scholarly journals Epidemiology, Staging and Management of Prostate Cancer

2020 ◽  
Vol 8 (3) ◽  
pp. 28 ◽  
Author(s):  
Adam Barsouk ◽  
Sandeep Anand Padala ◽  
Anusha Vakiti ◽  
Azeem Mohammed ◽  
Kalyan Saginala ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
External Beam Radiotherapy ◽  
Specific Antigen ◽  
Parp Inhibitors ◽  
Clinical Staging ◽  
Castration Resistance ◽  
National Guidelines ◽  
Psa Testing ◽  
Radium 223 ◽  
The Us

Prostate cancer is the second most common and fifth most aggressive neoplasm among men worldwide. It is particularly incident in high human development index (HDI) nations, with an estimated one in seven men in the US receiving a prostate cancer diagnosis in their lifetime. A rapid rise and then fall in prostate cancer incidence in the US and Europe corresponded to the implementation of widespread prostate specific antigen (PSA) testing in 1986 and then subsequent fall from favor due to high rates of false positives, overdiagnosis, and overtreatment (as many as 20–50% of men diagnosed could have remained asymptomatic in their lifetimes). Though few risk factors have been characterized, the best known include race (men of African descent are at higher risk), genetics (e.g., BRCA1/2 mutations), and obesity. The Gleason scoring system is used for histopathological staging and is combined with clinical staging for prognosis and treatment. National guidelines have grown more conservative over the past decades in management, recommending watchful waiting and observation in older men with low to intermediate risk disease. Among higher risk patients, prostatectomy (robotic is preferred) and/or external beam radiotherapy is the most common interventions, followed by ADT maintenance. Following progression on androgen deprivation therapy (ADT) (known as castration-resistance), next generation endocrine therapies like enzalutamide, often in combination with cytotoxic agent docetaxel, are standard of care. Other promising treatments include Radium-223 for bone metastases, pembrolizumab for programmed death ligand-1 (PDL1) and microsatellite instability (MSI) high disease, and poly ADP ribose polymerase (PARP) inhibitors for those with mutations in homologous recombination (most commonly BRCA2).

Healthcare resource use (HRU) in men with metastatic castration sensitive prostate cancer (mCSPC) receiving androgen deprivation therapy (ADT) only or no treatment in the United States (US).

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e19138-e19138
Author(s):  
Xuehua Ke ◽  
Marie-Hélène Lafeuille ◽  
Hela Romdhani ◽  
Frederic Kinkead ◽  
Peter St. John Francis ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Resource Use ◽  
Treatment Initiation ◽  
Specific Antigen ◽  
The United States ◽  
Abiraterone Acetate ◽  
Continuous Variables ◽  
Castration Resistance ◽  
Diagnosis Code ◽  
The Us

e19138 Background: mCSPC is clinically complex. Although consensus on treatments are evolving, ADT remains the backbone of therapy. This study assessed the proportion of mCSPC patients treated with ADT only or remaining untreated and their HRU during the mCSPC period in the US. Methods: The Optum Clinformatics Extended DataMart was used to identify men with ≥2 claims for prostate cancer (PC), ≥1 claim for metastasis, ≥1 castration sensitivity (CS) indicator (CS diagnosis code [dx]; castration and no prostate-specific antigen [PSA] rise; or hormone/castration naive for ≥18 months [mo] before index [date of 1st metastasis dx on or after 1st PC dx and between 2015-2018]). Patients were excluded if they had a pre-index castration-resistance (CR) indicator (CR dx; castration within ≥90 days pre-index or with PSA rise; or a claim for a drug solely recommended for metastatic CRPC). mCSPC period (F/U) was defined as time from index until CR (i.e., any post-index CR indicator or initiation of abiraterone acetate or docetaxel ≥12 mo after post-index ADT initiation or ≥12 mo post-index for those with no ADT) or end of data. The proportion of patients receiving ADT only or no mCSPC treatment during F/U was reported. Per-patient-per-year (PPPY) all-cause HRU were evaluated during baseline (12 mo pre-index) and F/U. Descriptive statistics were used: n (%) for binary and mean [SD] for continuous variables. Results: A total of 2,825 mCSPC patients were identified (age: 75 [9] years). Of these, 2,181 (77%) received ADT only or no treatment in a F/U of 10.9 [9.0] mo. Among them, there were more patients with ≥1 inpatient (IP) stay or ≥1 emergency room (ER) visit (F/U vs. baseline; IP: 50% vs. 20%; ER: 57% vs. 44%), and patients had more IP stays and ER visits (IP: 2.0 [4.0] vs. 0.3 [0.7] stays; ER: 3.2 [7.1] vs. 1.1 [2.2] visits) and more IP days (27 [61] vs. 3 [11] days) PPPY in F/U vs. baseline. Trends were similar among patients receiving ADT only (N=1,252 [44%]; F/U of 12.6 [9.0] mo; Table). Conclusions: The majority of mCSPC patients were treated with ADT only or remained untreated and incurred substantial HRU. These findings suggest that improvements in therapy and prompt treatment initiation in men with mCSPC are needed to improve outcomes. [Table: see text]

Bone modifying agents in veterans with castration-resistant prostate cancer.

