Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
HPO |
|
|
|
Breast Carcinoma
|
0.700 |
CausalMutation
|
disease |
CGI |
|
|
|
Breast Carcinoma
|
0.700 |
GenomicAlterations
|
disease |
CGI |
|
|
|
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
CTD_human |
PI3K pathway activation in breast cancer is associated with the basal-like phenotype and cancer-specific mortality.
|
19685490 |
2010 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
CTD_human |
Recurrent gross mutations of the PTEN tumor suppressor gene in breast cancers with deficient DSB repair.
|
18066063 |
2008 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
CTD_human |
Subtle variations in Pten dose determine cancer susceptibility.
|
20400965 |
2010 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
CTD_human |
Synchronous bilateral breast carcinoma in a patient with cowden syndrome: a case report with morphologic, immunohistochemical and genetic analysis.
|
19968660 |
2010 |
Breast Carcinoma
|
0.700 |
CausalMutation
|
disease |
CLINVAR |
|
|
|
Breast Carcinoma
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
PTEN coordinates G(1) arrest by down-regulating cyclin D1 via its protein phosphatase activity and up-regulating p27 via its lipid phosphatase activity in a breast cancer model.
|
11230179 |
2001 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Our data indicate PTEN as a key target of Bergapten action in breast cancer cells for the induction of autophagy.
|
26148846 |
2015 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Inherited or acquired mutations in specific genes involved in the DNA damage response, for example the breast cancer susceptibility genes 1/2 (BRCA1/2), phosphatase and tensin homolog (PTEN) and P53 are associated with various subtypes of breast cancer.
|
28034453 |
2017 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Alleles in PTEN and other breast cancer susceptibility genes would be responsible for approximately 25% of the familial component of breast cancer risk, BRCA1 and BRCA2 being the two major genes responsible for this inherited risk.
|
17636424 |
2007 |
Breast Carcinoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
The present results suggest that a wide range of germline PTEN mutations may play a role in the pathogenesis of breast cancer.
|
22320991 |
2011 |
Breast Carcinoma
|
0.700 |
GeneticVariation
|
disease |
BEFREE |
Additionally, we summarized breast cancer risk associated with the following genetic factors: breast cancer susceptibility high-penetrance genes (BRCA1, BRCA2, p53, PTEN, ATM, NBS1 or LKB1) and low-penetrance genes such as cytochrome P450 genes (CYP1A1, CYP2D6, CYP19), glutathione S-transferase family (GSTM1, GSTP1), alcohol and one-carbon metabolism genes (ADH1C and MTHFR), DNA repair genes (XRCC1, XRCC3, ERCC4/XPF) and genes encoding cell signaling molecules (PR, ER, TNFalpha or HSP70).
|
15784178 |
2005 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Mutation analysis of the putative tumor suppressor gene PTEN/MMAC1 in primary breast carcinomas.
|
9288766 |
1997 |
Breast Carcinoma
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
PTEN deletion increased PI(3,4)P<sub>2</sub> levels in a mouse model of prostate cancer, and it inversely correlated with PI(3,4)P<sub>2</sub> levels across several EGF-stimulated prostate and breast cancer lines.
|
29056325 |
2017 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
We identified that YAP1 promotes cell growth and inhibits cell apoptosis of BC through the phosphatase and tensin homolog deleted on chromosome 10-AKT signaling pathway, and thus suggest that YAP1 might serve as a new target for inhibiting BC progression.
|
30868052 |
2019 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
The exact mechanism of ATO's carcinostatic effects in breast cancer is related to downregulating PTEN/AKT pathway via promoting RhoB.
|
31011573 |
2019 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
METABIRC and TCGA breast cancer cohort mRNA expression data analysis revealed that a high expression of the anti‑angiogenesis‑associated genes, THBS2, SERPINF1 and serpin family B member 5 (SERPINB5), and of the tumor suppressor gene, PTEN, was associated with a better overall survival (OS) of breast cancer patients.
|
31059004 |
2019 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Together, our data revealed that lncRNA MAGI2-AS3 is involved in breast cancer cell progression by regulating the miR-374a-PTEN axis.
|
30883342 |
2019 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
miR-93 and PTEN: Key regulators of doxorubicin-resistance and EMT in breast cancer.
|
28765915 |
2017 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Furthermore, introduction of PTEN into human breast carcinoma cells induced apoptotic cell death and inhibited cell growth and tumor formation in nude mice.
|
10415336 |
1999 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
Epithelial to mesenchymal transition (EMT) is a process in which epithelial cells lose cell polarity and cell-cell adhesion and gain migratory and invasive properties to become mesenchymal cells that are very vital for development, wound healing and stem cell behavior and contribute pathologically to fibrosis and cancer progression. miR21, a potent regulator of the tumor suppressor gene PTEN, can be silenced to reverse EMT, thereby providing an attractive target for abrogating the malignant behavior of breast cancer.
|
30109002 |
2018 |
Breast Carcinoma
|
0.700 |
Biomarker
|
disease |
BEFREE |
IPA® enrichment analysis revealed known pathways ('mTOR Signaling', 'PI3K/AKT Signaling' and 'PTEN Signaling') as well as enriched canonical pathways not previously associated with human ovarian follicle development such as 'ErB Signaling' and 'NGF Signaling' in the down-regulated category and 'Regulation of eIF4 and P70S6K Signaling' and 'HER-2 Signaling in Breast Cancer' in the up-regulated group.
|
28854595 |
2017 |
Breast Carcinoma
|
0.700 |
AlteredExpression
|
disease |
BEFREE |
Human breast cancer cell lines with or without the expression of BRCA1 and/or PTEN were treated with PARP1 and PI3K inhibitors as single agents and in combination.
|
22266096 |
2012 |