Prostate Cancer MetastaticNCT05530395
BAseLine TEstosterone as a Prognostic and/or Predictive bioMARKer in mHSPC
An observational study of Prostate Cancer Metastatic, run by Ignacio Puche Sanz at 3 sites in Spain.
Trial summary
Despite large amounts of basic-science data supporting a role for androgens in PCa pathogenesis, there are conflicting clinical data on the role of endogenous testosterone in human de novo PCa pathogenesis. Read more about this study
- Who is it for?
- Ages 18 to 89 years, men only
- Conditions the study is for
- Prostate Cancer Metastatic
- What is being tested?
- Testosterone levels
- How many people
- 300 participants
- Where
- 3 sitesSpain
- Study dates
- 1 Jan 2023to 1 Jan 2026
- Phase
- Observational
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 89 years
- Men only
- No healthy volunteers
- Adult, Older adult
Study population: Metastatic hormone sensitive prostate cancer (mHSPC) patients diagnosed by any imaging test (at least CT and/or bone scan).
Who may be able to join
- Metastatic hormone sensitive prostate cancer (mHSPC) patients diagnosed by any imaging test (at least CT and bone scan) including:
- Any newly diagnosed mHSPC with no prior treatments.
- Primarily treated PCa that have progressed to mHSPC with no prior ADT in the last 2 years.
- Patients receiving ADT + EBRT as primary treatment will also be included.
- Patients who agree to be followed prospectively according to routine clinical practice in the context of this study.
Who cannot join
- Any prior androgen deprivation therapy (ADT) scheme 2 years before recruitment. - Any prior testosterone replacement therapy scheme 2 years before recruitment.
- Previous intermittent ADT schemes.
- Prior testicular excision surgery.
- Absence or testicular atrophy from any cause.
- Whenever further prospective clinical follow-up is not possible or patient do not accept follow-up in the context of this study.
Trial locations and contacts
3 sites in 1 country.
Spain3 sites
Hospital Universitario Reina Sofía
Córdoba, Andalusia
Hospital Universitario Virgen de las Nieves
Granada, Andalusia
Hospital Universitario Virgen del Rocio
Seville
About this study
Official title: Baseline Testosterone as a Prognostic and/or Predictive Biomarker in Metastatic Hormone Sensitive Prostate Cancer
Despite large amounts of basic-science data supporting a role for androgens in PCa pathogenesis, there are conflicting clinical data on the role of endogenous testosterone in human de novo PCa pathogenesis. The investigators hypothesize that lower baseline serum testosterone is significantly associated with worse clinical outcomes in mHSPC patients undergoing continuous medical castration
Read the detailed description
Biological rationale:
The 'androgen hypothesis' asserts that prostate cancer (PCa) development and progression is driven by androgens. There is significant evidence that androgens promote prostate cancer in experimental models. However, there is no clear evidence that elevations in endogenous testosterone levels promote the development of prostate cancer in humans. Indeed, despite large amounts of basic-science data supporting a role for androgens in PCa pathogenesis, there are conflicting clinical data on the role of endogenous testosterone in human PCa pathogenesis de novo. In reviewing the literature involving PCa development in PCa naive patients, there are studies implicating elevated testosterone, studies implicating lower testosterone, and studies with no association of testosterone and PCa risk.
A recent review in 2015 delved into the controversial role of androgens and prostate cancer and explains the different theories about the ambiguous action of testosterone on the prostate. In 2012, a research proposed the nonlinear U-shaped behaviour or time dependency theory, which postulates that the endocrine biology of the prostate tissue depends on exposure time at a given androgen concentration, which "relies on the fluctuation of the levels of circulating sex steroids during the lifespan of the individual". Another model is the saturation model based on the observations that prostate tissue is extremely sensitive to changes in serum testosterone at low concentrations. This model suggests that there is a nonprotective effect of low testosterone against PCa but tissue becomes indifferent to changes when increasing androgen concentration reach a limit (saturation point), beyond which no further androgen-driven changes are observed. Anyway, the lack of a satisfying model to explain the relationship between androgens and PCa is simply the consequence of insufficient knowledge of the real intrinsic physiopathology of this disease.
