Last reviewed by Dr. Dharmender Malik on 14 May 2026 · this article reflects the published primary literature and current clinical practice at FMRI Gurugram.
Introduction
Prostate cancer treatment is not a single decision — it is a sequence of decisions across the disease continuum from a man's first elevated PSA through localised disease management, possible biochemical recurrence, metastatic hormone-sensitive disease, the castration-resistant transition, and beyond. Each decision point has multiple evidence-based options with documented trade-offs. This pillar walks through, with primary-source citations, what the current evidence supports at each stage — based on AUA, EAU, NCCN, ESMO, and ESTRO guidelines, and the underlying randomised trials. Where radioligand therapy (Lu-177 PSMA-617, Ra-223) now fits in the standard sequence is explicit.
Risk stratification — the starting point
AI Overview · short answer
Prostate cancer treatment depends on disease stage, risk classification, and patient factors[1]. For localised disease, options include active surveillance (preferred for low-risk Grade Group 1), radical prostatectomy, external-beam radiation, brachytherapy, and focal therapy[2]. For metastatic hormone-sensitive disease, standard first-line treatment is androgen-deprivation therapy combined with a second-generation androgen-pathway inhibitor (abiraterone, enzalutamide, apalutamide, or darolutamide) or docetaxel, with triplet therapy increasingly standard for high-volume disease (ARASENS, PEACE-1)[3]. For metastatic castration-resistant prostate cancer (mCRPC), treatment options include docetaxel, cabazitaxel, abiraterone or enzalutamide (if not used earlier), Ra-223 for symptomatic bone-metastatic disease (ALSYMPCA), and Lu-177 PSMA-617 (Pluvicto) for PSMA-positive disease, FDA-approved 2022 post-taxane-and-ARPI and label-expanded 2025 to pre-chemotherapy use[4].
Every prostate cancer treatment decision begins with risk classification, which combines four core variables[5]:
- PSA at diagnosis — typically classified as <10, 10-20, and >20 ng/mL.
- Grade Group (Gleason score) — Grade Group 1 (Gleason 3+3=6), Grade Group 2 (Gleason 3+4=7), Grade Group 3 (Gleason 4+3=7), Grade Group 4 (Gleason 8), Grade Group 5 (Gleason 9-10).
- Clinical T-stage — T1c (impalpable, detected by raised PSA), T2 (palpable, organ-confined), T3 (extra-prostatic extension), T4 (involving adjacent structures).
- Imaging stage — multiparametric prostate MRI for local extent; Ga-68 PSMA PET-CT or conventional CT/bone scan for nodal and metastatic disease.
The NCCN, AUA, and EAU guidelines integrate these into risk groups[6]:
| Risk group | Definition |
|---|
| Very low risk | T1c, Grade Group 1, PSA <10, low percentage of cores positive, low core-burden disease |
| Low risk | T1-T2a, Grade Group 1, PSA <10 |
| Favourable intermediate | Grade Group 2 with favourable features (low PSA, low percent cores) |
| Unfavourable intermediate | Grade Group 3 or multiple intermediate-risk features |
| High risk | T3a, or Grade Group 4-5, or PSA >20 |
| Very high risk | T3b-T4, or primary Gleason 5, or >4 cores Grade Group 4-5 |
| Regional (N1) | Pelvic nodal involvement |
| Metastatic (M1) | Distant metastases (M1a node, M1b bone, M1c visceral) |
Localised disease — active surveillance
For low-risk Grade Group 1 disease, active surveillance is the preferred initial management strategy in current AUA, NCCN, and EAU guidelines[7]. Active surveillance is structured monitoring — PSA testing, MRI, periodic repeat biopsy — with curative treatment offered only if pathological reclassification occurs. The evidence base:
- Klotz et al. Toronto cohort (J Clin Oncol 2015) — long-term follow-up of 993 men on active surveillance showed 10-year prostate-cancer-specific survival of 98.1%, with 36% eventually receiving curative treatment for documented reclassification.
- ProtecT trial (Hamdy et al., NEJM 2023) — 1,643 men randomised to active monitoring, surgery, or radiotherapy. At 15 years, prostate-cancer-specific mortality was very low (~3%) and similar across all three arms, though the active-monitoring arm had higher metastasis rates than the curative arms.
