|
Colorectal Carcinoma
|
|
0.820 |
GeneticVariation
|
BEFREE |
We developed a sensitive, simple and rapid approach to detect the low-abundance PIK3CA (H1047R) mutation in real CRC specimens, providing an effective tool for guiding cancer targeted therapy.
|
27405731 |
2016 |
|
Colorectal Carcinoma
|
|
0.820 |
GeneticVariation
|
BEFREE |
Collectively, our data suggest that PF-04691502 exhibits potent anticancer activity in colorectal cancer by targeting both PIK3CA (H1047R) mutant CSCs and their derivatives.
|
23826249 |
2013 |
|
Colorectal Carcinoma
|
|
0.820 |
GeneticVariation
|
UNIPROT |
The prevalence of PIK3CA mutations in gastric and colon cancer.
|
15994075 |
2005 |
|
Colorectal Carcinoma
|
|
0.820 |
GeneticVariation
|
UNIPROT |
Functional analysis of PIK3CA gene mutations in human colorectal cancer.
|
15930273 |
2005 |
|
Colorectal Carcinoma
|
|
0.820 |
CausalMutation
|
CLINVAR |
|
|
|
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
We aimed to detect the tumor-derived free DNA in metastasis-free LNs in patients with breast cancers harboring the PIK3CA-H1047R mutation.
|
30805870 |
2019 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
Similarly, in human HCC cell lines, silencing of SGK3 reduced PIK3CA(E545K) -but not PIK3CA(H1047R)- induced accelerated tumor cell proliferation.
|
30975125 |
2019 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
In this study, we directly compared PIK3CA hotspot mutations (E545K, H1047R) in EpCAM-positive CTCs and paired plasma-ctDNA in breast cancer (BrCa).
|
31254443 |
2019 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
The hotspot mutation H1047R in the oncogenic PIK3CA gene is frequently detected in breast cancer and enhances the enzymatic activity of PI3K to activate AKT/mTOR signaling cascade.
|
30671946 |
2019 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
The aim of this study was to analyze the efficacy of PI3K/mTOR blockade in breast cancer brain metastases models.<b>Experimental Design:</b> The efficacy of GDC-0084 was evaluated in <i>PIK3CA</i>-mutant and <i>PIK3CA</i> wild-type breast cancer cell lines and the isogenic pairs of <i>PIK3CA</i> wild-type and mutant (H1047R/+) MCF10A cells <i>in vitro</i>.
|
30796030 |
2019 |
|
CLAPO Syndrome
|
|
0.800 |
GeneticVariation
|
UNIPROT |
CLAPO syndrome: identification of somatic activating PIK3CA mutations and delineation of the natural history and phenotype.
|
29446767 |
2018 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
PIK3CA mutations are seemingly the most common driver mutations in breast cancer with H1047R and E545K being the most common of these, accounting together for around 60% of all PIK3CA mutations and have promising therapeutic implications.
|
29523855 |
2018 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
Recently, PI3K H1047R mutation has been reported to sensitize breast cancer cells to PI3K inhibition by aspirin.
|
29504069 |
2018 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
Active mutations of PI3K catalytic subunit PIK3CA (e.g., H1047R) and amplification of its homolog PIK3CB are observed in a large number of breast cancers.
|
29545474 |
2018 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
This derivative showed low micromolar cytotoxic potency in all BrCa cell lines, a mild inhibition of the PI3Kα wild type and H1047R mutated enzyme and excellent pharmacokinetic parameters following oral and intraperitoneal administration at the designed dose of 10 mg/kg, with absence of in vivo phenotypic toxicity.
|
28006668 |
2017 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
Compared to MMTV-Her-2 transgenic mouse mammary tumors, H1047R tumors showed increased upregulation of Wnt/β-catenin/Axin2, hepatocyte growth factor (Hgf)/Stat3, insulin-like growth factor 2 (Igf-2), and Igf-1R pathways.
|
28296140 |
2017 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
Formalin-fixed paraffin-embedded tumour specimens from 118 HER2-overexpressing breast cancer patients treated with radical local therapy and trastuzumab in adjuvant setting were used for the assessment of: (1) PIK3CA gene mutations (p.H1047R and p.E545K) by qPCR, and (2) expression of Ki-67, EGFR, MUC4, HER3 and PTEN by immunohistochemistry.
|
28123607 |
2017 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
One tumour with a PIK3CA H1047R mutation also had a KRAS Q61H mutation.
|
27441415 |
2017 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
Formalin-fixed paraffin-embedded tumour specimens from 118 HER2-overexpressing breast cancer patients treated with radical local therapy and trastuzumab in adjuvant setting were used for the assessment of: (1) PIK3CA gene mutations (p.H1047R and p.E545K) by qPCR, and (2) expression of Ki-67, EGFR, MUC4, HER3 and PTEN by immunohistochemistry.
|
28123607 |
2017 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
Using a variety of physiologically relevant model systems with defined natural or knock-in PIK3CA mutations and/or PI3K hyperactivation, we show that PIK3CA-E545K mutations (found in ∼20% of PIK3CA-mutant breast cancers), but not PIK3CA-H1047R mutations (found in 55% of PIK3CA-mutant breast cancers), preferentially activate AKT1.
|
27197157 |
2016 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
The results suggest PIK3CA H1047R mutant cells have a selective advantage in breast, contribute to breast cancer susceptibility, and drive tumor progression during breast carcinogenesis, even when present as only a subpopulation of tumor cells.
|
27108388 |
2016 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
A positive association between the PIK3CA (H1047R) mutation and the patients' age was first found, except for the negative relationship with the degree of tumor differentiation.
|
27405731 |
2016 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
One metastatic sample with mutated KRAS also harbored a PIK3CA (H1047R) mutation. qPCR showed increased copy numbers of PIK3CA in 6 (33%) tumors, VEGFR1 in 0 (0%) tumors, VEGFR2 in 4 (22%) tumors, and VEGFR3 in 6 (33%) tumors.
|
25641339 |
2015 |
|
Malignant neoplasm of breast
|
|
0.800 |
GeneticVariation
|
BEFREE |
Using in situ genetic lineage tracing and limiting dilution transplantation, we have unravelled the potential of PIK3CA(H1047R), one of the most frequent mutations occurring in human breast cancer, to induce multipotency during tumorigenesis in the mammary gland.
|
26266975 |
2015 |
|
Neoplasms
|
|
0.800 |
GeneticVariation
|
BEFREE |
Interestingly, expression of Pik3ca(H1047R) in unipotent basal cells gave rise to luminal-like cells, while its expression in unipotent luminal cells gave rise to basal-like cells before progressing into invasive tumours.
|
26266985 |
2015 |