Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation phenotype BEFREE Activating mutations in the catalytic subunit of Phosphatidylinositol (3,4,5)-trisphosphate kinase (PI3K), encoded by the <i>Pik3ca</i> gene, are detected in approximately 20% of human anal cancers.<b>Experimental Design:</b> We asked if common activating mutations in <i>Pik3ca</i> contribute to anal carcinogenesis using an established mouse model for anal carcinogenesis in which mice are topically treated with the chemical carcinogen 7,12-Dimethylbenz(a)anthracene (DMBA). 30530704 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE The phosphoinositide 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) signaling has been shown to contribute to tumorigenesis, tumor progression, and resistance to therapy in most human cancer types, including lung cancer. 31262325 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Among them, three genes (PIK3CB, CAV2, and KANK1) are reportedly involved in tumorigenesis through the PI3K/Akt signaling pathway. 31642198 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway deregulation is closely associated with tumorigenesis. 30651769 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Notably, the EGFR, Ras, and PI3K/Akt pathways can lead to downregulation of RhoB, while simultaneously being associated with an increased propensity for tumorigenesis. 31200451 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Phosphoinositide 3-kinase (PI3K) is aberrantly activated in head and neck squamous cell carcinomas (HNSCC) and plays a pivotal role in tumorigenesis by driving Akt signaling, leading to cell survival and proliferation. 31393061 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE S1PR1 signaling can also trigger various other signaling pathways involved in carcinogenesis including activation of PI3K/AKT, MAPK/ERK1/2, Rac, and PKC/Ca, as well as suppression of cyclic adenosine monophosphate (cAMP). 31115798 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Our results suggested that S100A11 could activate the PI3K/Akt/mTOR signaling pathway in HSCC tumorigenesis. 31312359 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Numerous signaling pathways, such as PI3K/Akt/mTOR and Wnt‑β‑catenin have been demonstrated to be associated with the tumorigenesis and development of RCC. 31485634 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE High levels of NO drove LUAD tumorigenesis via activating MAPK and PI3K/Akt cascades. 31699997 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE In addition, we also examine how the knockdown of PTEN influences proliferation and invasion and correlate with CXCL12/CXCR4/PI3K/Akt, determination of PTEN up-down-stream targets that preferentially contribute to tumorigenesis. 31500630 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Comparing transcriptome profiles of human and mouse cell lines, miR-29b displayed common regulation pathways involving distinct downstream targets in macromolecular complex assembly, cell cycle regulation, and Wnt and PI3K-Akt signalling pathways; miR-29b also demonstrated specific functions reflecting cell characteristics, including fibrosis and neuronal regulations in NIH/3T3 cells and tumorigenesis and cellular senescence in HeLa cells. 31767948 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE <b>Background:</b> Phosphatidylinositol 3-kinase (PI3K) pathway activation plays a key role in tumorigenesis and has been associated with poor prognosis and resistance to multiple therapies in various cancers. 31741715 2019
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT) signaling pathway is related to tumorigenesis by up-regulating survivin. 30536312 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Together, our findings suggest that HBc promotes tumorigenesis of hepatoma cells by enhancing the expression of total Src and the active form of the kinase and subsequently activates Src/PI3K/Akt signaling pathway, revealing novel insights into the underlying mechanisms of HBV-associated hepatocarcinogenesis.-Liu, W., Guo, T.-F., Jing, Z.-T., Yang, Z., Liu, L., Yang, Y.-P., Lin, X., Tong, Q.-Y. 29401603 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Both mechanisms are correlated to the Pi3K/Akt/mTOR pathway which is a major tumorigenesis pathway in nearly all phacomatoses. 28265819 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Transcriptome analysis revealed that major transcription factors, such as SRF, HNF4A, ZEB1, and RUNX1, with potential regulatory roles in key pathways, including focal adhesion, the PI3K-Akt signaling pathway, and the MAPK signaling pathway, may play a role in the tumorigenesis of SRCC. 29747153 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 AlteredExpression phenotype BEFREE Although KRAS direct binding to and activation of PI3K is required for <i>KRAS</i>-driven lung tumorigenesis, the contribution of insulin receptor (IR) and insulin-like growth factor 1 receptor (IGF1R) in the context of mutant <i>KRAS</i> remains controversial. 29610318 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 GeneticVariation phenotype BEFREE Taken together, our results demonstrate that a subset of PIK3CAmut promote tumorigenesis and suggest that patients with helical domain mutations may be most sensitive to dual PI3Ki/MEKi treatment. 29975751 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Notch signaling via regulation of RB and p-AKT but not PIK3CG contributes to MIA PaCa-2 cell growth and migration to affect pancreatic carcinogenesis. 29434912 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE The development of molecular biology reveals that the PI3K-AKT-mTOR pathway plays a relevant role in tumorigenesis and progression of NENs. 29124519 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE Tumor silencing of NOS and LOX signaling mirrored the antitumor effect of the hit compounds, demonstrating their participation in Notch-PI3K/Akt-induced tumorigenesis. 29514083 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE PI3K/AKT/mTOR signaling pathway plays a crucial role in tumorigenesis and development. 29424922 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE It plays a crucial role in PI3K-mediated tumorigenesis, making it a potential therapeutic target for cancer. 30038340 2018
CUI: C0596263
Disease: Carcinogenesis
Carcinogenesis
0.100 Biomarker phenotype BEFREE <i>N</i>-Glycan deletion on β4-integrin impaired β4-dependent cancer cell migration, invasion, and growth <i>in vitro</i> and diminished tumorigenesis and proliferation <i>in vivo</i> The reduced abilities of β4-integrin were accompanied with decreased phosphoinositol-3 kinase (PI3K)/Akt signals and were restored by the overexpression of the constitutively active p110 PI3K subunit. 29549127 2018