|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
They noted a hypermutated phenotype with increased C>T transitions within the PPTID metastases and 2p amplification overlapping with the MYCN locus.
|
31653819 |
2019 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, using microarray and RNA-Seq-based gene expression profiling and ChIP-Seq analyses of breast cancer cells, we observed that the serum- and glucocorticoid-regulated kinase gene (<i>SGK1</i>) and the tumor metastasis-suppressor gene N-Myc downstream regulated gene 1 (<i>NDRG1</i>) are up-regulated and that the microRNAs <i>miR-29a</i> and <i>miR-101-1</i> targeting the 3'-UTR of <i>SGK1</i> are down-regulated in response to progesterone.
|
30337371 |
2018 |
|
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Neuroblastoma is the most common malignancy of childhood: high-risk patients, having N-MYC over-expression, undergo aggressive therapy and show high mortality or an increased risk of secondary malignancies.
|
30135355 |
2018 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Literature review identifies the poor prognosis of MYCN-amplified medulloblastomas as well as extraneural metastases; we review the current limitations and future directions of medulloblastoma treatment options.
|
29343221 |
2018 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Amplification of the MYCN gene in neuroblastoma is associated with a poor prognosis and is considered to remain unchanged in post-treatment specimens and metastases.
|
27465929 |
2017 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Historical risk stratification criteria for medulloblastoma rely primarily on clinicopathological variables pertaining to age, presence of metastases, extent of resection, histological subtypes and in some instances individual genetic aberrations such as MYC and MYCN amplification.
|
27040285 |
2016 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Patients with neuroblastoma due to N-Myc oncogene amplification have a high frequency of tumor metastasis.
|
24742640 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Patients with tumors harboring 2p gain or MYCN amplification showed unfavorable overall survival (P = .003 and P = .001, respectively).These markers were independent of the presence of metastases, which was indeed a clinical factor associated with poor overall survival (P = .01) in this series.
|
24470553 |
2014 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
N-Myc downstream-regulated gene 1 (NDRG1) plays vital roles in tumor metastasis suppression and is frequently silenced in metastatic colon cancers.
|
21184144 |
2011 |
|
Secondary Neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The combination of MYCN amplification, unfavorable histology and diploidy was noted in one patient who developed metastases within two months.
|
19012235 |
2008 |
|
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Neither MYCN nor expression of downstream targets significantly correlated with metastases at presentation, progression-free survival or overall survival in this small series.
|
17464317 |
2007 |
|
Secondary Neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Somatically acquired alterations at chromosome arms 3p and 11q are highly correlated with acquisition of metastases in the absence of MYCN amplification and may be useful as prognostic markers.
|
15659956 |
2005 |
|
Secondary Neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Here, we report on a patient who had a non-MYCN amplified 3p-/11q- neuroblastoma at diagnosis who subsequently developed a high level of MYCN amplification in bone marrow metastases 41 months after induction of complete remission.
|
15218241 |
2004 |