2021 ◽  
Vol 39 (15_suppl) ◽  
pp. 6582-6582
Author(s):  
Jordan Bauman ◽  
Kyle Kumbier ◽  
Jennifer A. Burns ◽  
Jordan Sparks ◽  
Phoebe A. Tsao ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Zoledronic Acid ◽  
Bone Metastases ◽  
Specific Antigen ◽  
Veterans Health ◽  
Health Administration ◽  
Castration Resistant Prostate Cancer ◽  
National Guidelines ◽  
Castration Resistant ◽  
Unit Increase

6582 Background: Skeletal related events (SREs) are a known complication for the 80% of men with metastatic prostate cancer who have bone metastases. Previous studies have demonstrated that bone modifying agents (BMAs) such as zoledronic acid and denosumab reduce SREs in men with metastatic castration-resistant prostate cancer who have bone metastases and are now recommended by national guidelines. We sought to investigate factors associated with use of BMAs in Veterans with CRPC across the Veterans Health Administration (VA). Methods: Using the VA Corporate Data Warehouse, consisting of aggregated medical record data from 130 facilities, we used an algorithm previously published to identify men with a diagnosis of castration-resistant prostate cancer (CRPC) based on rising prostate specific antigen (PSA) levels while on androgen deprivation therapy and who received systemic treatment for CRPC with one of the commonly used therapies: abiraterone, enzalutamide, docetaxel, ketoconazole between 2010 and 2017. To account for clustering among facilities, we used a multilevel multivariable logistic regression to determine the association of patient and disease-specific variables on the odds of a patient receiving a BMA after they started treatment for CRPC. Results: Of 4,998 patients with CRPC in our cohort, 2223 (44%) received either zoledronic acid or denosumab at some point after they were initiated on treatment for CRPC. After adjusting for other variables and accounting for a facility, the odds of receiving a BMA decreased by 3% for every additional year of age (odds ratio [OR] 0.97, 95% confidence interval [CI] 0.96-0.98), and decreased significantly with increasing comorbid conditions (OR 0.94, 95% CI 0.72-0.98 for Charlson Comorbidity Index [CCI] of 1; OR 0.69, 95% CI 0.59-0.81 for CCI 2+). Patients who were Black had 25% lower odds of receiving a BMA than patients who were White (OR 0.75, 95% CI 0.65-0.87). PSA at time of CRPC treatment start had a small but not significant effect on receipt of a BMA (OR 1.04, 95% CI 1.00-1.08) for every unit increase of PSA on the log scale. PSA doubling time was not associated with receipt of a BMA. The presence of a diagnosis code for bone metastases was far lower than expected in this cohort of patients with CRPC (40.7%), and thus was not included in the model. We did not expect the presence of bone metastases to vary significantly among the other independent variables. Conclusions: Despite most patients with CRPC historically having bone metastases, less than half of patients with CRPC received a BMA. Patients who are older, had more comorbidities, or were Black were less likely to receive a BMA after starting treatment for CRPC. Understanding factors that lead to different patterns of treatment can guide initiatives toward more guideline-concordant care.

Trends in Prostate Specific Antigen (PSA) testing and prostate cancer incidence and mortality in Australia: A critical analysis

2022 ◽  
Vol 77 ◽  
pp. 102093
Author(s):  
Thanya Pathirana ◽  
Rehan Sequeira ◽  
Chris Del Mar ◽  
James A. Dickinson ◽  
Bruce K. Armstrong ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Prostate Specific Antigen ◽  
Cancer Incidence ◽  
Critical Analysis ◽  
Specific Antigen ◽  
Prostate Cancer Incidence ◽  
Psa Testing ◽  
Incidence And Mortality

Hormonal therapy of prostate cancer

2011 ◽  
pp. 1622-1634
Author(s):  
Ciara O’Hanlon Brown ◽  
Jonathan Waxman
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Specific Antigen ◽  
Intraepithelial Neoplasia ◽  
Peripheral Zone ◽  
Molecular Feature ◽  
Molecular Defects ◽  
Psa Testing ◽  
Seer Data ◽  
Prostate Cancers

