|
Adenocarcinoma
|
0.010 |
AlteredExpression
|
group |
BEFREE |
We show that MAP17 expression is induced during lung tumourigenesis, particularly in lung adenocarcinomas, and provide in vitro and in vivo evidence that MAP17 levels predict sensitivity to therapies currently under clinical use in adenocarcinoma tumours, including cisplatin, carboplatin and EGFR inhibitors.
|
30119639 |
2018 |
|
Lung Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
Our results indicate a potential prognostic role for MAP17 in lung tumours, with particular relevance in lung adenocarcinomas, and highlight the predictive pot0065ntial of this membrane-associated protein for platinum-based therapy and EGFR inhibitor efficacy.
|
30119639 |
2018 |
|
Rectal Neoplasms
|
0.010 |
Biomarker
|
group |
BEFREE |
In the present manuscript, we examined the values of MAP17 and pH2AX as surrogate biomarkers of the response in rectal tumors.
|
30250642 |
2018 |
|
Adenocarcinoma of lung (disorder)
|
0.010 |
Biomarker
|
disease |
BEFREE |
In addition, we show that MAP17 expression predicts proteasome inhibitor efficacy in this context and that bortezomib, an FDA-approved drug, may be a novel therapeutic approach for MAP17-overexpressing lung adenocarcinomas.
|
30119639 |
2018 |
|
Malignant neoplasm of lung
|
0.010 |
Biomarker
|
disease |
BEFREE |
Collectively these findings suggest that MAP17 serves a role in TKI resistance through regulation of CSCs in lung cancer.
|
29616128 |
2018 |
|
Carcinoma of lung
|
0.010 |
Biomarker
|
disease |
BEFREE |
Collectively these findings suggest that MAP17 serves a role in TKI resistance through regulation of CSCs in lung cancer.
|
29616128 |
2018 |
|
Primary malignant neoplasm of lung
|
0.010 |
Biomarker
|
disease |
BEFREE |
Collectively these findings suggest that MAP17 serves a role in TKI resistance through regulation of CSCs in lung cancer.
|
29616128 |
2018 |
|
Atrial Fibrillation
|
0.010 |
Biomarker
|
disease |
BEFREE |
Paroxysmal AF comparing to permanent AF and SR individuals had higher estimated SPAP (56 versus 48 versus 47 mmHg, <i>p</i> = 0.01) and shorter ACT (58 versus 65 versus 70 ms, <i>p</i> = 0.04).
|
28280732 |
2017 |
|
Psoriasis
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Immunohistochemistry confirms local inflammation, mainly CD45<sup>+</sup> cells, at the site of expression of MAP17, at least in tumors, Crohn's and psoriasis.
|
29228712 |
2017 |
|
Liver carcinoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
Cox regression analysis indicated MAP17 was an independent prognostic factor for DFS (HR, 1.710; 95% CI, 1.156-2.449, <i>p</i> = 0.012) and OS (HR, 1.743; 95% CI, 1.152-2.639, <i>p</i> = 0.009) in HCC.
|
29190940 |
2017 |
|
Idiopathic pulmonary arterial hypertension
|
0.010 |
Biomarker
|
disease |
BEFREE |
(1) Compared with the control group, the PAH group had lower body mass and weight increment, and relative to the latter, 5-ASA-treated groups had larger body mass and weight increment except for groups 5-ASA-150 and 5-ASA-200 and greater overall survival rates; (2) SPAP, DPAP, MPAP, and RVHI in 5-ASA-treated groups, except for MPAP and RVHI in 5-ASA-200 group, were lower than those in the PAH group; (3) compared with the PAH group, Nur77 expression in the pulmonary arteries of 5-ASA-treated groups was increased; and (4) expression of inflammatory mediators (NF-κB p65) was lower, while that of IκBα was higher in the pulmonary arteries of 5-ASA-treated groups and control group than that in the PAH group (all P < 0.05).
|
28213866 |
2017 |
|
Intrahepatic Cholangiocarcinoma
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Differential gene expression analysis demonstrated significant upregulation of PDZK1IP1, EEF1A2 and RPL41 (ENSG00000279483) genes in the iCCA samples when compared with the matched para‑tumor samples.
