DNA topoisomerase 2-alpha Antibodies

DNA topoisomerase 2-alpha (TOP2A)

Control of topological states of DNA by transient breakage and subsequent rejoining of DNA strands. Topoisomerase II makes double-strand breaks.

Essential during mitosis and meiosis for proper segregation of daughter chromosomes. May play a role in regulating the period length of ARNTL/BMAL1 transcriptional oscillation (By similarity).

Gene Information

Human
Gene Name:	TOP2A
Uniprot:	P11388
Entrez:	7153

Family

Belongs to:
type II topoisomerase family

Alternative Names

DNA topoisomerase (ATP-hydrolyzing); DNA topoisomerase 2-alpha; DNA topoisomerase II, 170 kD; DNA topoisomerase II, alpha isozyme; EC 5.99.1.3; TOP2; TOP2A; TOP2DNA gyrase; topoisomerase (DNA) II alpha (170kD); topoisomerase (DNA) II alpha 170kDa; TP2A

Molecular Weight

Mass (kDA):
174.385 kDA

Genomic Context

Human
Location:	17q21.2
Sequence:	17; NC_000017.11 (40388525..40417902, complement)

Subcellular Localizations

Cytoplasm. Nucleus, nucleoplasm. Generally located in the nucleoplasm.

Diseases

• Malignant Neoplasms
• Neoplasms
• Malignant Neoplasm Of Breast
• Mammary Neoplasms
• Carcinoma
• Neoplasm Metastasis
• Adenocarcinoma
• Malignant Paraganglionic Neoplasm
• Leukemia
• Cell Transformation, Neoplastic
• Malignant Neoplasm Of Ovary
• Ovarian Neoplasm

• Lymphatic Metastasis
• Ductal Breast Carcinoma
• Lung Neoplasms
• Malignant Neoplasm Of Lung
• Invasive Breast Carcinoma
• Liver Carcinoma
• Ductal Carcinoma

Interacting Proteins

• BRCA1
• CTNNB1
• PRKCD

Pathways

• Cell Proliferation
• Cell Cycle
• Drug Resistance
• Pathogenesis
• Dna Replication
• Dna Repair
• Localization
• Translation
• Cell Division
• Chromosome Condensation
• Reverse Transcription
• Mitosis
• Metaphase

• Methylation
• Cell Adhesion
• Interphase
• Immune Response
• Chromosome Segregation
• Cell Death
• Cell Growth

PTMs

• Phosphorylation
• Methylation
• Acetylation

• Cleavage
• Oxidation
• Dephosphorylation

• Ubiquitination

Research Areas

• Cancer
• Cell Cycle and Replication
• Core ESC-Like Genes
• DNA Repair
• Phospho-Specific

• Stem Cell Markers

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TOP2A

Best Uses Of The TOP2A Marker

The TOP2A Cell-Based ELISA Kit offers a convenient, high-throughput way to measure the TOP2A protein expression profile in cells. This versatile kit also enables researchers to monitor the relative amounts of TOP2A in cultured cells and screen for the effects of different treatments. Although this product is not available for individual purchase, scientists and researchers can purchase it as part of a grant or earn product credits for sharing their results with the community.

High expression of TOP2A might be able to obtain more benefits from adjuvant chemotherapy

Patients with high expression of TOP2A may benefit more from adjuvant chemotherapy. The results of a study from Denmark suggest that patients with high expression of TOP2A may benefit more from adjuvant chemotherapy. The researchers analyzed data from 438 tumors of premenopausal women with node-positive breast cancer treated with cyclophosphamide, epirubicin, and 5-fluorouracil. Their tumors were analyzed for HER2 status and TOP2A expression. They also calculated recurrence-free survival.

The authors conducted an updated analysis on the individual patient data from five similar studies. The authors compared the effects of anthracycline-based and no-anthracycline-based chemotherapy regimens on patients with high expression of TOP2A. They also assessed the impact of TOP2A aberrations on prognosis in patients with high expression of this gene.

The researchers also studied the effects of TOP2A gene amplification on adjuvant chemotherapy for breast cancer. These tumors showed high expression of TOP2A, compared to those without. These patients benefited more from adjuvant chemotherapy than those with low expression. This is the first study to demonstrate that cancer patients with high TOP2A expression may benefit from adjuvant chemotherapy.

The researchers examined the impact of biologic markers on survival for MA.5 patients. HER2 gene amplification and TOP2A deletion had a negative impact on outcome. When combined with the CEP17 gene duplication, TOP2A deletion was significantly associated with worse outcome. Top2A amplification had no effect, but the combined effect was statistically significant.

The researchers analyzed the results of this study by grouping patients with altered TOP2A expression in their tumors into an "altered" group. Although they did not observe an overall difference in RFS and OS, patients with high TOP2A expression may benefit more from adjuvant chemotherapy. The authors also note that alterations in the expression of TOP2A may result in greater response to anthracyclines in patients with cancer with high ER protein levels and HER2 amplification.

Patients with tumors with high TOP2A expression may benefit more from adjuvant chemotherapy than patients with low TOP2A expression. Patients with normal expression of TOP2A had a significantly longer recurrence-free survival than those with abnormal tumors. Patients in CMF and CEF groups received different chemotherapy regimens. In the CEF group, patients with normal expression of TOP2A were treated with anthracycline-containing chemotherapy.