Prostate cancer is the most common cancer to effect men and the second most common cause of cancer-related death. Premalignant change or prostatic intraepithelial neoplasia has been detected within the prostate glands of men under 30 years of age. The incidence of prostate cancer remains negligible until men reach their 40s from whence it rises steadily and by 80 years 70% of men have detectable tumours at autopsy (1). A majority of prostate cancers arise from the peripheral zone of the prostate and rarely cause obstructive symptoms. Consequently, prostate cancers have historically presented late, with symptoms of metastatic disease. The advent of prostate-specific antigen (PSA) testing has produced a stage shift so that at present over 90% of prostate cancers are diagnosed as organ-confined disease. PSA diagnosis has unmasked a subset of prostate tumours that exhibit an indolent growth pattern and appear destined to remain organ-confined tumours the patient dies with, and not from. US SEER data estimates a 50-year-old man has a 42% chance of developing prostate cancer but only a 3.6% chance of dying from the disease. Features, either clinical or molecular, which would allow clinicians to clearly differentiate indolent from aggressive disease while still at the organ-confined stage, have yet to be identified (1). Adenocarcinoma is the predominant histological subtype of prostate cancer, accounting for 95% of tumours. Prostatic adenocarcinomas arise from androgen receptor-positive epithelial cells. On histological examination, prostate cancers appear multifocal and demonstrate heterogeneity both within individual tumours and across populations. This has created an obstacle as researchers attempt to subclassify prostate cancer and identify the molecular defects responsible for driving prostatic carcinogenesis (1). Of prostate cancers, 80–90% are androgen receptor-positive at diagnosis (2), thus to date the androgen–androgen receptor axis is the sole molecular feature of this disease that has been successfully harnessed as a therapeutic target.

scholarly journals Accuracy of Tumour-Associated Circulating Endothelial Cells as a Screening Biomarker for Clinically Significant Prostate Cancer

Cancers ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1064 ◽  
Author(s):  
Sebastian Chakrit Bhakdi ◽  
Prapat Suriyaphol ◽  
Ponpan Thaicharoen ◽  
Sebastian Tobias Karl Grote ◽  
Chulaluk Komoltri ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endothelial Cells ◽  
Predictive Value ◽  
Specific Antigen ◽  
Transrectal Ultrasound ◽  
Circulating Endothelial Cells ◽  
Index Test ◽  
Psa Testing ◽  
Diagnostic Potential ◽  
Clinically Significant

Even though more than 350,000 men die from prostate cancer every year, broad-based screening for the disease remains a controversial topic. Guidelines demand that the only commonly accepted screening tool, prostate-specific antigen (PSA) testing, must be followed by prostate biopsy if results are elevated. Due to the procedure’s low positive predictive value (PPV), however, over 80% of biopsies are performed on healthy men or men with clinically insignificant cancer—prompting calls for new ways of vetting equivocal PSA readings prior to the procedure. Responding to the challenge, the present study investigated the diagnostic potential of tumour-associated circulating endothelial cells (tCECs), which have previously been described as a novel, blood-based biomarker for clinically significant cancers. Specifically, the objective was to determine the diagnostic accuracy of a tCEC-based blood test to detect clinically significant prostate cancer (defined as Gleason score ≥ 3 + 4) in high-risk patients. Performed in a blinded, prospective, single-centre set-up, it compared a novel tCEC index test with transrectal ultrasound-guided biopsy biopsy as a reference on a total of 170 patients and found that a tCEC add-on test will almost double the PPV of a standalone PSA test (32% vs. 17%; p = 0.0012), while retaining a negative predictive value above 90%.

scholarly journals PARP Inhibitors in Prostate Cancer—The Preclinical Rationale and Current Clinical Development

Genes ◽  
2019 ◽  
Vol 10 (8) ◽  
pp. 565 ◽  
Author(s):  
Virtanen ◽  
Paunu ◽  
Ahlskog ◽  
Varnai ◽  
Sipeky ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Clinical Trials ◽  
Dna Repair ◽  
Therapeutic Potential ◽  
Parp Inhibitor ◽  
Parp Inhibitors ◽  
Treatment Modalities ◽  
Cancer Type ◽  
Castration Resistance ◽  
Single Strand Break

