5-Alpha Reductase 2 as a Marker of Resistance to 5ARI Therapy

• ClinicalTrials.gov Identifier: NCT04288427
• Recruitment Status: Recruiting
• First Posted: February 28, 2020
• Last Update Posted: March 14, 2023
• Sponsor: Beth Israel Deaconess Medical Center
• Collaborator: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
• Information provided by (Responsible Party): Aria F. Olumi, MD, Beth Israel Deaconess Medical Center

Study Description

Brief Summary:

The study is being conducted to learn why some patients with Benign Prostatic Hyperplasia (BPH) do not respond to a commonly used treatment drug, Finasteride. The hope is to find ways to predict which patients will not respond to Finasteride so that, in the future, these patients can be identified prior to offering this treatment and they can be offered alternative treatment strategies in its place. The aim is to see if noninvasive techniques such as MRI can detect inflammation of the prostate to assist with early detection of those who will and who will not respond to Finasteride.

Condition or disease	Intervention/treatment	Phase
Benign Prostatic Hyperplasia; Prostate Hyperplasia; Prostate Disease; Prostate Hypertrophy; Prostate Pain; Lower Urinary Tract Symptoms; Urinary Obstruction; Urinary Tract Disease	Drug: Finasteride	Not Applicable

Detailed Description:

Over 90% of adult males develop lower urinary tract symptoms (LUTS) secondary to bladder outlet obstruction by age 80, rendering benign prostatic hyperplasia (BPH) the most common proliferative abnormality in humans. LUTS secondary to BPH negatively impact the quality of life of 210 million men globally, accounting for significant life years lost, in addition to costing the US healthcare system over $4 billion per year. Medical therapy for the management of BPH, which includes α-adrenergic blockers (e.g., doxazosin, terazosin, tamsulosin or alfuzosin) and 5α reductase inhibitors (5ARI, i.e., finasteride or dutasteride) targets both stromal and epithelial cells in the prostate gland. Utilization of 5ARI remains ineffective in many patients, leading to invasive therapies in many patients. 5ARI's are the only class of BPH-related drugs that reduce prostate size for the alleviation of LUTS. However, the Medical Therapy of Prostatic Symptoms (MTOPS) trial, which randomized 3047 men, showed that 34% of BPH patients did not respond to individualized treatment with finasteride or doxazosin, while combining the 5ARI and α-blocker relieved LUTS in 66% of BPH patients. Resistance to 5ARI therapy is a major factor limiting the effectiveness of these agents in the management of BPH. Therefore, understanding the molecular pathogenesis of 5ARI resistance is a High-Priority Recommendation of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Prostate Research Strategic Plan. However, it is not yet possible to predict responders vs. non-responders to 5ARI therapy, which creates a significant gap in our ability to effectively manage patients with BPH.

5α reductase (5-AR) plays a critical role in the normal development of the human prostate and in the pathogenesis and progression of prostatic diseases. There are three types of 5-AR isozymes, Steroid 5 Alpha-Reductase 1, 2 3 (SRD5A1, SRD5A2 and SRD5A3), which are encoded by three distinct corresponding genes, SRD5A1, SRD5A2 and SRD5A3. Many studies suggest that all three 5-AR enzymes are expressed in prostate tissues; however, SRD5A2 is the predominant enzyme responsible for prostate development and growth. In addition, since the most commonly prescribed 5ARI, finasteride, is an inhibitor of SRD5A2, regulation of SRD5A2 will remain the focus of this study.

It was previously shown that the mechanism of somatic suppression of SRD5A2 during adulthood is dependent on epigenetic changes in the promoter region of the SRD5A2 gene. DNA methylation is one of the most common epigenetic mechanisms affecting gene expression. Methylation of Cytosine-Phosphate-Guanine (CpG) islands has been associated with the regulation of genes during development, cancer initiation, and metastasis. Since the prostate is the only solid organ that grows during adulthood as a result of androgen exposure, it can be considered a benign tumor growth throughout adulthood. Therefore, similar to the neoplastic initiation and progression of many cancers, including prostate cancer, epigenetic changes and variable expression of SRD5A2 in benign prostate tissue is a plausible molecular mechanism.

