scholarly journals Concordance between administrative claims and registry data for identifying metastasis to the bone: an exploratory analysis in prostate cancer

2014 ◽  
Vol 14 (1) ◽  
Author(s):  
Eberechukwu Onukwugha ◽  
Candice Yong ◽  
Arif Hussain ◽  
Brian Seal ◽  
C Daniel Mullins
2021 ◽  
Vol 39 (15_suppl) ◽  
pp. e17056-e17056
Author(s):  
Atul Batra ◽  
Shiying Kong ◽  
Winson Y. Cheung

e17056 Background: Prior cardio-oncology research has focused on examining the future risk of CVD as a result of cancer treatments. The impact of pre-existing CVD on cancer treatments is less clear. This study aimed to identify the associations of baseline CVD on treatment patterns and survival outcomes in metastatic prostate cancer where older age and exposure to androgen deprivation therapy can potentiate cardiac risks. Methods: We identified all patients diagnosed with metastatic prostate cancer in a large Canadian province from 2004 to 2017 using the population-based cancer registry. Administrative claims were linked to ascertain any diagnoses of pre-existing CVD, defined as any of arrythmias [AR], cerebrovascular accidents [CVAs], myocardial infarctions [MIs], or congestive heart failure [CHF] that preceded the diagnosis of metastatic prostate cancer. Logistic and Cox regression models were constructed to determine the associations of baseline CVD with receipt of cancer treatments (such as radiation, or systemic therapy) and overall survival (OS). Results: A total of 3,257 patients were included. The median age was 66 years (interquartile range, 46-95 years). At diagnosis of advanced prostate cancer, 993 (30.5%) had pre-existing CVD: 10.0% AR, 4.3% CVAs, 3.0% MIs, 2.8% CHF and 10.4% multiple CVDs. The Charlson comorbidity index (CCI) was 0, 1 and >1 in 53.4%, 27.3% and 19.3%, respectively. Overall, 2078 (63.8%) patients received chemotherapy, while 747 (22.9%) received radiotherapy. After adjusting for age and CCI, pre-existing CVD was associated with a lower likelihood of chemotherapy (odds ratio [OR], 0.67; 95% confidence interval [CI], 0.61-0.75; P=0.001) and radiotherapy (OR, 0.87; 95% CI, 0.85-0.91; P<0.001). Likewise, CVD was associated with worse OS, after adjusting for measured confounding variables (see table). Conclusions: One-third of patients with metastatic prostate cancer had pre-existing CVD, which was associated with a lower likelihood of chemotherapy and worse OS. In the context of an aging general population, early cardio-oncology consultations to optimize CVD management may lead to safer and broader uptake of appropriate prostate cancer treatments.[Table: see text]


2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 5036-5036
Author(s):  
Eddy Shih-Hsin Yang ◽  
Benjamin Leiby ◽  
Guru P. Sonpavde ◽  
David Johnson Einstein ◽  
Zachary L. Quinn ◽  
...  