Prostate cancer is globally the second most commonly diagnosed cancer type in men.Recent studies suggest that mutations in DNA repair genes are associated with aggressive forms ofprostate cancer and castration resistance. Prostate cancer with DNA repair defects may bevulnerable to therapeutic targeting by Poly(ADP‐ribose) polymerase (PARP) inhibitors. PARPenzymes modify target proteins with ADP‐ribose in a process called PARylation and are inparticular involved in single strand break repair. The rationale behind the clinical trials that led tothe current use of PARP inhibitors to treat cancer was to target the dependence of BRCA‐mutantcancer cells on the PARP‐associated repair pathway due to deficiency in homologousrecombination. However, recent studies have proposed therapeutic potential for PARP inhibitorsin tumors with a variety of vulnerabilities generating dependence on PARP beyond the syntheticlethal targeting of BRCA1/BRCA2 mutated tumors, suggesting a wider potential than initiallythought. Importantly, PARP‐associated DNA repair pathways are also closely connected toandrogen receptor (AR) signaling, which is a key regulator of tumor growth and a centraltherapeutic target in prostate cancer. In this review, we provide an extensive overview of publishedand ongoing trials exploring PARP inhibitors in treatment of prostate cancer and discuss theunderlying biology. Several clinical trials are currently studying PARP inhibitor mono‐andcombination therapies in the treatment of prostate cancer. Integration of drugs targeting DNArepair pathways in prostate cancer treatment modalities allows developing of more personalizedcare taking also into account the genetic makeup of individual tumors.

Overdiagnosis and Overtreatment of Prostate Cancer

2012 ◽  
pp. e35-e39 ◽  
Author(s):  
Ian M. Thompson
Keyword(s):  
Prostate Cancer ◽  
Active Surveillance ◽  
Specific Antigen ◽  
The United States ◽  
Assessment Tools ◽  
Low Grade ◽  
High Grade ◽  
Surveillance Strategy ◽  
Psa Testing ◽  
Prostate Cancer Prevention

Overview: Prostate cancer is a ubiquitous disease, affecting as many as two-thirds of men in their 60s. Through widespread prostate-specific antigen (PSA) testing, increasing rates of prostate biopsy, and increased sampling of the prostate, a larger fraction of low-grade, low-volume tumors have been detected, consistent with tumors often found at autopsy. These tumors have historically been treated in a manner similar to that used for higher-grade tumors but, more recently, it has become evident that with a plan of active surveillance that reserves treatment for only those patients whose tumors show evidence of progression, very high disease-specific survival can be achieved. Unfortunately, the frequency of recommendation of an active surveillance strategy in the United States is low. An alternative strategy to improve prostate cancer detection is through selected biopsy of those men who are at greater risk of harboring high-grade, potentially lethal cancer. This strategy is currently possible through the use of risk assessment tools such as the Prostate Cancer Prevention Trial Risk Calculator ( www.prostate.cancer.risk.calculator.com ) as well as others. These tools can predict with considerable accuracy a man's risk of low-grade and high-grade cancer, allowing informed decision making for the patient with a goal of detection of high-risk disease. Ultimately, other biomarkers including PCA3, TMPRSS2:ERG, and [-2]proPSA will likely aid in discriminating these two types of cancer before biopsy.

scholarly journals Prostate Cancer Screening in the Workplace

AAOHN Journal ◽  
1998 ◽  
Vol 46 (8) ◽  
pp. 379-384 ◽  
Author(s):  
Claire Snyder ◽  
Peggy N. Schrammel ◽  
Claudia B. Griffiths ◽  
Robert I. Griffiths
Keyword(s):  
Prostate Cancer ◽  
Cancer Screening ◽  
Prostate Cancer Screening ◽  
Specific Antigen ◽  
Screening Tests ◽  
Test Results ◽  
Total Cost ◽  
Screening Programs ◽  
Psa Testing ◽  
The Cost

Recognition of the mortality and morbidity associated with prostate cancer has resulted in employer based screening programs. This retrospective cohort study identified the employer costs of prostate cancer screening and referrals due to abnormal test results. The subjects were 385 men enrolled in a workplace screening program at a single employer between 1993 and 1995. Screening consisted of digital rectal examination (DRE) annually for enrolled employees aged 40 years and older, plus annual prostate specific antigen (PSA) testing for those 50 and older, and those 40 and older and considered at high risk. Data related to the health care and lost productivity costs of screening and referrals for abnormal test results were collected and analyzed. The total cost of screening was $44,355, or approximately $56 per screening encounter (788 DREs; 437 PSAs). Abnormal screening tests resulted in 52 referrals. Upon further evaluation, 42% were found to have an enlargement, 29% a node, and 12% benign prostatic hyperplasia. Only one malignancy was found. The total cost of additional referrals was $31,815, or 42% of the cost of screening plus referrals. As the cost per screening encounter was low, prostate cancer screening in the workplace is an efficient alternative.

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