-positive) density and tumor proliferation by Ki-67 labeling index, and the relationship with MYB-NFIB chimeric gene expression was analyzed.
|
29243184 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Retinoic acid agonists inhibited tumor growth in vivo in ACC patient-derived xenograft models and decreased MYB binding at translocated enhancers, thereby potentially diminishing the MYB positive feedback loop driving ACC.
|
30209067 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
MYB immunostaining was seen in 5 of 5 fusion-positive cases, and also 9 of 23 fusion-negative tumors.
|
29135517 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In recent years, the roles of MYB in tumor transformation have become increasingly clear.
|
29675107 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Aberrations in MYB and/or NFIB were found in the majority of cases in all three locations, whereas MYBL1 involvement was restricted to tumors in the salivary gland.
|
29467480 |
2018 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We have established cell cultures from two individual ACC PDX tumors that maintain the characteristic MYB translocation.
|
28900283 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We observed increasing tumor clonality during progression of B-cell lymphomas and identified gene players (especially TERT and MYB) and biological processes involved in tumor progression.
|
29099869 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Utilizing tissue microarrays, we studied a group of basal cell adenocarcinomas and basal cell adenomas to determine: (i) whether either tumor expressed MYB and (ii) the frequency of any expression in either tumors.
|
28727172 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
GATA3 and MYB Expression in Cutaneous Adnexal Neoplasms.
|
28323779 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Importantly, FISH for MYB rearrangement may be used as a diagnostic tool during pathological examination of lacrimal gland neoplasms.
|
28085142 |
2017 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We contribute with three additional cases of PCACC exhibiting MYB aberrations, the apparent driving genetic abnormality in these tumors.
|
27859477 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, 5'-NFIB fusions that did not involve MYB/MYBL1 genes were identified in a subset of t(6;9)-positive/fusion-negative tumors.
|
26631609 |
2016 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In vitro and in vivo functional studies show that MYB-QKI rearrangements promote tumorigenesis through three mechanisms: MYB activation by truncation, enhancer translocation driving aberrant MYB-QKI expression and hemizygous loss of the tumor suppressor QKI.
|
26829751 |
2016 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Although the c-Myb protein level in the tumor tissue correlated with its mRNA level, no significant association between MYB mRNA and any clinicopathological characteristics was observed.
|
26873484 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Adenoid Cystic Carcinoma Can Be Driven by MYB or MYBL1 Rearrangements: New Insights into MYB and Tumor Biology.
|
26851182 |
2016 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
FISH analysis indicated that nine AdCC tumors with high MYB protein expression were split gene-positive, while MYB gene splitting was not detected in the 11 cases with low or absent MYB protein expression.
|
26711587 |
2016 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Strategies based on detection of newly described genetic events (such as MYB activating super-enhancer translocations and alterations affecting another member of MYB transcription factor family-MYBL1) offer new hope for improved risk assessment, therapeutic intervention and tumor surveillance.
|
27533466 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We also identified several MYB-regulated genes in PC cells that might potentially mediate its effect on tumour growth and metastasis.
|
26657649 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The FISH assay, designed to detect the copy number of the RREB1 (6p25), MYB (6q23), and CCND1 (11q13) genes and of centromere 6 (Cep 6), was performed in a group of children and in a group of adults with a histopathologic diagnosis of spitzoid neoplasms.
|
25933206 |
2015 |