It remains an independent prognostic factor for BRFS

The TOP2A Marker has been found to be an independent prognostic factor in patients with BRFS. The higher the TOP2A expression, the shorter the BRFS. The tumor size also affects TOP2A expression. Tumors that are larger than 5 cm were associated with less TOP2A expression. Patients with a smaller tumor had higher TOP2A expression.

In multivariate analysis, the presence of the TOP2A Marker was an independent prognostic factor for bridging the survival curve of patients with BRFS. Cases with higher levels of TOP2A had a shorter BRFS than patients with lower levels. The presence of SV invasion did not affect the prognostic factor for BRFS.

Moreover, TOP2A expression correlated with node positivity and high nuclear grade, and with ER, PgR, and HER2 positivity. The association between tumor and TOP2A expression was significant in luminal and non-luminal BRFS. Although the study's results are not conclusive, the TOP2A Marker remains an independent prognostic factor for BRFS.

In a recent study, researchers found that patients with high TOP2A expression had significantly shorter BRFS than patients with low expression of the protein. Although this association cannot be verified clinically, these results indicate that TOP2A is a prognostic factor that is useful for clinical trials. Ultimately, TOP2A expression may be associated with the clinical progression of HCC and should be used in combination with other prognostic factors to predict the outcome of patients with BRFS.

Although a small percentage of patients with breast cancer show elevated TOP2A expression, it remained an independent prognostic factor in predicting disease-free survival. In addition to this, TOP2A overexpression was associated with higher Ki67 index and larger tumor size. Further, in early stages of the disease, it correlated with hormone receptor positivity. This suggests that TOP2A overexpression may be a superior prognostic factor compared to gene expression and universality.

While TOP2A is a prognostic marker, it remains controversial whether it is an independent factor in predicting BRFS. Although high TOP2A expression is associated with an improved outcome, there is still a lack of consensus on the optimal cutoff value. The current study included 1084 early breast cancer patients in China. The analysis used a minimum P value method to assess the optimal cut-off value.

Patients with high levels of TOP2A expression experienced significantly shorter overall survival than those with low TOP2A expression. Moreover, high levels of TOP2A are associated with an increased risk for cirrhosis. Furthermore, a poor prognosis after single HCC radical resection are associated with higher levels of liver cirrhosis. This study suggests that high levels of TOP2A are independent prognostic factors for BRFS.

It is a molecular target for many anticancer drugs

The TOP2A marker is a highly expressed gene in various types of cancer. It is responsible for transient DNA double-strand breaks in proliferating cells and resolves DNA topological entanglements during chromosome condensation, replication, and segregation. Several anticancer drugs target this gene. In this review, we discuss how TOP2a poisons inhibit the growth of resistant cells and discuss some of the molecular mechanisms that may contribute to the increased resistance of cancer cells to these drugs.

In addition, the TOP2A marker is a molecule that regulates the activity of a variety of anticancer drugs. Some of these drugs target this protein's LUMO region, a key structural motif in the anticancer molecule. The LUMO region of 38O plays a major role in establishing hydrogen bonds. In addition, there are three pi-alkyl interactions between D10 and TOP2A in the complex, two of which are caused by the Lys723.

Because TOP2A has a predictive value for the effects of anthracycline drugs, TOP2A is a promising biomarker for early diagnosis of cancer patients. In fact, some studies have shown that high TOP2A expression is associated with poor differentiation, metastasis, and death in cancer patients. Another large-scale retrospective study showed a correlation between high TOP2A expression and poor differentiation and neural invasion in esophageal cancer.

Several studies have shown that TOP2A is a biomarker for active proliferating cells. The TOP2A marker is sensitive and specific for malignant tumors. In addition, tumors with increased TOP2A expression exhibit increased cell proliferation. Furthermore, these tumors have invasive characteristics and a poor prognosis. Many anticancer drugs target this gene.

The data collected from the TCGA database were used to analyze the expression levels of TOP2A. Tumor samples with low TOP2A expression were associated with improved overall survival, whereas patients with high TOP2A expression had a worse outcome in all clinical stages. In a subsequent study, TOP2A expression was not associated with better survival among patients with metastatic disease.

Top2A is a molecular marker of human DNA topoisomerase IIa. It plays a vital role in DNA replication. Its ATP-dependent type IIb operates in a process called DNA topoisomerase. Various anticancer drugs target TOP2A to inhibit its function. But the research on TOP2A remains incomplete.

The results of these studies suggest that abnormal TOP2A and CEP17 are a biomarker for TNBC. In addition to this, both abnormal CEP17 and abnormal TOP2A are associated with large treatment effects. In addition, a combination of these two markers can provide consistent results across multiple trials and molecular subgroups. In addition to assessing tumor response, these studies may also help select appropriate treatment.

The TOP2A protein is 1436 amino acids in length. The translation product of TOP2a mRNA harbors exons one to 33 and a partially processed intron 33 that contains an in-frame stop codon and a consensus poly(A) site. TOP2a/160 lacks the C-terminal 108 amino acids (aaa) and NLS 1454-1497.