5036 Background: Rad is an alpha particle emitter that causes DNA double strand breaks and has been FDA-approved for use in mCRPC pts with bone metastases. PARP-1 activity critically supports androgen receptor (AR) activity in mCRPC and potentiates AR-dependent DNA damage response pathways that promote prostate cancer cell survival. Nira is a potent and selective PARP-1/2 inhibitor that has shown single agent clinical activity in mCRPC. We previously reported the safety of targeting the PARP-1/AR axis with Nira in combination with Rad. Herein we describe the results of an exploratory biomarker analysis. Methods: The primary objective of NiraRad is to determine the optimum Ph II dose of Nira plus Rad (55 kBq/kg of body weight IV every 4 weeks (wks) x 6) in pts with and without prior chemotherapy (docetaxel). Pts were enrolled to one of three dose levels of Nira (100, 200, or 300 mg PO daily). All cohorts were combined for exploratory biomarker analysis using Nanostring PanCancer Driver and Immune Pathways panels and the nSolver Advanced analysis module was performed on blood obtained from 23 pts at baseline, cycle (C) 1 day (D) 15, and C3D15. A favorable response was defined as any PSA reduction at week 12 or treatment (tx) duration > 18 wks, the median time on tx in the cohort of pts analyzed. A threshold of > 2 fold (X) differentially expressed genes was used. Results: Of the 23 pts with biomarker data, 7 (30%) experienced PSA reductions and 11 (48%) received tx for > 18 wks, 6 of which also had PSA reductions. Exploratory analysis revealed that the PI3K/Ras, MAPK, and transcriptional misregulation pathways were differentially regulated in pts who had favorable responses. The top downregulated gene, PAX5, which has been shown to promote prostate cancer growth, was decreased at C1D15 (2.7X, p < 0.01) and C3D15 (4.8X, p < 0.001) in pts with tx duration > 18 wks and at baseline in pts who had PSA reductions (3.1X, p < 0.05). Immune pathways analysis suggested downregulation of immunosuppressive B-cell (plasma cell) and upregulation of NK and T cell pathways in pts with tx duration > 18 wks. Conclusions: Previously Nira and Rad have been shown to have acceptable tolerability in mCRPC pts. This exploratory analysis suggests potential response biomarkers that warrant further investigation. Managed by: the Prostate Cancer Clinical Trials Consortium; Funded by: Janssen Pharmaceuticals and Bayer Healthcare Pharmaceuticals, Inc. Clinical trial information: NCT03076203.


2018 ◽  
Vol 42 (9) ◽  
pp. 593-599
Author(s):  
A.J. Virseda-Rodríguez ◽  
C. Salvatierra ◽  
F. García ◽  
A. Sanz ◽  
E. Gutiérrez ◽  
...  

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e13592-e13592 ◽  
Author(s):  
Katrine Wallace ◽  
Adrienne Landsteiner ◽  
Scott Bunner ◽  
Nicole Engel-Nitz ◽  
Amy Luckenbaugh

e13592 Background: To date, there has been a paucity of information in the literature describing the epidemiology of mCRPC within the prostate cancer population. We present a real-world data study describing characteristics and mortality of patients with mCRPC within an administrative claims database of an insured population within the United States. Methods: In an administrative claims database of ≈18,000,000 covered lives, adult male patients were included if they had ≥1 claim for prostate cancer (ICD-9: 185 or 233.4; ICD-10: C61 or D075), underwent pharmacologic or surgical castration, and had a code for metastatic disease during the identification period (January 1, 2008–March 31, 2018). The index date was the first metastatic claim; 6 months of continuous enrollment (CE) prior to (baseline period) and after (follow-up period) the index date was required. Patients with metastatic claims in the baseline period were excluded. Patients were followed until the earliest of: death (unless prior to the 6-month CE), end of study period, or disenrollment. A claims-based algorithm was employed to identify locally advanced and distant mCRPC patients in the prostate cancer study population. Mortality data were sourced from the Social Security Administration Medicare data, and a claims algorithm. Results: 343,089 patients were identified with a claim for prostate cancer; of those, 3690 mCRPC cases (1.1%) were identified using the claims-based algorithm and met the study inclusion criteria. Median age was 75 years. Insurance type included commercial plans (27%) and Medicare (73%). Castration type included pharmacologic (99%) and surgical (1%). First claims for metastases were most commonly in the bone (65%) or lymph nodes (15%), with 20% in other sites. The study population averaged a Charlson comorbidity index score of 3.05 at baseline, with 16% of patients receiving a score of ≥5. The most common baseline comorbidities were hypertension (67%), urinary disease (58%), dyslipidemia (52%), and cardiac disease (45%). Median follow-up time among the mCRPC group was 538 days, during which 1834 deaths occurred; 50% of the population experienced mortality during the study period. Conclusions: This study provides valuable insights into the epidemiology, clinical characteristics, prevalence rate, and mortality of patients with mCRPC. Given the high mortality proportion of this disease, the development of novel therapies to prolong life in patients with mCRPC is warranted.


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