Finasteride, the most commonly prescribed 5ARI, is an inhibitor of SRD5A2. Finasteride has been shown in several large clinical trials to reduce prostate size by 20%, improve urinary flow rate, and improve urinary bothersome symptom scores in men suffering from bladder outlet obstruction caused by BPH. Despite their widespread use and clinical effectiveness, 25% to 30% of patients are resistant to the therapeutic effects of 5ARIs and another 5% to 7% of patients develop worsening symptoms and ultimately may require surgery. Given their age and comorbidities, these patients are often not ideal candidates for surgery. Therefore, understanding the mechanisms of 5ARI treatment failure may pave the way for the development of new medical therapies appropriately targeted to these specific patient groups and is a desirable way to move forward with precision medicine. This proposed work is based on the premise that epigenetic changes to SRD5A2 account for the significant number of patients who are unresponsive to 5ARI therapy. The goal is to assess SRD5A2 methylation and expression as a gene signature to predict which patients will respond to 5ARI therapy.

The information gained from this proposal will pave the way toward the development of predictive biomarker assays that can be used to evaluate resistance to BPH-related therapies and allow clinicians to select alternate therapies for managing the most common proliferative disorder affecting men worldwide.

Study Design

• Study Type: Interventional (Clinical Trial)
• Estimated Enrollment: 120 participants
• Allocation: N/A
• Intervention Model: Single Group Assignment
• Masking: None (Open Label)
• Primary Purpose: Treatment
• Official Title: 5-Alpha Reductase 2 as a Marker of Resistance to 5ARI Therapy
• Actual Study Start Date: September 25, 2020
• Estimated Primary Completion Date: November 30, 2024
• Estimated Study Completion Date: April 30, 2025

Arms and Interventions

Arm

Intervention/treatment

Experimental: Finasteride Treatment; Patients who are eligible will be given 5ARI therapy, Finasteride, for medical management of Benign Prostatic Hyperplasia (BPH) symptoms. Only patients with lower urinary tract symptoms (LUTS) as assessed by American Urologic Association (AUA) urinary symptom score > than 8, (suggestive of moderate LUTS) prostate size > 40cc, no prostate nodule/tenderness/firmness and increased PSA between 4-10ng/ml requiring prostate biopsy will be enrolled. Then, they will have prostate MRIs/needle biopsies and blood/urine collection followed by treatment with Finasteride (standard of care). They will be followed in urology clinic for assessment of LUTS every 6 months and Finasteride responsiveness at the 12-month time point. Prostate biopsy samples will be evaluated for SRD5A2 gene expression/methylation, hormonal androgen/estrogen levels (which will be repeated in blood samples). Prostate MRIs will assess size/inflammatory changes at the start and 3-year time points.

Drug: Finasteride; Patients who are candidates to receive 5ARI therapy, Finasteride, for clinical medical management of lower urinary tract symptoms will begin treatment once deemed eligible. They will be assess every 6 months for changes in urinary symptom scores and their responsiveness to the Finasteride treatment will be assessed at the 12-month time point. MRIs of prostate taken at the start of study and at the 3 year time point will assess prostate size and changes in size as well as degree of inflammatory changes. Gene expression of SRD5A2 as well as methylation pattern will be tested on prostate tissue samples, where hormonal androgen/estrogen levels will also be assessed as they are in blood samples.; Other Name: Sequential Time Point Study

Outcome Measures

Primary Outcome Measures :

1. Finasteride treatment effect on lower urinary tract symptom improvement by urinary symptom score [ Time Frame: Assessment of Finasteride responsiveness through changes in urinary symptoms will be completed at 6 month intervals during clinic visits, and treatment efficacy will be determined after the first 12 months. ]
   Validated questions of the AUA Urinary Symptom Score will be used every 6 months to assess efficacy of Finasteride treatment in improving lower urinary tract symptoms in the patient population. Based on previous randomized trials, it will be determined whether the patient is responsive or resistant to the treatment dependent on changes in their AUA Urinary Symptom Score at the first 12 month mark. For patients who are resistant to Finasteride, other medical or surgical treatments will be offered, and the patients will be removed from the study.

