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. 2025 Jul 25;122(15):420–425. doi: 10.3238/arztebl.m2025.0099

The Early Detection, Diagnostic Evaluation, and Local Treatment of Prostate Cancer

A Paradigm Shift

Peter Albers 1,*, Tobias Franiel 2, Thomas Kötter 3, Glen Kristiansen 4, Ken Herrmann 5, Thomas Wiegel 6
PMCID: PMC12580837  PMID: 40536418

Abstract

Background

Approximately 75 000 men receive a diagnosis of prostate cancer in Germany each year. New data on the early detection, diagnostic evaluation, and treatment of prostate cancer provide the basis for a paradigm shift in the management of locally confined prostate cancer.

Methods

This narrative review is based on the systematic literature search that was carried out for the 2025 update of the German clinical practice guideline on prostate cancer.

Results

Risk-adapted early detection is now recommended. This involves the measurement of a baseline PSA value at age 45 whose magnitude determines the interval of follow-up testing: once every 5 years for baseline values below 1.5 ng/mL, and once every two years for baseline values between 1.5 and 3 ng/mL. Patients with PSA levels above 3 ng/mL should undergo a repeat PSA test and, if these levels are confirmed, receive a urological risk assessment including prostatic volume, family history, and past medical history. High risk patients should undergo magnetic resonance imaging (MRI) and, if necessary, prostate biopsy. This new PSA-MRI algorithm increases accuracy in detecting clinically significant prostate cancers, enabling the previously recommended annual testing and digital rectal examination to be avoided. Another novelty is that the indication for an active surveillance strategy for men with low-risk prostate cancer has been expanded to ISUP grade group 1 and 2 cancers with favorable risk.

Conclusion

The need for high-quality diagnostic testing, including MRI, with broad geographic coverage will be a major challenge to the health care system, especially with regard to accessibility. Patients can be expected to benefit greatly from the new PSA-MRI algorithm, as it eliminates unnecessary diagnostic testing and treatment while enabling necessary treatment to be initiated earlier and therefore with fewer side effects.


Information on CME

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With approximately 75 000 new cases per year in Germany (2022), prostate cancer is the most common type of cancer in men and the second most common cause of cancer-related deaths, after lung cancer and ahead of colorectal cancer (1). 10–15% of all men will receive a diagnosis of prostate cancer during their lifetime. The 5-year survival rate is approximately 90% (1). Three-quarters of tumors are diagnosed at an early stage (T1 or T2, i.e., confined to the prostate). Prostate cancer is more common in older men (average age at diagnosis in 2021: 71 years) (1). Latent, i.e., undetected and clinically indolent prostate cancer that does not cause any symptoms during the patient‘s lifetime or shorten his life span accounts for half of all diagnosed prostate cancers (2).

In the next 20 years, because of the aging population, the number of new cases worldwide is expected to double, and the number of deaths to rise by 85% (3).

The dilemma is that, with prostate cancer become more common, it is all the more important to distinguish clinically indolent tumors that will not harm a man during his lifetime from those that can metastasize, and to make this distinction as early as possible. The number of overdiagnoses, i.e., detected prostate cancers that will never become clinically manifest or affect longevity, must be kept as low as possible, while, at the same time, potentially dangerous cancers must not be overlooked. At present, for every man who is saved from dying of prostate cancer by early detection, 14 men receive a cancer diagnosis that is unnecessary in every respect, and some of them are treated for cancer as well (4).

Overdiagnosis cannot be completely avoided because no diagnostic procedure is so precise as to detect only cancers that will become life-threatening in the future. However, individualized, highly precise early detection and diagnostic evaluation can at least limit overdiagnosis and subsequent overtreatment. Accordingly, the new S3 guideline on the diagnosis and treatment of prostate cancer (2025) contains major changes in the recommendations for early detection, evaluation, and treatment.

Learning objectives

This article is intended to enable readers to:

  • state the current recommendations for the early detection of prostate cancer and be aware of their importance in practice,

  • understand new imaging techniques for prostate cancer and their clinical benefits,

  • explain the newly altered indications for active treatment (radical prostatectomy, radiation therapy) versus active surveillance and help make appropriate, individualized decisions on treatment jointly with the patient.

Methods

This review is based on the literature analyses that were carried out in order to update the S3 guideline on prostate cancer (AWMF registration number 043–022OL) in accordance with the rules laid down by the AWMF. 11 systematic literature searches were conducted for the overall guideline (Medline and Cochrane databases, years 2020–2024). The data were extracted and the evidence was evaluated according to the sign-grading system.

Personalized, risk-adapted early detection

If there is a reason to pursue early detection, e.g., the patient’s desire to do so, the advantages and disadvantages should be openly discussed before any decision is taken (Box). Early detection, if chosen, should begin at age 45 with a baseline measurement of prostate-specific antigen (PSA). This age was also recommended in the past as the starting point for early detection, in the absence of a genetic predisposition, but the reasoning has changed: with a baseline PSA value at this young age, most men can be spared the previously recommended annual early detection tests for at least five years. The less frequent performance of early detection tests will lower both the number of false-positive findings (abnormal PSA level without any further findings on follow-up tests) and the number of overdiagnoses (prostate cancer in fact present, but clinically irrelevant, with no need for treatment). At this age, the detection rate of clinically relevant prostate cancer (histologically defined by a grading group (GG) of 2–5 in the International Society of Urological Pathology (ISUP) classification) is 0.2–0.4% (5, 6). These relatively low prevalence figures for 45– and 50-year-olds are derived from the PROBASE study and from the publication of the first round of the Swedish OPT implementation study, respectively. If early detection is begun ten years later, the detection rate is already 10 times higher (7).

