Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The increased expression of MICA and MICB on CSC targets thereby enhanced NK cell mediated killing in vitro and ex vivo from both human primary tumor and patient-derived xenograft samples.
|
30646520 |
2019 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
MHC class I chain-related protein A and B (MICA and MICB) are predominantly expressed intracellularly in tumour and normal tissue.
|
28334733 |
2017 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Three downregulated and hypermethylated genes (KLF4, LGALS3, MICB) and one upregulated gene (ETV4) were identified in EE2 tumors and LCC9 breast cancer cells, and valproic acid and hydralazine normalized the altered expression of all four genes.
|
27609189 |
2017 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Our results suggest that locally sustained expression of MICA and MICB in the tumor may contribute to the malignant progression of GC and that expression of these ligands predicts an unfavorable prognosis in GC patients presenting large tumors.
|
26708143 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition to the immediate effects on the tumour cell growth, HDACi upregulates the expression of MHC class I-related chain molecules A and B (MICA and MICB), resulting in an enhanced susceptibility of tumour cells to natural killer cell-mediated lysis.
|
25393367 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The major histocompatibility complex class I-related molecules A and B (MICA and MICB) are NKG2D ligands that play important roles in tumor immune surveillance.
|
23917076 |
2014 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Irradiation of the KAS-6/1 cells induced mRNA and protein expression of NKG2D ligands, MICA, and MICB in a dose-dependent manner and enhanced delivery of CIK/MV to the irradiated tumors.
|
23403007 |
2013 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In conclusion, our results demonstrate the ability of hydralazine and valproate to increase the NK activity against epithelial cancer cell lines and suggest that these drugs could reduce the levels of soluble MICA and MICB helping in avoiding tumor-induced suppression of NK cytotoxicity against the tumor.
|
21805029 |
2011 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
One common strategy that employs tumor cells to elude a T-cell-mediated immune response is the downregulation or loss of expression of HLA class I molecules, often associated with an induction of the surface expression of HLA class II antigen, nonclassical HLA class I molecules, and/or NK cell-activating ligands such as MICA, MICB, or ULBP.
|
21626162 |
2011 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We used RT-PCR to analyze the mRNA expression of MICA and MICB in four oral cancer cell lines compared with three normal human oral keratinocyte (NHOK) cell lines and in tissues from 36 patients with OSCC comparing tumor tissue with non-cancerous matched tissue (NCMT).
|
17181741 |
2007 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
MICB was detected exclusively in the cytosol of primary tumors and cell lines.
|
15548365 |
2005 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The human NKG2DLs MICA and MICB are expressed on tumors of epithelial origin in vivo.
|
12714493 |
2003 |