Clinical rationale:
Approximately 15% of mHSPC patients primarily fail to respond to ADT. A recent consensus statement on circulating biomarkers for advanced prostate cancer highlighted the urgent need for prospective trials to clinically qualify circulating biomarkers, the greatest need being metastatic PCa. On the other hand, a very recent paper analysed baseline testosterone in hormone-naïve advanced PCa patients undergoing continuous medical castration and selected from 2 large Phase III RCTs. It demonstrated that lower baseline serum testosterone was significantly associated with worse survival end-points and warrants further prospective research in this scenario.
In this era of complex and expensive next-generation markers, this simple, cheap, and well-known biomarker may still have something to say in PCa.
- Conditions
- Prostate Cancer Metastatic
- Being tested
- Testosterone levels
- Keywords
- Testosterone, biomarker
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Testosterone levelsDiagnostic test
Blood sample to determine testosterone levels
What is being measured
The primary outcome is the main question the study is designed to answer.
Early treatment failure
Proportion of patients with PSA progression or death from PCa within 12 months after initiation of treatment.
Measured: 1 year
PSA response
Lowest PSA (nadir) reached after initiation of treatment
Measured: 6 months
Secondary outcomes (4)
Testosterone response.
%percent of decrease in testosterone levels at the moment of PSA nadir.
Measured: 6 months
Biochemical progression-free survival (bPFS)
PSA progression: 2 consecutive increase at least 50% or 5 ng/mL or more above PSA nadir on 2 consecutive measurements at least 2 weeks apart.
Measured: 1 year
Radiologic progression-free survival (rPFS)
Assessed by PCWG3 progression criteria on nodal, visceral and bone disease.
Measured: 1 year
Time to CRPC
Time (months) from treatment initiation to the development of a CRPC status.
Measured: 1 year
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted7 Sep 2022
- Study start1 Jan 2023 (estimated)
- Primary completion1 Jan 2025 (estimated)
- Study completion1 Jan 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (4)Papers the sponsor has linked to this study.
- Other trials for Prostate Cancer MetastaticStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 300 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Ignacio Puche Sanz
- Sponsor type
- University, hospital or other
- Collaborators
- Hospital Universitario Reina Sofia de Cordoba, Hospitales Universitarios Virgen del Rocío, Hospital Universitario Torrecárdenas, Hospital Neurotraumatologico de Jaen, Hospital San Carlos, Madrid, Institut Mutualiste Montsouris, San Raffaele University Hospital, Italy, Azienda Ospedaliera San Giovanni Battista, Chinese University of Hong Kong, Medical University Innsbruck, University of Padova, UMC Utrecht
- Responsible party
- Sponsor-investigator, Ignacio Puche Sanz, University Hospital Virgen de las Nieves
- Investigators
- Ignacio Puche, Principal investigator, Fundación para la Investigación Biosanitaria de Andalucía Oriental (FIBAO)
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05530395
- Sponsor's protocol ID
- BATEMARK-YAUPCa-21
- Status last verified
- Sep 2022
- First submitted
- 2 Sep 2022
- Last updated
- 14 Sep 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Michaud JE, Billups KL, Partin AW. Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Ther Adv Urol. 2015 Dec;7(6):378-87. doi: 10.1177/1756287215597633.
PubMed 26622322Pierorazio PM, Ferrucci L, Kettermann A, Longo DL, Metter EJ, Carter HB. Serum testosterone is associated with aggressive prostate cancer in older men: results from the Baltimore Longitudinal Study of Aging. BJU Int. 2010 Mar;105(6):824-9. doi: 10.1111/j.1464-410X.2009.08853.x. Epub 2009 Sep 14.