Box. The advantages and disadvantages of PSA-based prostate cancer screening.

Advangtages

  • lowering the probability of dying from prostate cancer or developing metastatic prostate cancer:

    • approximately 3 of 1000 men screened do not die of prostate cancer

    • approximately 4 out of 1000 men screened do not develop metastases of prostate cancer

  • lowering the need for early-detection testing when a PSA baseline value is measured at age 45:

    • 9 out of 10 men aged 45 have a PSA value below 1.5 ng/mL and need no further testing for 5 years

Disadvantages

  • psychological stress as a side effect of diagnostic testing for men with early-detected but non-life-threatening tumors

  • overdiagnosis – detection of cancer in 14 men to prevent one death; risk of overtreatment (surgery of radiotherapy of tumors that would never become life-threatening if left untreated)

  • unnecessary diagnostic testing if the baseline PSA level is elevated with no other evidence of tumor

  • false-positive findings: 3 out of 10 MRIs show normal findings, 3 out of 4 biopsies after elevated PSA levels show no tumor, 1 out of 4 biopsies after abnormal MRI show no tumor

  • low probability of a falsely negative (normal) PSA baseline value despite a demonstrable, clinically relevant tumor (false negative rate, 0.7 per 1000)

  • frequent repetition of PSA tests in 1 out of 10 men with a PSA baseline value of 1.5–3 ng/mL (every two years)

Modified according to AWMF registration number: 043–022OL S3 guideline for prostate cancer; MRI, magnetic resonance imaging; PSA, prostate-specific antigen

Prostate-specific antigen

Prostate cells express and secrete prostate-specific antigen (PSA), a serine protease that serves to liquefy the ejaculate. The serum PSA level is elevated whenever prostate cells are damaged, e.g., by prostatitis or trauma (cycling; digital rectal examinations), but also in prostate cancer. When, in men aged 55 to 69, an elevated PSA level is taken as an indication for invasive diagnostic testing (tissue sampling by prostate biopsy), prostate cancer will be found in approximately 25%, with this figure varying depending on the threshold that is set for an “elevated” PSA level. With modern magnetic resonance imaging (MRI)-guided biopsy techniques, the positive predictive value of an elevated PSA level rises to 42%, including 16% of clinically indolent carcinomas in ISUP grading group (GG) 1 (8).

Initial PSA measurement in men aged 45–50 has a further type of predictive value beyond a correlation with current, biopsy-proven prostate cancer: it can also predict the lifelong risk of developing metastatic prostate cancer (9). This predictive potential is highest in men aged 45–50 because they have not yet been affected by age-related benign prostatic enlargement (concept of the baseline PSA level). A major reason for the overdiagnosis and consequent overtreatment of prostate cancer in Germany at present is self-initiated testing at the wrong age. According to data from AOK, a German statutory health-insurance carrier, for the year 2022, most men undergo cancer screening for the first time in their lives when already over 75 years of age, probably in combination with a PSA test. Only 13% do so at the ideal diagnostic age of 45–50 (10).

Digital rectal examination (DRE)

DRE has been part of the annual cancer screening recommended by German statutory health insurance carriers for over 50 years, yet its sensitivity in the early detection of prostate cancer has been shown to be insufficient (5%). DRE is no longer recommended for the early detection of prostate cancer in the updated guidelines.

Risk-adapted early detection and clinical risk factors

Men aged 45–50 who undergo baseline PSA measurement for early detection are divided into three groups according to their PSA level, with different recommendations for further testing in each group Table. If the PSA level is below 1.5 ng/mL, the patient is considered to be at low risk and no further PSA measurements for early detection are indicated for at least five years. This is the case in 89% of men aged 45 and 82% of men aged 50 (12).

Table. The baseline PSA level determines the risk classification and the risk-adapted recommendation for subsequent testing intervals, or for an immediate diagnostic evaluation if indicated.

Baseline PSA value Risk classification Recommendations
< 1.5 ng/ml low risk 5-year intervals
1.5 ng/mL < 3.0 ng/ml intermediate risk 2-year intervals
≥3 ng/mL (confirmed) high risk evaluation (cf. Figure)

Modified from AWMF registration number 043–022OL, the S3-guideline on prostate cancerPSA, prostate-specific antigen

PSA levels between 1.5 and 3.0 ng/mL signify intermediate risk. For these patients, biennial follow-up examinations are recommended. Finally, PSA values of 3.0 ng/mL or above signify high risk, and these patients should undergo further testing, which will reveal prostate cancer in 25–30%. The first steps of further testing are confirmation of the PSA level within three months and a risk assessment. If the confirmed PSA level is still above 3 ng/mL and cannot be explained by an enlarged gland, acute inflammation, or any other known causes, an MRI of the prostate is recommended. These initial diagnostic steps obviate the need for invasive diagnosis by biopsy in half of men with an initially abnormal PSA level. Men with a suggestive family history (one first-degree relative (brother, father) who received a diagnosis of prostate cancer before age 60, or more than one first-degree relative with prostate cancer at any age) are offered the same early-detection strategy.

PSA-based screening is recommended from age 40 onward for men with a genetic predisposition (e.g., pathogenic variants of the BRCA2 gene or the Lynch-syndrome-associated genes MSH2 and MSH6). Smoking is not a risk factor for prostate cancer.

Diagnostic testing

Diagnostic testing for possible prostate cancer that is suspected on clinical/laboratory grounds (elevated PSA level, suspect findings on digital rectal examination, micturition symptoms) is of a different nature from population-based screening. Before non-invasive and/or invasive testing are decided upon, the consequences of a prostate cancer diagnosis must be discussed with the patient. In men with high comorbidity and limited life expectancy, testing should only be performed if prostate cancer would impair their quality of life (11).

