|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
The complex nature of APC/C and limited mutation analysis of its subunits has made it difficult to determine the relationship of each subunit to cancer.
|
31652364 |
2020 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Targeted next-generation sequencing identified 56 nonsynonymous alterations in 51 genes including TP53 and APC, which are commonly altered in GEJ cancer.
|
31292541 |
2020 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
APC/C contributes to chromosome segregation fidelity in mitosis raising the possibility that copy-number and expression changes in Cezanne observed in cancer contribute to the etiology of disease.
|
30874463 |
2020 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Here, we present the creation of a stable cell line system that constitutively expresses our dual-reporter vector harboring two cancer initiating nonsense mutations in the adenomatous polyposis coli (APC) gene.
|
31786671 |
2019 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Familial adenomatous polyposis (FAP) is a cancer predisposition syndrome driven by germline loss-of-function of the APC gene and phenotypically manifests with intestinal polyposis and a variety of extra-intestinal bone and soft tissue tumors.
|
30919136 |
2019 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Here, we show that the convergence of dietary factors (high-fat diet) and dysregulated WNT signaling (APC mutation) alters BA profiles to drive malignant transformations in Lgr5-expressing (Lgr5<sup>+</sup>) cancer stem cells and promote an adenoma-to-adenocarcinoma progression.
|
30794774 |
2019 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
In the training dataset, DNA methylation levels at 7 of 15 genomic loci (glutathione S-transferase Pi 1 [GSTP1], CCDC181, hyaluronan, and proteoglycan link protein 3 [HAPLN3], GSTM2, growth arrest-specific 6 [GAS6], RASSF1, and APC) showed large differences between cancer and benign samples.
|
31433512 |
2019 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Targeted APC Activation in Cancer Immunotherapy to Enhance the Abscopal Effect.
|
31001249 |
2019 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
There is now a consensus that efficient peptide vaccination against cancer requires that peptides should (i) be exclusively presented by professional APC and (ii) stimulate both CD4 and CD8-specific T cell responses.
|
30906653 |
2019 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Good concordance in cancer recording was found between CPRD and HES APC among type 2 diabetics and matched controls.
|
29804063 |
2018 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
In contrast, APC missense mutations that were rare in conventional pathway adenomas and cancers (3% in BRAF wild-type cancers) were more frequent in BRAF mutant cancers with microsatellite instability (32%).
|
29148535 |
2018 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Targeted next-generation sequencing of 7 APC/MUTYH mutation-negative DNA samples identified novel potentially pathogenic POLD1 variant (p.L460R) in 1 patient and known low-penetrant cancer-associated allele CHEK2 p.I157T in 3 patients.
|
29406563 |
2018 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Our results support the hypothesis that <i>APC</i>-mutant colorectal tumors are transcriptionally distinct from <i>APC</i>-wild-type colorectal tumors with canonical WNT signaling activated by other mechanisms, with possible implications for stratification and prognosis.<b>Significance:</b> These findings suggest that colon adenomas driven by APC mutations are distinct from those driven by WNT gain-of-function mutations, with implications for identifying at-risk patients with advanced disease based on gene expression patterns.<i>Cancer Res; 78(3); 617-30.©2017 AACR</i>.
|
29212857 |
2018 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Using NGS, the following mutations were detected: nonsense mutations in four tumor suppressor genes [APC R1114X (molecular argument that the cancer was a primary tumor of colon), TP53 R213X, RB1 E137X and FBWX7 R393X & S282X], mutations in three receptor tyrosine kinases (RET A919V of high transforming activity, EGFR E114K and FLT3 L601I) well known as oncogenes.
|
28730258 |
2017 |
|
Malignant Neoplasms
|
0.400 |
PosttranslationalModification
|
group |
BEFREE |
The APC gene promoter 1A methylation rate in cancer tissues was much higher than in autologous controls, with a pooled OR of 3.66 (95% CI 2.12-6.33).
|
28497891 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Cancer Biology: APC Delivers Kiss of Death to Focal Adhesions.
|
28829967 |
2017 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Familial adenomatous polyposis (FAP) is a cancer syndrome caused by a germline mutation in the adenomatous polyposis coli (APC) gene.
|
28668823 |
2017 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
DNA-methylation intensities of GSTP1, RASSF1, and APC were higher in biopsy cores from men diagnosed with GS ≥ 7 cancer compared to men with diagnosed GS 6 disease.
|
28762545 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
MSH3, MSH6, APC and PIK3CA genes seem to play a bigger role in the path to cancer in this population.
|
28002797 |
2017 |
|
Malignant Neoplasms
|
0.400 |
Biomarker
|
group |
BEFREE |
Lengthening of mitosis through APC/C modulation may be a common mechanism of resistance to cancer therapeutics that increase chromosome segregation errors.Cancer Discov; 7(2); 218-33.
|
28069571 |
2017 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
This approach classified CRC into two major groups consistent with previous classification systems: (1) ∼16 % hypermutated cancers with either microsatellite instability (MSI) due to defective mismatch repair (∼13 %) or ultramutated cancers with DNA polymerase epsilon proofreading mutations (∼3 %); and (2) ∼84 % non-hypermutated, microsatellite stable (MSS) cancers with a high frequency of DNA somatic copy number alterations, which showed common mutations in APC, TP53, KRAS, SMAD4, and PIK3CA.
|
27325016 |
2016 |
|
Malignant Neoplasms
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Regarding the relationship between COX-2 and cancer related proteins, we found that COX-2 expression is positively associated with APC (p = 0.006), and P53 (p = 0.026), supporting a cross link between these proteins in gastric carcinogenesis.
|
27314294 |
2016 |
|
Malignant Neoplasms
|
0.400 |
PosttranslationalModification
|
group |
BEFREE |
RUNX3 showed protein silencing in cancer and normal mucosa, compared to inflammatory peritumoural infiltrate in almost all cases, showing a non-lymphocytic predominant pattern and being correlated with epigenetic silencing.Our results show aberrant promoter's methylation in APC, CDH1, CDKN2A, MLH1 and RUNX3 associated with GC, as well as a non-lymphocytic predominant infiltrate with high expression of RUNX3.
|
27566570 |
2016 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Further, we experimentally validated some of the synthetic lethal relationships we predicted.We reported that mutations in some cancer driver genes mutations in some cancer driver genes such as APC, KRAS, or PIK3CA might correlate with cancer proliferation or drug resistance.
|
26937901 |
2016 |
|
Malignant Neoplasms
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Therefore, the increase in intracellular β-catenin protein initiated by APC mutations is sustained by ZBP-89-mediated feedforward induction of CTNNB1 mRNA.Cancer Res; 76(23); 6877-87.©2016 AACR.
|
27758879 |
2016 |