PubMed 19751256Yano M, Imamoto T, Suzuki H, Fukasawa S, Kojima S, Komiya A, Naya Y, Ichikawa T. The clinical potential of pretreatment serum testosterone level to improve the efficiency of prostate cancer screening. Eur Urol. 2007 Feb;51(2):375-80. doi: 10.1016/j.eururo.2006.08.047. Epub 2006 Sep 12.
PubMed 17005316Rajek NJ. Developing an evening clinical experience for baccalaureate community health nursing students. J Nurs Educ. 1987 May;26(5):197-200. doi: 10.3928/0148-4834-19870501-07.
PubMed 3035140
Study at a glance
From the registry record, last updated by the sponsor on 14 Sep 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Baseline Testosterone as a Prognostic and/or Predictive Biomarker in Metastatic Hormone Sensitive Prostate Cancer
- ClinicalTrials.gov ID
- NCT05530395
- Acronym / sponsor ID
- BATEMARK-YAUPCa-21
- Conditions
- Prostate Cancer Metastatic
- Keywords
- Testosterone, biomarker
- Study type
- Observational
- Recruitment status
- Unknown status
- Enrolment
- 300 participants (estimated)
- Lead sponsor
- Ignacio Puche SanzUniversity, hospital or other
- Collaborators
- Hospital Universitario Reina Sofia de Cordoba, Hospitales Universitarios Virgen del Rocío, Hospital Universitario Torrecárdenas, Hospital Neurotraumatologico de Jaen, Hospital San Carlos, Madrid, Institut Mutualiste Montsouris, San Raffaele University Hospital, Italy, Azienda Ospedaliera San Giovanni Battista, Chinese University of Hong Kong, Medical University Innsbruck, University of Padova, UMC Utrecht
- Study start
- 1 Jan 2023 (estimated)
- Primary completion
- 1 Jan 2025 (estimated)
- Study completion
- 1 Jan 2026 (estimated)
- First posted
- 7 Sep 2022 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Despite large amounts of basic-science data supporting a role for androgens in PCa pathogenesis, there are conflicting clinical data on the role of endogenous testosterone in human de novo PCa pathogenesis. The investigators hypothesize that lower baseline serum testosterone is significantly associated with worse clinical outcomes in mHSPC patients undergoing continuous medical castration
Detailed description
Biological rationale:
The 'androgen hypothesis' asserts that prostate cancer (PCa) development and progression is driven by androgens. There is significant evidence that androgens promote prostate cancer in experimental models. However, there is no clear evidence that elevations in endogenous testosterone levels promote the development of prostate cancer in humans. Indeed, despite large amounts of basic-science data supporting a role for androgens in PCa pathogenesis, there are conflicting clinical data on the role of endogenous testosterone in human PCa pathogenesis de novo. In reviewing the literature involving PCa development in PCa naive patients, there are studies implicating elevated testosterone, studies implicating lower testosterone, and studies with no association of testosterone and PCa risk.
A recent review in 2015 delved into the controversial role of androgens and prostate cancer and explains the different theories about the ambiguous action of testosterone on the prostate. In 2012, a research proposed the nonlinear U-shaped behaviour or time dependency theory, which postulates that the endocrine biology of the prostate tissue depends on exposure time at a given androgen concentration, which "relies on the fluctuation of the levels of circulating sex steroids during the lifespan of the individual". Another model is the saturation model based on the observations that prostate tissue is extremely sensitive to changes in serum testosterone at low concentrations. This model suggests that there is a nonprotective effect of low testosterone against PCa but tissue becomes indifferent to changes when increasing androgen concentration reach a limit (saturation point), beyond which no further androgen-driven changes are observed. Anyway, the lack of a satisfying model to explain the relationship between androgens and PCa is simply the consequence of insufficient knowledge of the real intrinsic physiopathology of this disease.