The new PSA-MRI diagnostic algorithm

An international consensus now holds that a man of any age whose life expectance is 10 years or more and whose PSA level is 3 ng/mL or higher should undergo diagnostic testing for prostate cancer. The life expectancy can be derived from the physician’s estimate or from the gait speed table of Studenski et al. (mean walking speed over a distance of 6 m [e1]). Such patients should, however, first undergo confirmaton of PSA and risk assessment, taking into account all possible factors that might elevate the PSA level (e.g., earlier diagnostic examinations, prostate size, inflammation, trauma, family history, ethnicity). Online risk calculators are available for objective risk assessment (e.g., ERSPC, Cancer Research UK). If these suggest an increased risk of having prostate cancer (e.g., >10% with the ERSPC No. 2 risk calculator), an MRI of the prostate should be performed next; one should not yet proceed directly to biopsy, as previously recommended. Multiple randomized trials (primarily in prostate screening) of this so-called PSA-MRI diagnostic algorithm (Figure) have revealed that it obviates the need for as many as 70% of prostate biopsies (see systematic review, [8]). Both the technical quality of prostate MRI and the radiologist‘s experience in interpreting it are crucial. For this reason, the new S3 guideline recommends that the MRI should be performed in accordance with the currently applicable quality standards, and that the interpreting radiologist should be one who is specially trained and certified in prostate MRI (Q2 special certificate from the German Society of Radiology). The information available in the images should guide the performance of the biopsy. The new guidelines specify precisely when a biopsy is indicated: A so-called MRI-ultrasound fusion biopsy is indicated only when the suspicion of prostate cancer on MRI is rated at PI-RADS (Prostate Imaging – Reporting and Data System) 4 or 5, or at PI-RADS 3 if the patient is at high individual risk (e.g., when the PSA density – the PSA level in ng/mL, divided by the prostate volume in mL – is greater than 0.15) (Figure 1). This increases the tumor detection rate for clinically relevant prostate cancer in screening studies to nearly 50% (8). The rationale behind these recommendations is to avoid unnecessary biopsies of clinically indolent carcinomas (ISUP GG 1) on the basis of high-level evidence (1316). PI-RADS 1–2 lesions should not be biopsied (17, 18).

Figure.

Figure

Algorithm for risk-adapted early detection

ERSPC, European Randomized Study of Screening for Prostate Cancer;

MRI, magnetic resonance imaging; PSA, prostate-specific antigen

Figure 1.

Figure 1

Multiparametric magnetic resonance imaging (MRI)

The patient is a 73-year-old man with a confirmed elevated PSA level of 9.5 ng/mL. In the peripheral zone of the mid-prostate, right anterior to posterolateral, there is a suspect area of highly probable carcinoma (arrows) with a PI-RADS of 5. Subsequent targeted MRI-ultrasound fusion biopsy led to the diagnosis of prostate cancer with a Gleason score of 3+4 (60%/40%).

Prostate biopsy technique

In view of the findings of multiple randomized trials, both perineal and transrectal fusion biopsies can be recommended, although transrectal biopsies should only be performed with antibiotic protection (1921). Both types of biopsy can be performed under either local or general anesthesia (eFigure).

eFigure.

eFigure

Targeted MRI/ultrasound fusion biopsy system

Computer used to combine MRI images with ultrasound images (left), high-resolution ultrasound scanner (middle), exam table with leg support (right, foreground)

PSMA-PET-/CT imaging

Initial evidence suggests that positron emission tomography (PET) with prostate-specific membrane antigen (PSMA) as the target molecule can also provide valuable information in primary diagnostic testing, e.g., with respect to the aggressiveness of prostate cancer (ISUP GG). In the new guideline, PSMA-PET/CT is recommended primarily to rule out lymph node and distant metastases in locally advanced prostate cancer (ISUP GG ≥ 3 or cT3/cT4 or PSA > 20 ng/mL) (Figure 2). This method has been found in randomized trials to be significantly superior to conventional imaging (computed tomography [CT] and bone scintigraphy) (22). The accuracy of staging with regard to lymph node metastases was 92% [88; 95] in PSMA-PET-CT examinations versus 65% [60; 69] in conventional staging with CT and bone scintigraphy (p < 0.0001) (22).

Figure 2.

Figure 2

PSMA-PET/CT in a 55-year-old man with an initial diagnosis of prostate cancer (iPSA 25.8 ng/mL). 18F-PSMA positron emission tomography (PET) for primary staging.

The images in the upper row include coronal sections from computed tomography (CT) scans, a PET scan, and a fused PET/CT scan.

The images in the lower row include a transaxial CT and a fused PET/CT. The PSMA PET/CTs show focal, intensified PSMA uptake in the prostate, without uptake in the lymph nodes or other organs (miTNM codeline: mT3b [LM, RM, LSV] N0 M0).

The detection of lymph node or distant metastases in prostate cancer has significant therapeutic consequences, because local therapy alone can no longer be performed.

Genetic counseling and testing

Genetic counseling and the offer of germline testing for patients with metastatic prostate cancer are mentioned for the first time in the new S3 guideline. The background to this recommendation is the high prevalence (>10%) of pathogenic variants in DNA repair genes in these patients (23).

The treatment of localized prostate cancer

68% of cases of prostate cancer are localized and non-metastatic, in UICC stages I and II (T1-T2c N0 M0), when initially diagnosed (1). In addition to clinical staging, prostate cancer is classified into different ISUP GG after biopsy. These groups are clinical risk groups, each with its own risk of mortality. The most commonly used and best validated classification is now that of the NCCN (National Comprehensive Cancer Network), but the D‘Amico risk classification is still in use. The new subdivision of the large group of intermediate-risk prostate cancers has important implications for treatment.