Active surveillance is also appropriate for selected favourable intermediate-risk Grade Group 2 disease. The decision balances cancer-specific risk against the morbidity of definitive treatment (incontinence and erectile dysfunction after surgery; bowel and bladder side effects after radiation). The trade-offs are individualised through shared decision-making.
Localised disease — surgery and radiation
For intermediate-risk, high-risk, and selected low-risk patients who prefer definitive treatment, the principal options are radical prostatectomy and external-beam radiation therapy[8]:
- Radical prostatectomy — robotic-assisted or open. Removes the prostate and seminal vesicles; nodal dissection for higher-risk disease. Recovery 4-8 weeks; longer-term considerations include erectile function and continence outcomes.
- External-beam radiation therapy (EBRT) — modern intensity-modulated radiation therapy (IMRT), volumetric modulated arc therapy (VMAT), or stereotactic body radiation therapy (SBRT). Typical fractionation 28-39 daily treatments or 5-fraction SBRT. For higher-risk disease, combined with androgen-deprivation therapy (ADT) for 4 months to 3 years per risk group.
- Brachytherapy — low-dose-rate (LDR, permanent seeds) or high-dose-rate (HDR, temporary catheters). Used as monotherapy in selected low-risk or as boost in combination with EBRT for higher-risk disease.
- Focal therapy — HIFU, cryotherapy, focal laser, or focal brachytherapy for selected localised disease where the dominant lesion can be precisely targeted. Active research area; outcomes data still evolving.
The ProtecT 15-year data showed similar prostate-cancer-specific mortality across active monitoring, surgery, and radiotherapy, with different morbidity patterns — important context for the surgery-vs-radiation discussion[9]. For high-risk and very-high-risk disease, current evidence supports definitive treatment plus ADT-containing systemic therapy.
Biochemical recurrence after definitive treatment
Biochemical recurrence (BCR) — a rising PSA after definitive treatment without imaging evidence of disease — is a common scenario. The 2025 standard pathway uses Ga-68 PSMA PET-CT to identify the source of recurrence, which then determines treatment[10]:
- Post-prostatectomy BCR — PSA >0.2 ng/mL on two consecutive measurements. Ga-68 PSMA PET-CT typically detects disease above PSA 0.5-1.0 ng/mL; salvage radiotherapy is the standard for local recurrence; ADT-based systemic therapy for nodal or distant recurrence.
- Post-radiation BCR — Phoenix criteria (PSA nadir + 2 ng/mL). PSMA PET-CT identifies local vs distant recurrence; salvage prostatectomy, salvage cryotherapy, or salvage HIFU for selected local recurrence; ADT-based systemic therapy for distant disease.
The proPSMA, OSPREY, and CONDOR trials established PSMA PET-CT as superior to conventional imaging (CT, bone scan) in this setting. Detection sensitivity is meaningfully better at low PSA levels — important because earlier identification of recurrence supports better-targeted salvage treatment.
The castration-resistant transition (CRPC and mCRPC)
Castration resistance is defined as disease progression (PSA rise, radiographic progression, or symptomatic deterioration) despite castrate testosterone levels[13]. The transition is critical clinically because the treatment landscape changes:
- Non-metastatic CRPC (nmCRPC) — PSA rising on ADT but no radiographic evidence of metastatic disease (with conventional imaging). Apalutamide (SPARTAN), enzalutamide (PROSPER), and darolutamide (ARAMIS) all showed metastasis-free survival benefit in this setting. PSMA PET-CT increasingly identifies disease earlier; many "nmCRPC" by conventional imaging show PSMA-positive disease on modern PET, raising questions about whether the distinction will persist long-term.
- Metastatic CRPC (mCRPC) — radiographically evident metastatic disease that has progressed on ADT. The treatment landscape includes multiple modalities with varied evidence bases.
