|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The participation of TOP2 in generating persistent DNA breaks and leading to diseases such as cancer, could have an impact on disease treatment and prevention.
|
31614754 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Taken together with the recent clinical data obtained with AML patients targeted with TOP2 poisons, our study suggests a novel mechanism of cancer chemoresistance toward combination therapies administering TOP2 poisons or inhibitors.
|
31271486 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
And both GEPIA analysis and immunohistochemistry experiment (IHC) confirmed that TOP2A was aberrant gain of expression in cancer comparing to normal tissues.
|
31528121 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Novel Deazaflavin Analogues Potently Inhibited Tyrosyl DNA Phosphodiesterase 2 (TDP2) and Strongly Sensitized Cancer Cells toward Treatment with Topoisomerase II (TOP2) Poison Etoposide.
|
30998359 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
As a DNA replication- and cell division-regulating enzyme, TOP2A is the main target of many anticancer therapy regimens; however, the exact role of TOP2A in cancer remains elusive.
|
30672125 |
2019 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Bioinformatics analyses conducted on the co-expressed genes of TOP1 and TOP2A revealed that the topoisomerases were involved in several key cancer-related pathways, including the 'p53 pathway', 'pathway in cancer' and 'apoptosis signaling pathway'.
|
30132517 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The aim of this meta-analysis was to elucidate whether TOP2A could predict prognosis of cancer.
|
29937926 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The proportion of TOP2A-positive cancer cells was significantly higher among anthracycline responders than among nonresponders in HR-negative cancer (15.4% ±17.5% vs. 2.0% ± 2.4%, respectively, P = 0.048), whereas TOP2A and TIMP-1 expression statuses did not differ in HR-positive cancer.
|
29516929 |
2018 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Poisons of topoisomerase II (TOP2) kill cancer cells by preventing religation of intermediate DNA breaks during the enzymatic process and thus by accumulating enzyme-drug-DNA complexes called TOP2 cleavage-complex (TOP2cc).
|
28611105 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Importantly, TOP2A and EZH2 in prostate cancer cells act as key driving oncogenes, a fact highlighted by sensitivity to combination-targeted therapy.<b>Conclusions:</b> Overall, our data support further assessment of TOP2A and EZH2 as biomarkers for early identification of patients with increased metastatic potential that may benefit from adjuvant or neoadjuvant targeted therapy approaches.<i>Clin Cancer Res; 23(22); 7072-83.©2017 AACR</i>.
|
28899973 |
2017 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
For this reason, TOP2A is the target of the most widely successful drugs in cancer chemotherapy, such as TOP2A poisons, which stabilize TOP2A-DNA cleavage complexes and create DSBs, leading to chromosome damage and cell death.
|
23928695 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Overexpression of mir-23a could significantly potentiate the in vitro and in vivo anti-tumor effect of etoposide; however, ectopic expression of miR-23a fails to sensitize HCC cells to 5-fluorouracil treatment, indicating the miR-23a-induced cancer cell hypersensitivity in chemotherapy is TOP2A-specific though miR-23a overexpression could not directly up-regulate TOP2A expression.
|
24103454 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Topoisomerase II (TOP2)-targeting poisons such as anthracyclines and etoposide are commonly used for cancer chemotherapy and kill tumor cells by causing accumulation of DNA double-strand breaks (DSB).
|
23222298 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Our results suggest that TOP2 isozymes contribute to NO-induced mutagenesis and subsequent cancer development during chronic inflammation.
|
22998676 |
2013 |
|
Primary malignant neoplasm
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This study is to evaluate the expression of Topo-IIα in glioblastoma cancer stem cells (CSCs) and its effects on cell proliferation and apoptosis.
|
22569122 |
2012 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
During a median follow-up period of 55 months (range, 6 to 81 months), the subgroup of patients with hormone receptor-negative cancer and without TOP2A amplification showed the worst survival (relapse-free survival: hazard ratio (HR) = 0.29, 95% confidence interval (95% CI), 0.13 to 0.65, P = 0.001; and overall survival: HR = 0.28, 95% CI, 0.10 to 0.76, P = 0.008).
|
21288332 |
2011 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The genes MTIM and RRM2 appeared in nine and TOP2A in eight lists of significantly altered genes in cancer.
|
21165954 |
2011 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
By tissue microarray analysis of 172 HCC, we found TOP2A expressions correlated with advance histological grading (p<0.001), microvascular invasion (p=0.004) and an early age onset of the malignancy (<or=40 years; p=0.007).
|
19003983 |
2009 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
HER2 and TOP2A genes, located on 17q, can be coamplified in cancer.
|
17363613 |
2007 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
Simultaneous amplification of HER-2 (ERBB2) and topoisomerase IIalpha (TOP2A) genes--molecular basis for combination chemotherapy in cancer.
|
17100565 |
2006 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Considering the relevance of the TOP2A gene product to anthracycline therapy and the wealth of other cancer-associated genes within the ERBB2/TOP2A region, the pattern of amplification and deletion near ERBB2 and TOP2A may have a dramatic effect on the malignant potential of breast carcinomas and their response to therapy.
|
15034864 |
2004 |
|
Primary malignant neoplasm
|
0.100 |
GeneticVariation
|
group |
BEFREE |
This finding together with the concept that TOP2A gene amplification and deletion seem to account for both relative chemosensitivity and resistance to topoII-inhibitor therapy further highlights the importance of screening for TOP2A gene copy number aberrations when topoII-inhibitors are considered either alone or in combination of other chemotherapeutic drugs for the treatment of cancer patients.
|
14632727 |
2003 |
|
Primary malignant neoplasm
|
0.100 |
Biomarker
|
group |
BEFREE |
The DNA topoisomerase II alpha titration assay is a highly sensitive new technique to study the role of DNA topoisomerase II alpha in drug resistance and may help to identify cancer types and patients most likely to respond to DNA topoisomerase II targeted drugs.
|
8041119 |
1994 |