The findings of the British ProtecT trial at 15 years were published in 2023 and serve as the most important basis for the new treatment recommendations (24). The classic forms of treatment—radical prostatectomy, radiotherapy, and active monitoring—were compared in a randomized trial; at 15 years, there was no difference in cancer-specific survival (>97% in each case). Patients with localized prostate cancer must therefore be informed neutrally by urologists and radiation oncologists about all three forms of treatment, with due consideration to their comorbidity and life expectancy. This analysis implies that low-risk tumors should be managed with active surveillance, as is recommended in the new S3 guideline.

Active surveillance

Patients in the NCCN low-risk and very-low-risk groups make up approximately half of patients with localized prostate cancer and can be managed with active surveillance. In Germany, a decision was made to define in detail a further group of patients who are at “favorable intermediate risk,” for whom active surveillance is also appropriate.

Large-scale histopathological studies of prostatectomy specimens have revealed a clear correlation between the frequency of Gleason pattern 4 (out of 5) and the PSA recurrence rate after radical prostatectomy. This suggests that patients with ISUP GG 2 prostate cancer and no more than a small amount of Gleason pattern 4 can also be managed primarily with active surveillance. This would correspond in practice to, e.g., less than 25% of Gleason pattern 4 without cribriform or intraductal growth patterns (25).

All patients with low risk (ISUP GG 1) should primarily undergo active surveillance; neither surgery nor radiotherapy is recommended any more for these patients. The active surveillance recommended in the new German S3 guideline is to be carried out more frequently than that described in the ProtecT trial. Active surveillance is recommended only with a prostatic MRI that meets the current quality criteria and an MRI-guided biopsy of the prostate to avoid misclassification. During active surveillance, the PSA level should be checked every 3 months (ISUP GG 2) or every 6 months (ISUP GG 1) for the first two years. In addition, an MRI-guided re-biopsy is recommended at 12–18 months. In the event of histological progression, but not in the event of a PSA increase alone, active surveillance should be discontinued in favor of surgery or radiotherapy. Purely MRI-guided active surveillance without re-biopsy is possible but has not yet been sufficiently evaluated.

Radical prostatectomy

Radical prostatectomy (RP) is recommended for patients with localized prostate cancer and an ISUP grading group above 2, or 2 with an unfavorable risk profile. A German randomized trial comparing laparoscopic and robot-assisted surgical techniques revealed a significant difference in early continence at 3 months, in favor of robotics (26). The 3-month continence rate after robot-assisted radical prostatectomy was 54%, compared to 46% after open surgery (p = 0.027). A systematic review of randomized trials of open surgery vs. robot-assisted techniques did not reveal any significant difference in oncological outcomes or long-term side effects (27). Patients with a high-risk profile and/or locally advanced tumors (pT3/pT4 and ISUP 4–5) should be offered adjuvant radiotherapy. This can be performed in patients with multifocal positive margins (28). The alternative for patients with a high-risk profile is delayed percutaneous salvage radiotherapy, if biochemical recurrence (BCR) from the nadir (PSA below the detection limit) is detected after surgery (29). In patients with BCR and a favorable risk profile (PSA doubling time > 12 months, ISUP GG < 4), watchful waiting is an acceptable approach (30). PSMA-PET/CT examinations may be useful if PSA levels rise above >0.2 ng/mL to localize the recurrence and assist in treatment planning (31).

Primary curative radiation therapy

Intensity-modulated percutaneous radiotherapy (IMRT) of localized prostate cancer should be carried out with image guidance (IGRT). The standard dose is at least 74 Gy to 80 Gy in normofractionated form. For localized intermediate-risk and localized high-risk prostate cancer, either moderate hypofractionation (e.g., over four weeks instead of eight) or normofractionated radiotherapy is indicated (32, 33). In patients with an intermediate-risk profile, this should be accompanied by hormone ablation therapy for four to six months. For high- to very- high-risk profiles according to the NCCN, hormone ablation therapy should be given for 24 to 36 months. Proton therapy has no greater clinical benefit than IMRT and IGRT (34). In patients with an intermediate-risk profile, extreme hypofractionation (5–7 fractions over one or two weeks of radiotherapy) can also be performed under certain conditions (35). A so-called focal boost has also been added to the recommendations: this consists of a local dose increase above 78 Gy up to a total dose of approximately 90 Gy, with the boost covering the major portion of the carcinoma that is visible in multiparametric MRI. A focal boost can be used for locally confined tumors with a high risk profile (36). In patients with a very-high-risk profile and stage cN0 (PSMA-PET/CT negative), supplementary radiotherapy of the pelvic lymphatic drainage areas can be performed as adjuvant treatment (37).

As implied by new data from the randomized STAMPEDE trial, patients with pelvic lymph node metastases (cN1 in conventional CT staging) should be given not only radiotherapy of the prostate and pelvic lymphatic drainage areas, but also extended systemic treatment with abiraterone for two years in addition to androgen deprivation therapy (ADT) (38).

Low-dose-rate (LDR) brachytherapy

On the basis of findings from a randomized trial, LDR mono-brachytherapy has been reevaluated and can now be considered a standard treatment option for patients with a favorable intermediate risk profile (39). Brachytherapy is generally supplemented with androgen-deprivation treatment for the same length of time as percutaneous radiotherapy (4–6 months or 24–36 months).