Eligibility Criteria

• Ages Eligible for Study: 50 Years and older (Adult, Older Adult)
• Sexes Eligible for Study: Male
• Gender Based Eligibility: Yes
• Gender Eligibility Description: Prostatic disease are limited to biologically male individuals.
• Accepts Healthy Volunteers: No

Criteria

Inclusion Criteria:

• Male (physiological);
• Age ≥ 50;
• Eligible for treatment with 5ARI therapy;
• Presence of lower urinary tract symptoms secondary to BPH;
• Prostate size >40cc by digital rectal examination;
• Absence of prostate nodule, tenderness or firmness;
• Mildly elevated PSA's >1.5 ng/ml and ≤ 40 ng/ml;
• Undergoing clinically indicated prostate biopsy for elevated prostate-specific antigen (PSA).

Exclusion Criteria:

• Diagnosis of any prostatic malignancy or precancerous lesions (atypical glandular foci and prostatic intraepithelial neoplasia);
• Treatment with 5ARI (Finasteride or Dutasteride) within six months of study enrollment;
• Current urinary tract infection;
• Previous pelvic radiation;
• Previous treatment with demethylating drugs;
• Diagnosis of multiple sclerosis, Alzheimer's, Parkinson's, neurological deficits in the judgment of the investigator;
• Unable or unwilling to undergo MRI due to implants, claustrophobia, etc.

Contacts and Locations

Contacts

Contact: Abigail Escobar, BS; 617-903-0153; aescoba2@bidmc.harvard.edu

Contact: Christopher Mistretta, RN; 617-632-8432; cmistret@bidmc.harvard.edu

Locations

United States, Massachusetts

Beth Israel Deaconess Medical Center; Recruiting

Boston, Massachusetts, United States, 02215

Contact: Chris Mistretta, RN 978-821-0889 cmistret@bidmc.harvard.edu

Contact: Abigail Escobar, B.S. 617-903-0153 aescoba2@bidmc.harvard.edu

Principal Investigator: Aria Olumi, MD

Sponsors and Collaborators

Beth Israel Deaconess Medical Center

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)

Investigators

• Principal Investigator: Aria F. Olumi, MD; Beth Israel Deaconess Medical Center

More Information

Publications:

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• Responsible Party: Aria F. Olumi, MD, Principal Investigator; Chief of Urologic Surgery at Beth Israel Deaconess Medical Center; Janet & William DeWolf Professor of Surgery/Urology at Harvard Medical School; American Urological Association Chair of Research, Beth Israel Deaconess Medical Center
• ClinicalTrials.gov Identifier: NCT04288427
• Other Study ID Numbers: 2020P000202; R01DK124502 ( U.S. NIH Grant/Contract )
• First Posted: February 28, 2020
• Last Update Posted: March 14, 2023
• Last Verified: March 2023

• Studies a U.S. FDA-regulated Drug Product: No
• Studies a U.S. FDA-regulated Device Product: No
• Product Manufactured in and Exported from the U.S.: No

Keywords provided by Aria F. Olumi, MD, Beth Israel Deaconess Medical Center:

Finasteride; 5 Alpha Reductase

Additional relevant MeSH terms:

Prostatic Hyperplasia; Prostatic Diseases; Urologic Diseases; Hyperplasia; Hypertrophy; Lower Urinary Tract Symptoms; Pathologic Processes; Genital Diseases, Male; Genital Diseases; Urogenital Diseases; Male Urogenital Diseases; Pathological Conditions, Anatomical; Urological Manifestations; Female Urogenital Diseases; Female Urogenital Diseases and Pregnancy Complications; Finasteride; 5-alpha Reductase Inhibitors; Steroid Synthesis Inhibitors; Enzyme Inhibitors; Molecular Mechanisms of Pharmacological Action; Hormone Antagonists; Hormones, Hormone Substitutes, and Hormone Antagonists; Physiological Effects of Drugs; Urological Agents