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If castration-resistant prostate cancer (CRPC) goes undetected in patients receiving ADT…

an UNCONTROLLABLE THREAT may soon emerge

PSA Monitoring Helps to Identify Disease Progression


Keep your eyes on the rise

Routine PSA monitoring may help you identify castration resistance in your patients before metastases emerge.

The RADAR Group* recommended PSA testing every 3 months for patients with1:

  • Biochemically recurrent prostate cancer
  • Non-metastatic CRPC

*The Prostate Cancer Radiographic Assessments for Detection of Advanced Recurrence (RADAR) Group was a multidisciplinary group that included urologists and oncologists. It was convened to review the currently available imaging guidelines for metastatic disease in prostate cancer and found no consensus on eligibility criteria, type of imaging modality, and the frequency of scanning for detecting metastatic disease. The aim of their review was to present the recommendations from the group to identify optimal strategies for early identification of metastases in patients with prostate cancer.

Monitoring PSA when patients visit to receive their ADT may help you identify CRPC before the development of metastases.

Test your knowledge

Learn about non-metastatic CRPC by taking the quiz below featuring 2 hypothetical patients.

JOHN
  • Aged 70 years
  • No radiographically detectable metastases
  • Has CRPC
  • PSA doubling time is 6 months
Not an actual patient.
KEVIN
  • Aged 77 years
  • No radiographically detectable metastases
  • Has CRPC
  • Currently receiving ADT
Not an actual patient.
John

JOHN

  • Aged 70 years
  • Has CRPC
  • No radiographically detectable metastases
  • PSA doubling time is 6 months
Not an actual patient.

How much more likely is John to develop a bone metastasis than a patient with non-metastatic CRPC who has a PSA doubling time ≥10 months?3

Based on a study that examined PSA doubling time and the risk of progression, what is the expected median time to metastasis for John?4

Based on his diagnosis of non-metastatic CRPC, and his rapid PSA doubling time, how frequently should John have his PSA measured?1,2

+
Kevin

KEVIN

  • Aged 77 years
  • Has CRPC
  • No radiographically detectable metastases
  • Currently receiving ADT
Not an actual patient.

When was Kevin’s therapy (androgen-deprivation therapy) first used in the treatment of prostate cancer?6

Like many men, Kevin initially responded to ADT. But after 4 years, he developed CRPC. According to one study, what was the median time to PSA progression after ADT initiation in men with non-metastatic CRPC?7

Kevin understands that he is at risk for developing metastases. According to one study, 46% of men with non-metastatic CRPC taking ADT alone developed ≥1 bone metastasis after a median of8:

+

Thank you for taking the quiz and learning more about non-metastatic CRPC.

Important Consideration:

PSA doubling time is an important predictor of the risk of developing metastases.1,5

+

Thank you for taking the quiz and learning more about non-metastatic CRPC.

Important Consideration:

After biochemical recurrence, most men on ADT develop CRPC.6,9

+

Learn more about 3 key characteristics of patients with non-metastatic CRPC1

Receiving Androgen-Deprivation Therapy

Explore

Receiving Androgen-Deprivation Therapy

In a randomized controlled trial, 46% of men with non-metastatic CRPC receiving ADT alone developed at least 1 bone metastasis within 2 years.8Study description

Rapidly Rising PSA

Explore

Rapidly Rising
PSA

Based on PCWG2 criteria, PSA progression is defined as: an increase in PSA of 25% or greater and 2 ng/mL or more from the nadir, confirmed by a second value obtained ≥3 weeks later.10

No radiographically detectable Metastases

Explore

No Radiographically Detectable Metastases

In one study, men with CRPC and a PSA doubling time (PSADT) <3 months developed metastasis after a median of 9 months. Men with CRPC and a PSADT ≥15 months developed metastasis after a median of 50 months.4
Study description

CRPC and the Development of Metastases

10% TO  20%
of men diagnosed with prostate cancer are estimated to develop CRPC within 5 years of follow-up.11

Patients with prostate cancer receiving ADT may develop CRPC.

After biochemical recurrence, most men on ADT develop CRPC.6,9

A study has shown that within 2 years
33%

of patients initially diagnosed with non-metastatic CRPC had developed at least 1 bone metastasis.†5

Based on data from 201 men with prostate cancer, no bone metastases, and rising PSA despite ADT in the placebo control group of a terminated randomized controlled trial. These patients were assessed to describe the natural history of non-metastatic prostate cancer and rising PSA despite ADT.