The treatment of patients with lymph node metastases (cN1)

The increasing use of PSMA-PET/CT staging has led to an increasing number of diagnoses at stage cN+. It remains unclear which form of treatment should be recommended for these patients. False-positive PSMA PET findings are very rare in conjunction with an unfavorable NCCN risk profile (40). In all cases, treatment of the primary tumor with surgery or radiotherapy is recommended. The STAMPEDE trial with conventional staging provides strong evidence for combined radiotherapy of the prostate and its lymphatic drainage pathways (38).

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Questions on this article

Participation is possible at cme.aerzteblatt.de.

The submission deadline is 24 July 2026.

Only one answer is possible per question. Please select the answer that is most appropriate.

Question 1

What is the probability that a man will receive a diagnosis of prostate cancer during his lifetime?

  1. 3–5%

  2. 10–15%

  3. 20–25%

  4. 30–35%

  5. > 35%

Question 2

What is the meaning of “overdiagnosis” in prostate cancer screening?

  1. the diagnosis of a tumor that has already metastasized

  2. the diagnosis of a locally advanced tumor

  3. the diagnosis of a tumor with lymph node metastases

  4. the diagnosis of a tumor that will not become life-threatening in the rest of the patient’s life

  5. the diagnosis of a tumor that will metastasize at some point in the rest of the patient’s life

Question 3

Which of the following is not a risk factor for prostate cancer?

  1. age

  2. BRCA1 mutation

  3. BRCA2 mutation

  4. smoking

  5. a first-degree relative with prostate cancer

Question 4

Which statement about prostate-specific antigen (PSA) is correct?

  1. PSA is a threonine protease.

  2. PSA is a serine protease.

  3. A low PSA level increases the risk of erectile dysfunction.

  4. PSA phosphorylates intracellular tyrosine kinases.

  5. PSA levels follow a circadian rhythm.

Question 5

Why is a digital rectal examination (DRE) no longer recommended for early detection?

  1. Its low specificity leads to a high rate of false-negative findings.

  2. It is no longer accepted by patients.

  3. It can only detect locally advanced tumors with high sensitivity and specificity.

  4. It is only useful in patients with a PSA level above 3 ng/mL.

  5. It is only suitable for verifying the success of radiation therapy.

Question 6

At what age should a baseline PSA level be determined for early detection if there is no genetic predisposition?

  1. 35 years

  2. 40 years

  3. 45 years

  4. 50 years

  5. 55 years

Question 7

What role does magnetic resonance imaging (MRI) play in the diagnosis of prostate cancer?

  1. It is an integral part of the diagnostic process and helps obviate the need for biopsy.

  2. It is only suitable for treatment planning in metastatic prostate cancer.

  3. It is mainly used in patients with a genetic predisposition.

  4. It is a supplementary method that is only recommended when the PSA level exceeds 10 ng/mL.

  5. It replaces biopsy in patients with a PI-RADS score of 3–4.

Question 8

For which patients is active surveillance a suitable management?

  1. those whose PSA level is in the 1.5–2.5 ng/mL range

  2. those with ISUP-GG-2 prostate cancer, with a Gleason pattern 4 fraction under 25% and without cribriform or intraductal growth patterns

  3. those with locally advanced tumors (pT3/pT4)

  4. those with an ISUP-GG of 4–5

  5. those with no more than 2 metastases of diameter no more than 2 cm

Question 9

Which statement about curative radiation therapy for the prostate is correct?

  1. 60–70 Gy must be delivered in normofractionated form.

  2. For patients at intermediate risk, it must be combined with hormone deprivation therapy.

  3. It must be performed by Q2-certified radiation oncologists.

  4. It must be performed after radical prostatectomy (R1 resection).

  5. It is best given as proton therapy.

Question 10

Which statement about radical prostatectomy (RP) is correct?

  1. It is the only available treatment for patients with locally advanced prostate cancer.

  2. Robot-assisted RP yields a higher early continence rate but no difference in oncological outcomes or long-term side effects compared to open surgery.

  3. RP should always be combined with adjuvant radiotherapy, regardless of the patient‘s risk profile.

  4. It is an alternative to radiotherapy for patients with prostate cancer in grading group 1.

  5. It is mandatory for all patients with biochemical recurrence (PSA doubling time > 24 months) after surgery.

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eBox. Collaborators of the S3 guideline on prostate cancer:

  • Nikolaus Becker, German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ), section for personalized early detection of prostate cancer (early detection working group)

  • Dirk Böhmer, Department of Radiation Oncology, Charité, Berlin

  • Christian Bolenz, Department of Urology and Pediatric Urology, Universitätsklinikum Ulm (head of working group on active surveillance)

  • Angelika Borkowetz, Department of Urology, Universitätsmedizin Rostock (head of working group on diagnostic testing)

  • Ernst-Günter Carl, German Association for Prostate Cancer Self-Help (Bundesverband Prostatakrebsselbsthilfe, BPS) and eUOMO (working group on early detection)

  • Ute Ganswindt, University Department of Radiation Therapy – Radio-Oncology, Innsbruck, Austria

  • Marc-Oliver Grimm, Department of Urology, Universitätsklinikum Jena (guideline coordinator)

  • Boris Hadaschik, Department of Urology, Universitätsklinikum Essen (head of working group on staging)

  • André Karger, Department of Psychosomatic Medicine, Universitätsklinikum Düsseldorf (working group on treatment)

  • Lars Schimmöller, Department of Diagnostic and Interventional Radiology, Universitätsklinikum der Ruhruniversität Bochum und des Universitätsklinikums Düsseldorf

  • Stefanie Schmidt, UroEvidence, DGU Berlin

  • Alexander E. Volk, Institute of Human Genetics, Universitätsklinikum Hamburg-Eppendorf (working group on early detection)

  • Bernhard Wörmann, Department of Hematology, Oncology, and Tumor Immunology, Charité, Berlin (working group on treatment)

Acknowledgments

Translated from the original German by Ethan Taub, M.D.