|
27082702 |
2016 |
|
Primary cholangiocarcinoma of intrahepatic biliary tract
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
Differential gene expression analysis demonstrated significant upregulation of PDZK1IP1, EEF1A2 and RPL41 (ENSG00000279483) genes in the iCCA samples when compared with the matched para‑tumor samples.
|
27082702 |
2016 |
|
Multiple Myeloma
|
0.010 |
Biomarker
|
disease |
BEFREE |
To analyze whether MAP17 could also alter this process, we used the proteasome inhibitor bortezomib (Velcade, PS-341), which is approved for the treatment of multiple myeloma and mantle cell lymphoma, although it has a high rate of resistance emergence and poor efficacy in solid tumors.
|
25837675 |
2015 |
|
Solid Neoplasm
|
0.010 |
Biomarker
|
phenotype |
BEFREE |
To analyze whether MAP17 could also alter this process, we used the proteasome inhibitor bortezomib (Velcade, PS-341), which is approved for the treatment of multiple myeloma and mantle cell lymphoma, although it has a high rate of resistance emergence and poor efficacy in solid tumors.
|
25837675 |
2015 |
|
Malignant lymphoma, lymphocytic, intermediate differentiation, diffuse
|
0.010 |
Biomarker
|
disease |
BEFREE |
To analyze whether MAP17 could also alter this process, we used the proteasome inhibitor bortezomib (Velcade, PS-341), which is approved for the treatment of multiple myeloma and mantle cell lymphoma, although it has a high rate of resistance emergence and poor efficacy in solid tumors.
|
25837675 |
2015 |
|
Hematologic Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
We propose that the levels of MAP17 could be used as a prognostic marker to predict the response to bortezomib in hematologic malignancies and in other tissues that are not commonly responsive to the drug.
|
25837675 |
2015 |
|
Mantle cell lymphoma
|
0.010 |
Biomarker
|
disease |
BEFREE |
To analyze whether MAP17 could also alter this process, we used the proteasome inhibitor bortezomib (Velcade, PS-341), which is approved for the treatment of multiple myeloma and mantle cell lymphoma, although it has a high rate of resistance emergence and poor efficacy in solid tumors.
|
25837675 |
2015 |
|
Malignant neoplasm of thyroid
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In addition, we show that aberrant promoter hypomethylation-associated overexpression of MAP17 might promote tumor growth in thyroid cancer.
|
23666970 |
2013 |
|
Thyroid Neoplasm
|
0.010 |
AlteredExpression
|
disease |
BEFREE |
In addition, we show that aberrant promoter hypomethylation-associated overexpression of MAP17 might promote tumor growth in thyroid cancer.
|
23666970 |
2013 |
|
Mammary Neoplasms
|
0.010 |
AlteredExpression
|
group |
BEFREE |
MAP17 levels increased with breast tumor stage and were strongly correlated with mammary tumoral progression.
|
22266858 |
2012 |
|
Dermatitis, Atopic
|
0.010 |
Biomarker
|
disease |
BEFREE |
Interestingly, MAP17 was originally reported to interact with PDZK1; in turn, the PDZK1 gene is localized within the atopic dermatitis-linked region on human chromosome 1q21.
|
19601982 |
2010 |
|
Eczema
|
0.010 |
Biomarker
|
disease |
BEFREE |
Interestingly, MAP17 was originally reported to interact with PDZK1; in turn, the PDZK1 gene is localized within the atopic dermatitis-linked region on human chromosome 1q21.
|
19601982 |
2010 |
|
Dermatologic disorders
|
0.010 |
AlteredExpression
|
group |
BEFREE |
Taken together, the Th cell cytokine-induced up-regulation of MAP17 expression may be linked to the down-regulation of filaggrin in NHEK, which may be associated with the abnormal epidermal differentiation observed in the dermatological diseases.
|
19601982 |
2010 |
|
Mesothelioma
|
0.010 |
GeneticVariation
|
disease |
LHGDN |
Transcriptome sequencing of malignant pleural mesothelioma tumors.
|
18303113 |
2008 |