|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Elevated S100A9 expression is thought to serve an important role in tumorigenesis; however, the exact role of S100A9 in the modulation of cervical cancer and the underlying molecular mechanism remain unknown.
|
31059008 |
2019 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Whether there are synergistic actions between calgranulin B and HPV-16/HPV-45 infection on the squamous cervical carcinogenesis or progression need further study.
|
29497331 |
2018 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
We previously revealed that S100a8 and S100a9 are highly activated and play an important role in the process of colitis-associated carcinogenesis, which suggests an attractive therapeutic target for ulcerative colitis and related colon cancer.
|
29326691 |
2017 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Members of the S100 protein family, S100A8, S100A9 and their heterodimer complex known as calprotectin are thought to be involved not only in inflammatory pathways but also in tumorigenesis and cancer progression.
|
28609200 |
2017 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
In ovarian epithelial carcinogenesis, p16 and p53 show higher immunohistochemical staining frequencies in malignant tumors and are associated with poor prognoses. p14 was only analyzed in carcinomas, with conflicting results.
|
27770808 |
2016 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Researches have provided valuable insights into the tumorigenesis of S100A9 in some cancers.
|
27020242 |
2016 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Chronic liver inflammation and hepatocellular carcinogenesis are independent of S100A9.
|
25331529 |
2015 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
In addition to increasing cell migration and invasion, ectopic S100A9 expression in tumor cells promoted xenograft tumorigenesis as well as the dominant expression of myeloid cell markers and pro-inflammatory IL-6.
|
26315114 |
2015 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Using RNAi-mediated stable gene knockdown in human ATC cell lines and bioluminescent imaging of orthotopic and lung metastasis mouse models of human ATC, we investigated the effects of S100A8 and S100A9 on tumorigenesis and metastasis.
|
25423568 |
2015 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
HBV infection is associated with p14 (ARF) , p15 (INK4B) , p16 (INK4A) , and RB gene methylation (P = 0.048, 0.035, 0.02); HBV-DNA replication is associated with p14 (ARF) , p15 (INK4B) , p16 (INK4A) , and RB gene methylation (P = 0.048, 0.035, 0.02); high rate of p14 (ARF) , p15 (INK4B) , and p16 (INK4A) in HCC with HBV infection suggests that HBV-induced hypermethylation may be one of the mechanisms of HBV involved in hepatocellular carcinogenesis.
|
24254306 |
2014 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Both S100A8 and S100A9 are highly expressed in cutaneous SCC and play important roles in tumorigenesis.
|
24550082 |
2014 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Taken together, these results indicate that the tumorigenesis potential of CSCs arises from highly expressed S100A9.
|
23836528 |
2013 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
Upregulated genes in chemoresistant tumors included cell cycle regulating genes (TOP2A, BCAT1, CDCA8, CCNA2, CENPE), and genes with previously known mechanisms in tumorigenesis (S100A9, APOA1, RNF125, IFI16).
|
20066894 |
2009 |
|
Carcinogenesis
|
0.100 |
Biomarker
|
phenotype |
BEFREE |
The present findings of the frequent and variable p14 gene abnormalities, including rare-type ones with or without sufficient mutational effect in glioma cell lines, might be of value for better understanding of the p14 gene and its related pathways in glioma carcinogenesis.
|
18415661 |
2008 |
|
Carcinogenesis
|
0.100 |
AlteredExpression
|
phenotype |
BEFREE |
Our observation of frequent p14 gene abnormalities (90%) and inactivation (40-60%) was in striking contrast to the same pathological subtype of systemic lymphoma in which p14 gene abnormalities and inactivation were infrequent, suggesting a difference in carcinogenesis between PCNSL and systemic lymphoma.
|
15649253 |
2005 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Of 91 fully characterized cases, 41 (45%) had p53 mutations alone, 17 (19%) had p14 methylation alone, 30 (33%) had neither, but only 3 (3%) had both p53 mutations and p14 methylation. p14 methylation is an early event in colorectal carcinogenesis, being detectable in normal aging epithelium by using sensitive assays.
|
12612901 |
2003 |
|
Carcinogenesis
|
0.100 |
PosttranslationalModification
|
phenotype |
BEFREE |
Recent studies indicated that p16 and p14 inactivation owing to promoter methylation was important for colorectal tumorigenesis.
|
12716465 |
2002 |
|
Carcinogenesis
|
0.100 |
GeneticVariation
|
phenotype |
BEFREE |
Although the number of cases we analyzed was not large, alterations identified in the Rb, p53, p16, p15 and p14 genes are of significance and might be associated with tumorigenesis in NK cell neoplasms.
|
11676855 |
2001 |