References (abbreviated)

1. www.krebsdaten.de/Krebs/DE/Content/Publikationen/Krebs_in_Deutschland/krebs_in_deutschland_node.html

2. Worst TS, et al.: Urologie 2024; 63: 681–92.

3. James ND, et al.: Lancet 2024; 403: 1683–722.

4. de Vos II, et al.: Eur Urol 2023; 85: 426–34.

5. Arsov C, et al.: Int J Cancer 2022; 150: 1861–9.

6. Bratt O, et al.: Eur Urol 2024; 85: 207–14.

7. Hugosson J, et al.: N Engl J Med 2022; 387: 2126–37.

8. Fazekas T, et al.: JAMA Oncol 2024; 10: 745–54.

9. Vickers AJ, et al.: BMJ 2013; 346: f2023.

10. www.wido.de/fileadmin/Dateien/Dokumente/Publikationen_Produkte/GGW/2020/wido_ggw_0320_widothemen.pdf

11. Krilaviciute A, et al.: Eur Urol Oncol 2023; 6; 566-73.

12. Krilaviciute A, et al.: Eur Urol 2024; 86: 493–500.

13. Drost FH, et al.: Cochrane Database Syst Rev 2019; 4: Cd012663..

14. Franiel T, et al.: RoFo 2021; 193: 763–77.

15. Schoots IGet al.: BJU Int 2021; 127: 175–8.

16. Quentin M, et al.: Eur J Radiol 2024; 175: 111436.

17. Pagniez MA, et al.: J Urol 2020; 204: 24–32.

18. Alberts AR, et al.: Eur Urol 2019; 75: 310–8.

19. Hu JC, et al.: Eur Urol 2024; 86: 61–8.

20. Mian BM, et al.: J Urol 2024; 211: 205–13.

21. Ploussard G, et al.: Eur Urol Oncol 2024; 7: 1080–7.

22. Hofman MS, et al.: Lancet 2020; 395: 1208–16.

23. Pritchard CC, et al.: N Engl J Med 2016; 375: 443–53.

24. Hamdy FC, et al.: N Engl J Med 2023; 388: 1547–58.

25. Sauter G, et al.: Eur Urol 2016; 69: 592–8.

26. Stolzenburg JU, et al.: Eur Urol 2021; 79: 750–9.

27. Haney CM, et al.: Eur Urol Focus 2023; 9: 930–7.

28. Tilki D,et al.: J Clin Oncol 2021; 39: 2284–93.

29. Parker CC, et al.: T Ann Oncol 2024; 35: 656–66.

30. Van den Broeck T, et al.: Eur Urol Focus 2020; 6: 231–4.

31. Bottke D, et al.: Front Oncol 2021; 11: 665304.

32. Lee WR, et al.: J Clin Oncol 2024; 42: 2377–81.

33. Niazi T, et al.: Int J Radiat Oncol Biol Phys. 2024; 118: 52–62.

34. Corrao G, et al.: Radiother Oncol 2024; 195: 110264.

35. van As N, et al.: N Engl J Med 2024; 391: 1413–25.

36. Groen VH, et al.: Eur Urol 2022; 82: 252–7.

37. Murthy V, et al.: Clin Oncol 2021; 39: 1234–42.

38. Attard G, et al.: Lancet 2022; 399: 447–60.

39. Michalski JM, et al.: J Clin Oncol 2023; 41: 4035–44.

40. Luining WI, et al.: Eur Urol Open Sci 2024; 59: 55–62.

Footnotes

Conflict of interest statement

The authors state that they have no conflict of interest.

