|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Overexpression of AURKA is common in cancer, resulting in acquisition of alternate non-mitotic functions.
|
23334327 |
2014 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
However, the role of AURKA in osteosarcoma (OS), the most common type of primary malignancy arising from bone, has not been clarified.
|
24452445 |
2014 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Targeting the AURKA-EIF4E-c-MYC axis using alisertib is a novel therapeutic strategy that can be applicable for everolimus-resistant tumors and/or subgroups of cancers that show overexpression of AURKA and activation of EIF4E and c-MYC.<i>Clin Cancer Res; 23(14); 3756-68.©2017 AACR</i>.
|
28073841 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
AURKA (aurora kinase A) has been identified as an oncogene in cancer development; however, its potential role and underlying mechanisms in the progression of BC remain unknown.
|
30547784 |
2018 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
This analysis predicts that cancer cells manifesting a stem cell-like expression profile of a death-from-cancer signature would exhibit the following features: a concomitantly increased expression of certain members of inhibitor of apoptosis protein (IAP) family (Survivin and XIAP); activation of mitotic spindle check point proteins (BUB1, BUB3, KNTC2, Mad2, PLK1, PLK4, STK6/Aurora A); and elevated levels of certain cell cycle control/marker proteins (CCNB1, CCNB2, CCND1, CCNA2, CDC2, CDC25, Ki67, USP22).
|
16760651 |
2006 |
|
Malignant Neoplasms
|
0.400 |
PosttranslationalModification
|
group |
BEFREE |
Mechanically, AURKA-mediated phosphorylation of LKB1 impairs LKB1 interaction with and phosphorylation of its downstream target AMPKα, which has critical roles in governing cancer cell energy metabolic homeostasis and tumorigenesis.
|
28967900 |
2018 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Overall, our study showed that selinexor treatment restored tumor suppressive function of IGFBP5 and inhibited aurora kinase A and B in liposarcoma cells supporting the usefulness of selinexor as a potential therapeutic strategy for the treatment of this cancer.
|
27893412 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
While overexpression of AURKA induced epithelial-mesenchymal transition (EMT) and cancer stem cell (CSC) behaviors though PI3K/AKT pathway, silencing AURKA suppressed radiation-enhanced cell invasiveness of HCC.
|
28322787 |
2017 |
|
Malignant Neoplasms
|
0.400 |
PosttranslationalModification
|
group |
BEFREE |
Phosphorylation-dead Twist1 serves as a dominant-negative and fully reverses the EMT phenotype induced by Twist1, underscoring the crucial role of AURKA-mediated phosphorylation in mediating Twist1-induced malignancy.
|
28167680 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
The Aurora-A/STK15 gene encodes a kinase that is frequently amplified in cancer.
|
17935280 |
2007 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Furthermore, we find that AURKA activity is critical to the propagation and self-renewal of sphere-enriched MPNST cancer stem-like cells.
|
23328114 |
2013 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Aurora kinase A (AURKA) has been implicated in the regulation of cell cycle progression, mitosis and a key number of oncogenic signaling pathways in various malignancies.
|
28218735 |
2017 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Hence, we performed a meta-analysis to investigate the association between cancer susceptibility and STK15 F31I (42,315 cases and 50,542 controls from 62 studies) and V57I polymorphisms (12,891 cases and 17,391 controls from 18 studies) in different inheritance models.
|
25154511 |
2015 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
First, we demonstrate that SQ1274 has a much lower IC<sub>50</sub> than paclitaxel in both ARK1 (1.26 nM vs. 15.34 nM, respectively) and OVCAR8 (1.34 nM vs. 10.29 nM, respectively) cancer cell lines.
|
30190114 |
2018 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Recent studies have demonstrated STK15 to be significantly associated with many tumors, with aberrant expression obseved in many human malignancies.
|
25124567 |
2014 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Aurora kinase A has been demonstrated to be involved in the malignant progression of many types of cancer including prostate cancer, we therefore hypothesized that Aurora kinase A might work as a valuable target for prostate cancer treatment.
|
18404163 |
2008 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Clinical studies with polyploidy inducers, such as aurora kinase A inhibitors, are under way for a wide variety of malignancies, whereas trials specifically for AMKL and PMF are in development.
|
23963861 |
2013 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Numerous microarray-based gene expression studies performed on several types of solid tumors revealed significant changes in key genes involved in progression and regulation of the cell cycle, including AURKA that is known to be overexpressed in many types of human malignancies.
|
23925655 |
2013 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
SIGNIFICANCE: The identification of a synthetic lethal interaction between <i>RB1</i> and AURKA inhibition, and the discovery of a drug that can be dosed continuously to achieve uninterrupted inhibition of AURKA kinase activity without myelosuppression, suggest a new approach for the treatment of RB1-deficient malignancies, including patients progressing on CDK4/6 inhibitors.<i>See related commentary by Dick and Li, p. 169</i>.<i>This article is highlighted in the In This Issue feature, p. 151</i>.
|
30373917 |
2019 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
We aimed to determine polymorphisms of F31I and V57I codons of AURKA gene and their association with cancer prognosis in patients compared with controls in an eastern population of Iran.A case-control study was conducted on specimens from 100 patients and 100 age- and gender-matched controls.
|
28906374 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Recent data from The Cancer Genome Atlas analysis have revealed that Aurora kinase A (AURKA) amplification and overexpression characterize a distinct subset of human tumors across multiple cancer types.
|
27624071 |
2016 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
The Cancer Genome Atlas data mining in the University of Alabama interactive web resource for pathways associated with poor survival of patients with adrenocortical carcinoma revealed significant upregulation of genes involved in DNA damage and regulation of cell-cycle pathways, such as AURKA, AURKB, CDK1, CDK4, CDK6, PLK1, CHEK1, CHEK2, CDC7, BUB3, and MCM3 (P < .001-.05).
|
30413320 |
2019 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
The findings from this study are consistent with the evidence from invitro and in vivo experiments, implicating an etiologic role of the STK15 gene in human breast cancer, and provide evidence for the modifying effects of genetic background on human cancer risk.
|
15598762 |
2004 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
STK15 is considered a potential cancer susceptibility gene owing to its functions in normal cell mitosis.
|
15271853 |
2004 |