Metastatic CRPC treatment options
For mCRPC, current 2026 treatment options include[14]:
| Treatment | Evidence base | Indication |
|---|
| Abiraterone + prednisone | COU-AA-301 (post-docetaxel), COU-AA-302 (pre-docetaxel) | If not used earlier in mHSPC |
| Enzalutamide | AFFIRM (post-docetaxel), PREVAIL (pre-docetaxel) | If not used earlier in mHSPC |
| Docetaxel | TAX 327, SWOG 9916 | Standard first-line cytotoxic chemotherapy in mCRPC if not used earlier |
| Cabazitaxel | TROPIC, CARD | Post-docetaxel; CARD established cabazitaxel over second ARPI after docetaxel + ARPI |
| Ra-223 dichloride | ALSYMPCA | Symptomatic bone-metastatic CRPC; OS HR 0.70 vs placebo |
| Lu-177 PSMA-617 (Pluvicto) | VISION (Sartor 2021, NEJM); TheraP (Hofman 2021, Lancet); PSMAfore (2024) | PSMA-positive mCRPC: post-taxane and ARPI (VISION) or pre-chemotherapy (PSMAfore, 2025 label expansion) |
| PARP inhibitors (olaparib, rucaparib, talazoparib, niraparib) | PROfound, TRITON3, TALAPRO-2, MAGNITUDE | Selected patients with BRCA1/2, ATM, or other HRR pathway mutations |
| Pembrolizumab + chemotherapy | Selected indications | MSI-H or specific contexts |
| Sipuleucel-T | IMPACT trial | Asymptomatic or minimally symptomatic mCRPC (limited use in current practice) |
The optimal sequence and combination for any individual patient depends on prior treatment, disease characteristics, biomarker status (PSMA expression, HRR mutations, MSI status), patient performance status, and patient values. Decisions are made at multidisciplinary tumour board review.
Lu-177 PSMA-617 — where it fits in the mCRPC sequence
Lu-177 PSMA-617 (Pluvicto) is the principal recent addition to the mCRPC treatment landscape and represents the integration of theranostic radioligand therapy into standard care[15]:
- VISION trial (Sartor et al., NEJM 2021) — 831 men with PSMA-positive mCRPC post-taxane and ARPI randomised to Lu-177 PSMA-617 plus standard of care vs standard of care alone. Median radiographic PFS 8.7 vs 3.4 months (HR 0.40); median OS 15.3 vs 11.3 months (HR 0.62); FDA-approved 2022.
- TheraP trial (Hofman et al., Lancet 2021) — 200 men randomised to Lu-177 PSMA-617 vs cabazitaxel. PSA response 66% vs 37%; PFS HR 0.63; supported the regulatory case.
- PSMAfore trial (2024) — Lu-177 PSMA-617 vs ARPI switch in pre-chemotherapy mCRPC. rPFS benefit; led to FDA label expansion 2025 to include the pre-chemotherapy setting.
- Eligibility — anchored to Ga-68 PSMA PET-CT confirming PSMA expression; FDG PET may add information in selected patients to identify PSMA-discordant disease.
- Standard protocol — six cycles of 7.4 GBq Lu-177 PSMA-617 at 6-8 week intervals.
For deeper coverage see our companion Lu-177 PSMA published outcomes article. For cost and access see cost considerations in India.
Ra-223 and bone-targeted therapy
Ra-223 dichloride (Xofigo) is the established alpha-emitter radiopharmaceutical for symptomatic bone-metastatic CRPC[16]. ALSYMPCA randomised 921 patients to Ra-223 vs placebo plus best supportive care: median overall survival 14.9 vs 11.3 months (HR 0.70); time-to-first-symptomatic-skeletal-event 15.6 vs 9.8 months. FDA and EMA approved 2013. Standard regimen: six monthly intravenous infusions.
Other bone-supportive treatments in mCRPC include zoledronic acid and denosumab — both reduce skeletal-related events but do not extend overall survival as monotherapy in this setting. They are used adjunctively to systemic disease-modifying therapy.
Sequencing of Ra-223 and Lu-177 PSMA-617 is a current clinical question: both target bone-dominant mCRPC, both have safety profiles affecting marrow, and the available evidence does not clearly establish which to use first or whether they can be combined. Decisions are individualised[17].
Supportive care and symptom management
Supportive care is integral to prostate cancer treatment across the disease continuum[18]:
- Hormone-deprivation side effects — hot flushes, sexual dysfunction, fatigue, muscle and bone loss, metabolic changes. Specific interventions: exercise (proven OS benefit in some settings), bisphosphonate or denosumab for bone-health, lifestyle counselling.
- Bone-pain management — escalation through paracetamol, NSAIDs (with renal considerations), weak opioids, strong opioids, neuropathic agents, palliative external-beam radiation to symptomatic sites, Ra-223 for diffuse bone disease.
