BRCA2: The Potential Drug Target and Biomarker for Ovarian Cancer

Target Name: BRCA2

NCBI ID: G675

BRCA2

BRCA2: The Potential Drug Target and Biomarker for Ovarian Cancer

Ovarian cancer is a leading cause of cancer death in women, with estimates suggesting that in the United States alone, over 21,000 women will be diagnosed with ovarian cancer this year. Despite advances in treatment, the survival rate for ovarian cancer remains relatively poor, with a five-year survival rate of only 40%. The discovery ofBRCA2, a gene that has been identified as a potential drug target and biomarker for ovarian cancer, has brought new hope to researchers and patients alike.

BRCA2: The Gene and Its Function

BRCA2 is a tumor suppressor gene that is located on the X chromosome. It is responsible for producing a protein known as BRCA2, which plays a critical role in the development and maintenance of cancer cells. BRCA2 mutations have been identified in a variety of ovarian cancer types, including epithelial, endometrial, and fallopian tube cancers.

BRCA2 also has been shown to be involved in the regulation of cell growth and division, as well as the development of resistance to chemotherapy. These functions make it an attractive target for drug development in ovarian cancer.

Drugs that target BRCA2 have the potential to disrupt the growth cycle of cancer cells, leading to a reduction in cell division and a decrease in the production of new cancer cells. This can lead to a reduction in the size and severity of tumors, as well as improved survival.

BRCA2 as a Biomarker

The identification of BRCA2 as a potential drug target for ovarian cancer has also led to the development of a new biomarker for the disease. The detection of BRCA2 mutations can be done through a variety of techniques, including DNA sequencing and array-based assays. Once BRCA2 mutations are identified, they can be used to predict the risk of ovarian cancer and to identify patients who may benefit from targeted therapy.

BRCA2 also has the potential to be used as a biomarker for tracking the effectiveness of treatments. By measuring the levels of BRCA2 in cancer cells before and after treatment, researchers can determine the effectiveness of different treatments and identify potential areas for improvement.

BRCA2: The Potential Drug Target

BRCA2 has been shown to be involved in the development and maintenance of ovarian cancer, as well as the regulation of cell growth and division. This makes it an attractive target for drug development in ovarian cancer.

One potential drug that targets BRCA2 is called \"PARP inhibitor.\" These drugs work by inhibiting the activity of the PARP enzyme, which is responsible for repairing damaged DNA. When DNA is damaged, the PARP enzyme helps to repair it, but in the case of cancer cells, this repair process can lead to the continued growth and division of damaged cells.

PARP inhibitors have been shown to be effective in the treatment of ovarian cancer, particularly in cases where the cancer has a BRCA2 mutation. These drugs have been shown to reduce the size and severity of tumors, as well as improve survival.

Another potential drug that targets BRCA2 is called a \"CDK inhibitor.\" These drugs work by inhibiting the activity of the CDK4 enzyme, which is involved in cell growth and division. CDK4 inhibitors have been shown to be effective in the treatment of breast and ovarian cancer, particularly in cases where the cancer has a BRCA2 mutation.

BRCA2: The Biomarker

BRCA2 mutations have been identified in a variety of ovarian cancer types, including epithelial, endometrial, and fallopian tube cancers. The detection of BRCA2 mutations can be done through a variety of techniques, including DNA sequencing and array-based assays.

Once BRCA2 mutations are identified, they can be used to predict the risk of ovarian cancer

Protein Name: BRCA2 DNA Repair Associated

Functions: Involved in double-strand break repair and/or homologous recombination. Binds RAD51 and potentiates recombinational DNA repair by promoting assembly of RAD51 onto single-stranded DNA (ssDNA). Acts by targeting RAD51 to ssDNA over double-stranded DNA, enabling RAD51 to displace replication protein-A (RPA) from ssDNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis. Part of a PALB2-scaffolded HR complex containing RAD51C and which is thought to play a role in DNA repair by HR. May participate in S phase checkpoint activation. Binds selectively to ssDNA, and to ssDNA in tailed duplexes and replication fork structures. May play a role in the extension step after strand invasion at replication-dependent DNA double-strand breaks; together with PALB2 is involved in both POLH localization at collapsed replication forks and DNA polymerization activity. In concert with NPM1, regulates centrosome duplication. Interacts with the TREX-2 complex (transcription and export complex 2) subunits PCID2 and SEM1, and is required to prevent R-loop-associated DNA damage and thus transcription-associated genomic instability. Silencing of BRCA2 promotes R-loop accumulation at actively transcribed genes in replicating and non-replicating cells, suggesting that BRCA2 mediates the control of R-loop associated genomic instability, independently of its known role in homologous recombination (PubMed:24896180)

The "BRCA2 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about BRCA2 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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