Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
FABP5 overexpression is frequent in PCa, but seems to be restricted to TMPRESS2:ERG fusion-negative tumors and is associated with SPOP and FOXA1 mutations.
|
30701334 |
2020 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results demonstrate that FASN is a crucial mediator of SPOP-induced inhibition of PCa cell growth.
|
30955223 |
2019 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Altogether, we have revealed a novel mechanism for SPOP in suppressing prostate cancer and provided evidence to show SPOP has dual functions in prostate cancer and CCRC.
|
30237511 |
2019 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here, we identified a previously unrecognized mutation Q165P at the edge of SPOP MATH domain in primary and metastatic PCa of a patient.
|
31559706 |
2019 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we report that NANOG is degraded by SPOP, a frequently mutated tumor suppressor of PCa.
|
30595535 |
2019 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Disability or mutation of the SPOP gene has been reported to contribute to prostate cancer incidence and prognosis.
|
31392082 |
2019 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Knockout of SPOP or expression of prostate cancer-associated SPOP mutants conferred resistance to death caused by SG inducers (e.g. docetaxel, sodium arsenite and H<sub>2</sub>O<sub>2</sub>) in prostate cancer cells.
|
31771591 |
2019 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
IQGAP2 (5q13.3) genomic alterations were observed in SPOP-marked PCs and co-occurred with deletion in the RN7SK (16p12.2), SNORA50A (16q21), and SNORA50C (17q23.3) genes; the co-occurrence associated with reductions in DFS (P=4.14e-4).
|
30428404 |
2019 |
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
SPOP and FOXA1 mutations are associated with PSA recurrence in ERG wt tumors, and SPOP downregulation with ERG-rearranged prostate cancer.
|
31090082 |
2019 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our structural and biophysical data confirm the suggested loss-of-function in prostate cancer-associated SPOP mutants and provide mechanistic explanation.
|
31026449 |
2019 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Class-1 activating mutations originate in early prostate cancer without alterations in ETS or SPOP, selectively recur within the wing-2 region of the DNA-binding forkhead domain, enable enhanced chromatin mobility and binding frequency, and strongly transactivate a luminal androgen-receptor program of prostate oncogenesis.
|
31243372 |
2019 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Importantly, cancer-derived mutations in SPOP or at the Nanog-degron (S68Y) disrupt SPOP-mediated destruction of Nanog, leading to elevated cancer stem cell traits and PrCa progression.
|
30595538 |
2019 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In summary, we found no evidence that ERG is an effector of SPOP mutation in human prostate cancer or mouse models.
|
29202479 |
2018 |
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
TRIM24 and AR coactivated gene signature of SPOP-mutant PCa is similarly activated in human PCa with high TRIM28 expression.
|
30479348 |
2018 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Mutations in SPOP, the gene most frequently point-mutated in primary prostate cancer, are associated with a high degree of genomic instability and deficiency in homologous recombination repair of DNA but the underlying mechanisms behind this defect are currently unknown.
|
30124983 |
2018 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The aim of this work was to investigate how SPOP mutations contribute to prostate cancer development and progression.
|
29996942 |
2018 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Prostate cancer-associated mutation in SPOP impairs its ability to target Cdc20 for poly-ubiquitination and degradation.
|
27780719 |
2017 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Specifically, we provide a molecular rationale for the use of BET inhibitors to treat patients with endometrial but not prostate cancer who harbor SPOP mutations.
|
28805821 |
2017 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
More importantly, our results also provide a molecular basis for using combination with BET inhibitors and other inhibitors to treat prostate cancer patients with SPOP mutations.
|
29108467 |
2017 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data show that resistance to BET inhibitors in SPOP-mutant prostate cancer can be overcome by combination with AKT inhibitors and further support the evaluation of SPOP mutations as biomarkers to guide BET-inhibitor-oriented therapy in patients with prostate cancer.
|
28805822 |
2017 |
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Therefore, our study not only underlines an oncogenic role of EglN2 in prostate cancer, but also highlights SPOP as a tumor suppressor to down-regulate EglN2 in prostate cancer.
|
28089830 |
2017 |
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
In summary, PRISM-SRM enables multiplexed, isoform-specific detection of mutant SPOP proteins in cell lysates, providing significant potential in biomarker development for prostate cancer.
|
28810879 |
2017 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Using next-generation sequencing to analyze the mutations in PC, the main molecular PC subtypes were identified, which depended on the presence of fusion genes and FOXA1, CHD1, and SPOP point mutations; other driver mutations responsible for the progression of PC subclones were also characterized.
|
28659719 |
2017 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here, the authors show that a non-coding polymorphic regulatory element at 7p14.3 may predispose to SPOP mutant prostate cancer subclass through a hormone dependent DNA damage response.
|
28663546 |
2017 |
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Taken together, our study provided new insights in understanding the relationship between metabolic pathways and <i>SPOP</i> mutations in PCa.
|
29262542 |
2017 |