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Analysis was done using random and fixed models and both were reported. For effect sizes, a 95% CI was used, and a P value of less than.
#COMPREHENSIVE META ANALYSIS EXCEL SOFTWARE#
The meta-analysis was performed using Comprehensive Meta-analysis software version 3. The extracted data included HRs for PFS and OS. Information was extracted from the papers by reading through the main texts and tables, and a second author reviewed the information collected to ensure its accuracy. Information was extracted using a prespecified extraction table. Risk of bias for selected papers was assessed using the Cochrane Collaboration tool and then classified as high, uncertain, or low. Three authors independently reviewed all articles and abstracts and excluded the irrelevant trials. Papers that did not meet the above criteria were excluded. included only patients 18 years or older andĤ. compared PARP inhibitors against SOC in patients with mCRPC ģ. To be included, however, the papers had to report on RCTs that:ġ.
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Papers had no restrictions in terms of date or status of publications. Search terms used were PARP inhibitors, prostate cancer, prostate neoplasm, olaparib (Lynparza), veliparib. The databases accessed were Cochrane Central Registry of Clinical Trials, Embase, and PubMed. The aim of this meta-analysis is to analyze the efficacy of these drugs in the treatment of mCRPC in terms of progression-free survival (PFS) and overall survival (OS), using the results of completed trials. 9,13 In 2020, for the first time, the FDA approved PARP inhibitors for use in mCRPC. 12 Previous study results have shown that these PARP inhibitors are synergistic when used with agents affecting the AR pathway regardless of HRR mutation status. 9-11 The mechanism of action of PARP inhibitors includes physical obstruction of the replication fork (PARP trapping), which affects HRR, resulting in DNA double-strand breaks. 9 Several cancers, including prostate cancer, exhibit increased PARP1 activity or expression. 6-8 An example of such an enzyme is PARP1, which is involved in identifying single-stranded DNA breaks and their repair through the base excision method. Recent study results indicate that the androgen receptor (AR) regulates the DNA repair pathways, and reciprocally, several enzymes involved in DNA repair can moderate AR activity. PARP1 (or PARP) inhibitors are used in patients with mutations in homologous recombination repair (HRR) genes (most commonly, BRCA1/2). Other treatment options include pembrolizumab (Keytruda) for PD-L1–positive and microsatellite instability (MSI)–high disease, and radium-223 (Xofigo) for bone metastasis. Previously, CRPC was called “androgen-independent prostate cancer” and “hormone-refractory prostate cancer.” 4 Subsequently, results of several studies showed that intratumoral (intracrine and paracrine) androgen production plays a significant role in the development of resistance among prostate cancer cells to testosterone suppression therapy. 3įor decades the standard-of-care (SOC) treatment for metastatic CRPC (mCRPC) has been composed of cytotoxic agents, including taxanes (docetaxel or cabazitaxel ), and second-generation antihormonal agents (antihormonal therapy AHT) such as abiraterone (Zytiga) or enzalutamide (Xtandi). Unfortunately, the majority of patients with prostate cancer progress to castration-resistant disease within 2 to 3 years. If disease progression occurs while the patient is receiving ADT, the disease is noted to be castration-resistant prostate cancer (CRPC). Patients with high-risk disease are treated with prostatectomy and/or external beam radiotherapy followed by androgen deprivation therapy (ADT) as maintenance therapy. Gleason scoring is commonly used for histopathologic evaluation and for clinical and pathologic staging of disease. 2 The best-known risk factors for prostate cancer are race (ie, African American descent), obesity, and genetics (eg, BRCA1/2 mutations).
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1 According to one estimate, 1 in 7 US men and 1 in 25 men worldwide will be diagnosed with prostate cancer during his lifetime.1 Despite the advanced screening methods available, such as measurement of prostate-specific antigen levels, the incidence of metastatic disease remains as high as 20%. Prostate cancer is the second most common and fifth most aggressive cancer among men worldwide.