References

  • 1.RKI; Krebsregisterdaten Zf, editors. Robert Koch Institut; 2022. Krebs in Deutschland. [Google Scholar]
  • 2.Worst TS, Surovtsova I, Vogel T, et al. [Incidence, therapy, and prognosis of prostate cancer in Baden-Württemberg: Analysis based on cancer registry data] Urologie. 2024;63:681–692. doi: 10.1007/s00120-024-02275-w. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 3.James ND, Tannock I, N‘Dow J, et al. The Lancet Commission on prostate cancer: Planning for the surge in cases. Lancet. 2024;403:1683–1722. doi: 10.1016/S0140-6736(24)00651-2. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.de Vos II, Meertens A, Hogenhout R, Remmers S, Roobol MJ. ERSPC Rotterdam Study Group: A detailed evaluation of the effect of prostate-specific antigen-based screening on morbidity and mortality of prostate cancer: 21-year follow-up results of the Rotterdam section of the European Randomised Study of Screening for Prostate Cancer. Eur Urol. 2023;85:426–434. doi: 10.1016/j.eururo.2023.03.016. [DOI] [PubMed] [Google Scholar]
  • 5.Arsov C, Albers P, Herkommer K, et al. A randomized trial of risk-adapted screening for prostate cancer in young men—results of the first screening round of the PROBASE trial. Int J Cancer. 2022;150:1861–1869. doi: 10.1002/ijc.33940. [DOI] [PubMed] [Google Scholar]
  • 6.Bratt O, Godtman RA, Jiborn T, et al. Population-based Organised Prostate Cancer Testing: Results from the First Invitation of 50-year-old Men. Eur Urol. 2024;85:207–214. doi: 10.1016/j.eururo.2023.11.013. [DOI] [PubMed] [Google Scholar]
  • 7.Hugosson J, Månsson M, Wallström J, et al. Prostate cancer screening with PSA and MRI followed by targeted biopsy only. N Engl J Med. 2022;387:2126–2137. doi: 10.1056/NEJMoa2209454. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 8.Fazekas T, Shim SR, Basile G, et al. Magnetic resonance imaging in prostate cancer screening: A systematic review and meta-analysis. JAMA Oncol. 2024;10:745–754. doi: 10.1001/jamaoncol.2024.0734. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Vickers AJ, Ulmert D, Sjoberg DD, et al. Strategy for detection of prostate cancer based on relation between prostate specific antigen at age 40-55 and long term risk of metastasis: case-control study. BMJ. 2013;346 doi: 10.1136/bmj.f2023. f2023. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 10.Tillmanns H. Früherkennung: Die Teilnahmeraten sind oft noch zu niedrig. WIDO—Wissenschaftliches Institut der AOK. 2020 [Google Scholar]
  • 11.Krilaviciute A, Lakes J, Radtke JP, et al. Digital rectal examination (DRE) is not useful as a solitary screening tool for prostate cancer in young men—results from the PROBASE trial. Eur Urol Oncol. 2023;6:566–573. doi: 10.1016/j.euo.2023.09.008. [DOI] [PubMed] [Google Scholar]
  • 12.Krilaviciute A, Kaaks R, Seibold P, et al. Risk-adapted Screening for Prostate Cancer - Re-defining the Low-Risk Group by data from the PROBASE trial. Eur Urol. 2024;86:493–500. doi: 10.1016/j.eururo.2024.04.030. [DOI] [PubMed] [Google Scholar]
  • 13.Drost FH, Osses DF, Nieboer D, et al. Prostate MRI, with or without MRI-targeted biopsy, and systematic biopsy for detecting prostate cancer. Cochrane Database Syst Rev. 2019;4 doi: 10.1002/14651858.CD012663.pub2. Cd012663. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Franiel T, Asbach P, Beyersdorff D, et al. mpMRI of the Prostate (MR-Prostatography): Updated recommendations of the DRG and BDR on patient preparation and scanning protocol. RoFo. 2021;193:763–777. doi: 10.1055/a-1406-8477. [DOI] [PubMed] [Google Scholar]
  • 15.Schoots IG, Padhani AR. Risk-adapted biopsy decision based on prostate magnetic resonance imaging and prostate-specific antigen density for enhanced biopsy avoidance in first prostate cancer diagnostic evaluation. BJU Int. 2021;127:175–178. doi: 10.1111/bju.15277. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 16.Quentin M, Boschheidgen M, Radtke JP, et al. MRI in-bore biopsy following MRI/US fusion-guided biopsy in patients with persistent suspicion of clinically significant prostate cancer. Eur J Radiol. 2024;175 doi: 10.1016/j.ejrad.2024.111436. 111436. [DOI] [PubMed] [Google Scholar]
  • 17.Pagniez MA, Kasivisvanathan V, Puech P, Drumez E, Villers A, Olivier J. Predictive factors of missed clinically significant prostate cancers in men with negative magnetic resonance imaging: A systematic review and meta-analysis. J Urol. 2020;204:24–32. doi: 10.1097/JU.0000000000000757. [DOI] [PubMed] [Google Scholar]
  • 18.Alberts AR, Roobol MJ, Verbeek JFM, et al. Prediction of high-grade prostate cancer following multiparametric magnetic resonance imaging: Improving the Rotterdam European Randomized Study of Screening for Prostate Cancer Risk Calculators. Eur Urol. 2019;75:310–318. doi: 10.1016/j.eururo.2018.07.031. [DOI] [PubMed] [Google Scholar]
  • 19.Hu JC, Assel M, Allaf ME, et al. Transperineal versus transrectal magnetic resonance imaging-targeted and systematic prostate biopsy to prevent infectious complications: The PREVENT Randomized Trial. Eur Urol. 2024;86:61–68. doi: 10.1016/j.eururo.2023.12.015. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 20.Mian BM, Feustel PJ, Aziz A, et al. Complications following transrectal and transperineal prostate biopsy: Results of the ProBE-PC randomized clinical trial. J Urol. 2024;211:205–213. doi: 10.1097/JU.0000000000003788. [DOI] [PubMed] [Google Scholar]
  • 21.Ploussard G, Barret E, Fiard G, et al. Transperineal versus transrectal magnetic resonance imaging-targeted biopsies for prostate cancer diagnosis: Final results of the randomized PERFECT trial (CCAFU-PR1) Eur Urol Oncol. 2024;7:1080–1087. doi: 10.1016/j.euo.2024.01.019. [DOI] [PubMed] [Google Scholar]
