|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Here, we show that CD103<sup>+</sup> cDC1 and, to a much lesser extent CD11b<sup>+</sup> cDC2, are the only populations expressing TLR3 at the tumor site, and consequently could be potential targets of poly A:U.
|
30949170 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We comprehensively characterized myeloid cells in tumor draining lymph nodes (tdLN) of mice and identified two subsets of conventional type-2 dendritic cells (cDC2) that traffic from tumor to tdLN and present tumor-derived antigens to CD4<sup>+</sup> T<sub>conv</sub>, but then fail to support antitumor CD4<sup>+</sup> T<sub>conv</sub> differentiation.
|
30955881 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
POLE/POLD1 gene variants have been suggested as potential markers for immunotherapy due to their significant association with the tumor mutational burden (TMB), an effective indicator for response prediction in immunotherapy.
|
31673068 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Next generation sequencing of the MMR, POLE and POLD1 genes was performed in leukocyte and tumor DNA of the remaining nine patients, as well as in two patients with MMR-proficient tumors, but with severe family history.
|
31114938 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The increase of the tumor-node-metastasis (TNM) staging of osteosarcoma and the high expression of CDC2 are the risk factors affecting the prognosis of osteosarcoma patients (P<0.05), and Cox regression analysis showed that the expression level of CDC2 was a risk factor affecting the prognosis of osteosarcoma patients (P<0.05).
|
29731906 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Additionally, increased expression of POLD1 was associated with shorter DFS at early-stage (P=0.037), late-stage cases (P=0.023) and with the presence of triple-negative tumors (TNBC; P=0.049).
|
30344713 |
2018 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Germline mutations in POLE and POLD1 have been shown to cause predisposition to colorectal multiple polyposis and a wide range of neoplasms, early-onset colorectal cancer being the most prevalent.
|
28423643 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The results provide compelling evidence for the pathogenic role of the POLD1-R689W mutation in the development of the human tumor and emphasize the need to experimentally determine the significance of Polδ variants present in sporadic tumors.
|
28368425 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Somatic POLE mutations have been found in a subset of endometrioid ECs particularly in FIGO grade 3 tumors while POLD1 mutations are reportedly rare in ECs.
|
26748215 |
2016 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Six of these POLE/POLD1-EDM mutated tumors also carried somatic MMR variants.
|
26648449 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We also found that p-Cdc2 was decreased in the USP39-overexpressing cells and was upregulated in the xenografted tumors derived from the HepG2/KD cells from nude mice.
|
26081192 |
2015 |
|
Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
The results indicated that the tumor suppressive activity of SASH1 derived from G2/M arrest in A-375 cells, and that the phosphorylation of Cdc2 or the disruption of cyclin B-Cdc2 binding may be responsible for the G2/M arrest.
|
23023727 |
2012 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Assessment of the previously described gene sets relative to training data sets of head and neck squamous cell carcinoma samples, one including data on tumor differentiation and patient outcome and one present in the Human Gene Expression Map, identified four genes with association to poor survival (COX7A1, MFAP5, MPDU1, and POLD1).
|
22142811 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Cell cycle regulation and CCNE1 and CDC2 were the only significant overlapping pathway and genes differentially expressed between tumors with high and low levels of miR-26a and EZH2, respectively.
|
22094936 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The overexpressions of cdc2 and p16 were correlated with an infiltrative tumor border pattern and this was statistically significant (p<0.05).
|
21488187 |
2011 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We found a significant upregulation in CCNB1 (1.5-fold), CDC2 (1.4-fold), and MKI67 (1.8-fold) expression in recurrent tumors in comparison with primary tumors (P<0.05).
|
22137483 |
2011 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
HTMC treatment also led to an inhibition of cell-cycle regulatory proteins phosphorylation of cdc2 (Tyr(15) and Tyr(161)) and Rb (Ser(795) and Ser(807/811)), which was accompanied by the accumulation of tumor suppressor genes p53 and p21.
|
20926293 |
2010 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
OSU-HDAC42, (i) unlike most HDACIs, elicited a more than five-fold increase in G(2)-phase cells, at 2.5 microM, with G(2) arrest followed by apoptosis; (ii) at 1.0 microM, completely repressed messenger RNA expression of the cell cycle progression gene cdc2; (iii) at low doses (0.25-1.0 microM for 24 hours), induced tumor cell epithelial differentiation, as evidenced by morphology changes and a more than five-fold up-regulation of epithelium-specific cytokeratins; (iv) potently abrogated the growth of numerous ovarian cancer cells, with IC(50) values of 0.5 to 1.0 microM, whereas also remaining eight-fold less toxic (IC(50) of 8.6 microM) to normal ovarian surface epithelial cells; and (v) chemosensitizated platinum-resistant mouse xenografts to cisplatin.
|
19484144 |
2009 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Following ex vivo study, viral particles containing small interfering RNA for CDC2 were subsequently injected into xenogeneic graft tumor of nude mice and the weight of human glioma xenografts, survival and resulting phenotypic changes of target gene were investigated.
|
18230152 |
2008 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Interestingly, Cdc2 over-expression was observed in all and cyclin E1 was over-expressed in half of the late-stage tumors regardless of p27 status; and p27 inactivation led to significant activation of Cdk2 or Cdc2 only in half of the p27-deficient tumors.
|
17434927 |
2007 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Elevation of cyclin B1, active cdc2, and HuR in cervical neoplasia with human papillomavirus type 18 infection.
|
16458113 |
2006 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We show that the recently discovered tumor suppressor pdcd4 represses the transcription of the mitosis-promoting factor cyclin-dependent kinase (CDK)1/cdc2 via upregulation of p21(Waf1/Cip1). p21(Waf1/Cip1) inhibits CDK4/6 and CDK2.
|
15317660 |
2004 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Although activation of the cyclin-dependent kinase CDC2 mediates G2/M transition in all tumor cells studied to date, regulation of CDC2 varies between tumor types.
|
11305412 |
2001 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In particular, two of the kinases, cdk3 and PISSLRE and PITALRE, the cdc2-related kinases recently cloned by us, map to regions previously shown to exhibit loss of heterozygosity in breast and other tumors.
|
7882308 |
1995 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In addition, using proliferating normal vs. human tumor breast cells as a model system, we observed a number of alterations in cyclin expression: (i) an 8-fold amplification of cyclin E gene in one tumor line, a 64-fold overexpression of its mRNA, and altered expression of its protein; (ii) deranged expression of cyclin E protein in all (10 of 10) tumor cell lines studied; (iii) increased cyclin mRNA stability, resulting in (iv) general overexpression of RNAs and proteins for cyclins A and B and CDC2 in 9 of 10 tumor lines and (v) deranged order of appearance of cyclins in synchronized tumor vs. normal cells, with mitotic cyclins appearing prior to G1 cyclins.
|
8430082 |
1993 |