Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The blast crisis of CML has been variably associated with abnormalities of proto-oncogenes, such as RAS and MYC, or of tumour suppressor genes, in particular RB, p53 and p16, or with the generation of chimeric transcription factors, as in the AML1-EVI1 gene fusion.
|
8656667 |
1996 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
It also indicates that although the t(3;3)/EVI1 rearrangement is mostly related to myelocytic neoplasms, the t(3;3)/EVI1-rearrangement may also play an important role in the development of ALL.
|
23054648 |
2012 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The RUNX1-EVI1 gene generated by the t(3;21) translocation encodes a chimeric transcription factor and is a causative gene in the development of de novo acute megakaryoblastic leukemia and leukemic transformation of hematopoietic stem cell tumors.
|
30278283 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Chemokine receptors CCR6 and CCR7 have been reported to play important roles in T cell migration and organ-specific metastasis of various tumors.
|
23835793 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We conclude that EVI1 is a critical player in tumor growth in a subset of MLL-rearranged AMLs.
|
22553314 |
2012 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Evidence supports a role for EVI1 in inducing cellular quiescence, and this may contribute to the resistance to chemotherapy seen in patients with neoplasms that overexpress EVI1.
|
24495476 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These findings open the way to further studies aimed at identifying the culprit EVI1 implicated tumour suppressor genes on 7q.
|
20084277 |
2010 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
High-intensity IHC staining for CXCR4 was associated with larger tumor size (P = .02), while PTCs exhibiting ETE, ALI, or lymph node metastasis showed higher-intensity IHC staining for CCR7 than those without (P = .01, .03, and .01, respectively).
|
18696160 |
2008 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Strong cytoplasmic staining for CCR7 correlated with the presence of epithelioid cells (P = 0.037), tumor thickness (P = 0.011), lymphocytic infiltration (P = 0.041), and necrosis (P = 0.045).
|
24052640 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The chemokine receptor CCR7 and its ligands CCL19/21 mediate the tumor mobility, invasion, and metastasis (Wu et al.Curr Pharm Des.15:742-57, 2009).
|
25168373 |
2014 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Experimental re-expression of MS4A3 in an EVI1 overexpressing cell line counteracted the tumor promoting effect of EVI1 in a murine xenograft model by increasing the rate of apoptosis.
|
25886616 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Freshly sorted metastatic cells and tumour cell lines derived from the liver of BALB/c mice overexpressed functional CCR6 and CCR7 molecules compared with primary tumour.
|
12791091 |
2003 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CCR7(+) tumor cells and FOXP3(+) Tregs were assessed by immunohistochemistry in tissue microarrays containing gastric cancer from 133 patients.
|
24040244 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results indicate that specific HDAc inhibitors may be useful in the treatment of Evi-1-induced neoplastic tumors, including myeloid leukemias.
|
11587364 |
2001 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Moreover, the prognosis of patients with CCR7-positive tumors was better than that of patients with CCR7-negative tumors, but no such correlation was observed for CXCR4 expression.
|
15867478 |
2005 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
As tyrosine kinase inhibitors for metastatic renal cell carcinoma (mRCC) mostly emphasized on vascular inhibition, whether the CCR7 expressing tumor cells with potential lymphatic invasion function could have an impact on mRCC patient's drug response and survival, was unknown.
|
28114889 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Monoclonal antibodies to CCR7 showed intense staining in the patient's tumor epithelium.
|
16018941 |
2005 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The anti-CCR7 therapy significantly delayed the tumor appearance and also reduced the volumes of tumors in the subcutaneous model.
|
24305507 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The EVI1 gene locus was amplified in 43% of the tumors, and there was a significant correlation (P = 0.029) between gene copy number and EVI1 gene expression.
|
16951150 |
2006 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In the aspect of potential therapeutic approaches, some pharmaceutical drugs or antisense oligonucleotides that repress Evi-1 expression would be useful for the treatment of Evi-1-induced neoplastic tumors.
|
10641791 |
1999 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Chemokine and chemokine receptor patterns in patients with benign and malignant salivary gland tumors: a distinct role for CCR7.
|
28840842 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Imbalanced expression of MECOM isoforms is observed in multiple malignancies, implicating EVI1 as an oncogene, while PRDM3 has been suggested to function as a tumor suppressor through an unknown mechanism.
|
30462309 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CAR-engineered CCR7(-) T cells more efficiently accumulated at the tumor site, secreted more IFN-γ, expressed higher amounts of cytotoxic molecules, and showed superior tumor cell lysis compared to the younger CCR7(+) cells.
|
23350854 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, functional genomic studies using genomic editing and genome engineering have shown that the reallocation of the GATA2 distal hematopoietic enhancer to the proximity of the promoter of ectopic virus integration site 1 (EVI1) without the formation of a new oncogenic fusion transcript is the molecular mechanism underlying these inv(3)/t(3;3) myeloid neoplasms.
|
27628325 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
A PDPN expressing model of CAFs made it possible to demonstrate the same CCL21/CCR7 axis involvement in the tumor cells to CAFs recognition mechanism through PDPN binding of CCL21.
|
28416768 |
2017 |