  • 22.Hofman MS, Lawrentschuk N, Francis RJ, et al. Prostate-specific membrane antigen PET-CT in patients with high-risk prostate cancer before curative-intent surgery or radiotherapy (proPSMA): A prospective, randomised, multicentre study. Lancet. 2020;395:1208–1216. doi: 10.1016/S0140-6736(20)30314-7. [DOI] [PubMed] [Google Scholar]
  • 23.Pritchard CC, Mateo J, Walsh MF, et al. Inherited DNA-repair gene mutations in men with metastatic prostate cancer. N Engl J Med. 2016;375:443–453. doi: 10.1056/NEJMoa1603144. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.Hamdy FC, Donovan JL, Lane JA, et al. Fifteen-year outcomes after monitoring, surgery, or radiotherapy for prostate cancer. N Engl J Med. 2023;388:1547–1558. doi: 10.1056/NEJMoa2214122. [DOI] [PubMed] [Google Scholar]
  • 25.Sauter G, Steurer S, Clauditz TS, et al. Clinical utility of quantitative gleason grading in prostate biopsies and prostatectomy specimens. Eur Urol. 2016;69:592–598. doi: 10.1016/j.eururo.2015.10.029. [DOI] [PubMed] [Google Scholar]
  • 26.Stolzenburg JU, Holze S, Neuhaus P, et al. Robotic-assisted versus laparoscopic surgery: Outcomes from the first multicentre, randomised, patient-blinded controlled trial in radical prostatectomy (LAP-01) Eur Urol. 2021;79:750–759. doi: 10.1016/j.eururo.2021.01.030. [DOI] [PubMed] [Google Scholar]
  • 27.Haney CM, Kowalewski KF, Westhoff N, et al. Robot-assisted versus conventional laparoscopic radical prostatectomy: A systematic review and meta-analysis of randomised controlled trials. Eur Urol Focus. 2023;9:930–937. doi: 10.1016/j.euf.2023.05.007. [DOI] [PubMed] [Google Scholar]
  • 28.Tilki D, Chen MH, Wu J, et al. Adjuvant versus early salvage radiation therapy for men at high risk for recurrence following radical prostatectomy for prostate cancer and the risk of death. J Clin Oncol. 2021;39:2284–2293. doi: 10.1200/JCO.20.03714. [DOI] [PubMed] [Google Scholar]
  • 29.Parker CC, Petersen PM, Cook AD, et al. Timing of radiotherapy (RT) after radical prostatectomy (RP): Long-term outcomes in the RADICALS-RT trial ( NCT00541047) Ann Oncol. 2024;35:656–666. doi: 10.1016/j.annonc.2024.03.010. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Van den Broeck T, van den Bergh RCN, Briers E, et al. Biochemical recurrence in prostate cancer: The European Association of Urology Prostate Cancer Guidelines Panel Recommendations. Eur Urol Focus. 2020;6:231–234. doi: 10.1016/j.euf.2019.06.004. [DOI] [PubMed] [Google Scholar]
  • 31.Bottke D, Miksch J, Thamm R, et al. Changes of radiation treatment concept based on (68)Ga-PSMA-11-PET/CT in early PSA-recurrences after radical prostatectomy. Front Oncol. 2021;11 doi: 10.3389/fonc.2021.665304. 665304. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 32.Lee WR, Dignam JJ, Amin MB, et al. Long-term analysis of NRG oncology RTOG 0415: A randomized phase III noninferiority study comparing two fractionation schedules in patients with low-risk prostate cancer. J Clin Oncol. 2024;42:2377–2381. doi: 10.1200/JCO.23.02445. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 33.Niazi T, Nabid A, Malagon T, et al. Hypofractionated dose escalation radiotherapy for high-risk prostate cancer: The survival analysis of the prostate cancer study 5, a groupe de radio-oncologie génito-urinaire du Quebec-led phase 3 trial. Int J Radiat Oncol Biol Phys. 2024;118:52–62. doi: 10.1016/j.ijrobp.2023.05.014. [DOI] [PubMed] [Google Scholar]
  • 34.Corrao G, Marvaso G, Mastroleo F, et al. Photon vs proton hypofractionation in prostate cancer: A systematic review and meta-analysis. Radiother Oncol. 2024;195 doi: 10.1016/j.radonc.2024.110264. 110264. [DOI] [PubMed] [Google Scholar]
  • 35.van As N, Griffin C, Tree A, et al. Phase 3 trial of stereotactic body radiotherapy in localized Prostate Cancer. N Engl J Med. 2024;391:1413–1425. doi: 10.1056/nejmoa2403365. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.Groen VH, Haustermans K, Pos FJ, et al. Patterns of failure following external beam radiotherapy with or without an additional focal boost in the randomized controlled FLAME trial for localized prostate cancer. Eur Urol. 2022;82:252–257. doi: 10.1016/j.eururo.2021.12.012. [DOI] [PubMed] [Google Scholar]
  • 37.Murthy V, Maitre P, Kannan S, et al. Prostate-only versus whole-pelvic radiation therapy in high-risk and very high-risk prostate cancer (POP-RT): Outcomes from phase III randomized controlled trial. Clin Oncol. 2021;39:1234–1242. doi: 10.1200/JCO.20.03282. [DOI] [PubMed] [Google Scholar]
  • 38.Attard G, Murphy L, Clarke NW, et al. Abiraterone acetate and prednisolone with or without enzalutamide for high-risk non-metastatic prostate cancer: A meta-analysis of primary results from two randomised controlled phase 3 trials of the STAMPEDE platform protocol. Lancet. 2022;399:447–460. doi: 10.1016/S0140-6736(21)02437-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 39.Michalski JM, Winter KA, Prestidge BR, et al. Effect of brachytherapy with external beam radiation therapy versus brachytherapy alone for intermediate-risk prostate cancer: NRG oncology RTOG 0232 randomized clinical trial. J Clin Oncol. 2023;41:4035–4044. doi: 10.1200/JCO.22.01856. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 40.Luining WI, Hagens MJ, Meijer D, et al. The probability of metastases within different prostate-specific antigen ranges using prostate-specific membrane antigen positron emission tomography in patients with newly diagnosed prostate cancer. Eur Urol Open Sci. 2024;59:55–62. doi: 10.1016/j.euros.2023.12.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • E1.Studenski S, Perera S, Patel K, et al. Gait speed and survival in older adults. JAMA. 2011;305:50–58. doi: 10.1001/jama.2010.1923. [DOI] [PMC free article] [PubMed] [Google Scholar]

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