In the placebo arm of a randomized controlled trial, men with non-metastatic CRPC received ADT alone.

After 2 years
46%

had developed at least 1 bone metastasis; 20% had died.8

Data from 331 participants in the placebo group of a randomized controlled trial were evaluated to describe the natural history of non-metastatic CRPC.

PSA Doubling Time (PSADT) and Risk Assessment

PSADT is an important predictor of the risk of developing metastases.1,5

Men with non-metastatic CRPC have a greater risk of metastasis development and death when their PSADT is less than 10 months. When compared with patients who experienced a PSADT ≥10 months, those with a PSADT <10 months had§3:

12x

greater risk of developing a bone metastasis

4x

greater risk of death

§Retrospective study of 347 patients with CRPC from a cohort of 9547 patients who underwent treatment for prostate cancer, using the Center for Prostate Disease Research database.

A faster PSA doubling time (PSADT) is linked to shorter time to metastasis in patients with non‑metastatic castration‑resistant prostate cancer (nmCRPC).II 4

PSADT
(months)
Median Time to Metastasis (months)
<3 9
3 TO 8.9 19
9 TO 14.9 40
≥15 50

PSADT calculated by log(2) divided by the slope of the linear regression of log(PSA) over time in months. Study included data from 441 men with M0 CRPC at 5 Veterans Affairs Medical Centers obtained from the SEARCH database.

Resources


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  ADT = androgen-deprivation therapy; M0 = non-metastatic; PCWG2 = Prostate Cancer Working Group 2; PSA = prostate-specific antigen.

Review publications by clicking on the reference citations

References:

1. Crawford ED, Stone NN, Yu EY, et al; and the Prostate Cancer Radiographic Assessments for Detection of Advanced Recurrence (RADAR) Group. Challenges and recommendations for early identification of metastatic disease in prostate cancer. Urology. 2014;83(3):664-669.

2. Virgo KS, Basch E, Loblaw A, et al. Second-line hormonal therapy for men with chemotherapy-naïve, castration-resistant prostate cancer: American Society of Clinical Oncology provisional clinical opinion. J Clin Oncol. 2017. doi:10.1200/JCO.2017.72.8030.

3. Metwalli AR, Rosner IL, Cullen J, et al. Elevated alkaline phosphatase velocity strongly predicts overall survival and the risk of bone metastases in castrate-resistant prostate cancer. Urol Oncol. 2014;32(6):761-768.

4. Howard LE, Moreira D, De Hoedt A, et al. Thresholds for PSA doubling time in men with non-metastatic castration-resistant prostate cancer. BJU Int. 2017;120(5B):E80-E86.

5. Smith MR, Kabbinavar F, Saad F, et al. Natural history of rising serum prostate-specific antigen in men with castrate nonmetastatic prostate cancer. J Clin Oncol. 2005;23(13):2918-2925.

6. Pomerantz M, Kantoff P. Clinical progression to castration-recurrent prostate cancer. In: Tindall DJ, Mohler J, eds. Androgen Action in Prostate Cancer. Verlag, New York: Springer; 2009.

7. Ross RW, Xie W, Regan MM, et al. Efficacy of androgen deprivation therapy (ADT) in patients with advanced prostate cancer: association between Gleason score, prostate-specific antigen level, and prior ADT exposure with duration of ADT effect. Cancer. 2008;112(6):1247-1253.

8. Smith MR, Cook R, Lee KA, Nelson JB. Disease and host characteristics as predictors of time to first bone metastasis and death in men with progressive castration-resistant nonmetastatic prostate cancer. Cancer. 2011;117(10):2077-2085.

9. Knudsen KE, Scher HI. Starving the addiction: new opportunities for durable suppression of AR signaling in prostate cancer. Clin Cancer Res. 2009;15(15):4792-4798.

10. Scher HI, Halabi S, Tannock I, et al; Prostate Cancer Clinical Trials Working Group. Design and end points of clinical trials for patients with progressive prostate cancer and castrate levels of testosterone: recommendations of the Prostate Cancer Clinical Trials Working Group. J Clin Oncol. 2008;26(7):1148-1159.

11. Kirby M, Hirst C, Crawford ED. Characterising the castration-resistant prostate cancer population: a systematic review. Int J Clin Pract. 2011;65(11):1180-1192.