Clinical rationale:
Approximately 15% of mHSPC patients primarily fail to respond to ADT. A recent consensus statement on circulating biomarkers for advanced prostate cancer highlighted the urgent need for prospective trials to clinically qualify circulating biomarkers, the greatest need being metastatic PCa. On the other hand, a very recent paper analysed baseline testosterone in hormone-naïve advanced PCa patients undergoing continuous medical castration and selected from 2 large Phase III RCTs. It demonstrated that lower baseline serum testosterone was significantly associated with worse survival end-points and warrants further prospective research in this scenario.
In this era of complex and expensive next-generation markers, this simple, cheap, and well-known biomarker may still have something to say in PCa.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
Who may qualify
- Ages
- 18 to 89 years
- Sex
- Male only
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Metastatic hormone sensitive prostate cancer (mHSPC) patients diagnosed by any imaging test (at least CT and/or bone scan).
Key inclusion criteria (5 listed)
- Metastatic hormone sensitive prostate cancer (mHSPC) patients diagnosed by any imaging test (at least CT and bone scan) including:
- Patients who agree to be followed prospectively according to routine clinical practice in the context of this study.
Key exclusion criteria (5 listed)
- Any prior androgen deprivation therapy (ADT) scheme 2 years before recruitment. - Any prior testosterone replacement therapy scheme 2 years before recruitment.
- Previous intermittent ADT schemes.
- Prior testicular excision surgery.
- Absence or testicular atrophy from any cause.
- Whenever further prospective clinical follow-up is not possible or patient do not accept follow-up in the context of this study.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Testosterone levelsBlood sample to determine testosterone levels | Diagnostic test | – |
Primary outcome
Early treatment failure
Time frame: 1 year
Proportion of patients with PSA progression or death from PCa within 12 months after initiation of treatment.
PSA response
Time frame: 6 months
Lowest PSA (nadir) reached after initiation of treatment
4 secondary outcomes
Testosterone response.
Time frame: 6 months
Biochemical progression-free survival (bPFS)
Time frame: 1 year
Radiologic progression-free survival (rPFS)
Time frame: 1 year
Time to CRPC
Time frame: 1 year
Results and safety
Results are not available in the source record.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 14 Sep 2022.
- Background: PubMed 26622322Michaud JE, Billups KL, Partin AW. Testosterone and prostate cancer: an evidence-based review of pathogenesis and oncologic risk. Ther Adv Urol. 2015 Dec;7(6):378-87. doi: 10.1177/1756287215597633.
- Background: PubMed 19751256Pierorazio PM, Ferrucci L, Kettermann A, Longo DL, Metter EJ, Carter HB. Serum testosterone is associated with aggressive prostate cancer in older men: results from the Baltimore Longitudinal Study of Aging. BJU Int. 2010 Mar;105(6):824-9. doi: 10.1111/j.1464-410X.2009.08853.x. Epub 2009 Sep 14.
- Background: PubMed 17005316Yano M, Imamoto T, Suzuki H, Fukasawa S, Kojima S, Komiya A, Naya Y, Ichikawa T. The clinical potential of pretreatment serum testosterone level to improve the efficiency of prostate cancer screening. Eur Urol. 2007 Feb;51(2):375-80. doi: 10.1016/j.eururo.2006.08.047. Epub 2006 Sep 12.
- Background: PubMed 3035140Rajek NJ. Developing an evening clinical experience for baccalaureate community health nursing students. J Nurs Educ. 1987 May;26(5):197-200. doi: 10.3928/0148-4834-19870501-07.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Ignacio Puche principal investigator
Fundación para la Investigación Biosanitaria de Andalucía Oriental (FIBAO)
3 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Prostate Cancer Metastatic, run by Ignacio Puche Sanz at 3 sites in Spain.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 5 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: status not confirmed, as of the sponsor's last update on 14 Sep 2022. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 3 sites in Spain. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
Results are not available in the source record.
How can a doctor refer a patient or contact the research team?
Contact Ignacio Puche Sanz (0034 958 023 158, naho.puchesanz@gmail.com), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Early treatment failure (time frame: 1 year). The study lists 2 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05530395, which also lists 4 linked publications.
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 14 Sep 2022.