- Urinary symptoms — obstruction from local disease may require urethral stenting, transurethral resection, or palliative radiation.
- Psychological support — clinical psychology and structured cancer-support groups are part of comprehensive care.
- Specialist palliative care — early specialist palliative care integration improves quality of life and may improve survival; recommended alongside disease-modifying treatment, not only at end of life.
Prognosis and individualised decision-making
Prostate cancer outcomes vary substantially by stage and risk group. Approximate 5-year prostate-cancer-specific survival figures (Globocan 2022 / SEER 2020-2024):
- Localised disease (~75-80% of new diagnoses in screened populations) — 5-year prostate-cancer-specific survival approaches 100%.
- Regional (nodal) disease — 5-year prostate-cancer-specific survival approximately 90%.
- Metastatic disease at diagnosis — 5-year prostate-cancer-specific survival approximately 30%; substantially improved with modern systemic therapy (ARPI, docetaxel, triplet, PSMA-RLT) compared with historic data.
Individual prognosis depends on more than stage: tumour biology (Grade Group, biomarker status, genomic features), prior treatment response, organ reserve, performance status, and patient age. Quantitative individual-patient prognostic tools (MSKCC nomograms, NCCN-based predictors) support but do not replace clinical judgement and informed-consent discussion[19].
Where multidisciplinary review fits
Every major prostate cancer treatment decision benefits from multidisciplinary tumour board review[20]. The relevant disciplines typically include:
- Medical oncology — for systemic therapy decisions across mHSPC, mCRPC, biomarker-targeted therapy.
- Urology / urological oncology — for surgical decisions, post-prostatectomy management, local salvage.
- Radiation oncology — for definitive radiotherapy, salvage radiotherapy, palliative radiation, SBRT for oligometastatic disease.
- Nuclear medicine — for PSMA PET-CT staging and biochemical-recurrence imaging, Lu-177 PSMA-617 therapy eligibility, Ra-223 delivery.
- Radiology — for prostate MRI interpretation, PI-RADS scoring, body-imaging response assessment.
- Genetic counselling — for HRR-pathway testing (BRCA1/2, ATM, CHEK2, HOXB13), family screening implications.
- Specialist palliative care — for symptom management and care planning across the continuum.
This multidisciplinary structure is what current AUA, EAU, NCCN, and ESMO guidelines explicitly endorse for high-risk and metastatic disease decisions, and increasingly for localised-disease decisions as well.
The bottom line
- Prostate cancer treatment is determined by risk classification (PSA, Grade Group, T-stage, imaging stage) integrated through NCCN, AUA, and EAU risk groups[5][6].
- For low-risk Grade Group 1 disease, active surveillance is the preferred initial management strategy; long-term cohort and randomised data (Klotz; ProtecT) support its safety[7].
- For localised disease requiring treatment, options include radical prostatectomy, external-beam radiation (IMRT/VMAT/SBRT), brachytherapy, and focal therapy; ProtecT showed similar 15-year prostate-cancer-specific mortality across modalities with different morbidity patterns[9].
- Biochemical recurrence is managed with Ga-68 PSMA PET-CT guidance; salvage radiotherapy for local recurrence, ADT-based therapy for nodal/distant recurrence[10].
- Metastatic hormone-sensitive disease: standard first-line is ADT + ARPI or ADT + docetaxel, with triplet therapy (ARASENS, PEACE-1) increasingly standard for high-volume disease[11].
- mCRPC: docetaxel, cabazitaxel, abiraterone, enzalutamide, Ra-223, Lu-177 PSMA-617 (Pluvicto), PARP inhibitors per biomarker status — sequenced based on prior therapy and disease characteristics[14].
- Lu-177 PSMA-617 is FDA-approved (2022) and EMA-approved (2023) for PSMA-positive mCRPC, label expanded 2025 to pre-chemotherapy setting based on VISION, TheraP, and PSMAfore trials[15].
Important
This article is a patient-level pillar guide to prostate cancer treatment. Individual treatment decisions depend on multiple clinical and personal factors and should be made through informed shared decision-making with the urology, oncology, and nuclear medicine teams. The article does not replace clinical consultation.
"Prostate cancer treatment is not a single decision but a sequence of decisions across the disease continuum. The current evidence base supports active surveillance for low-risk disease, intensified systemic therapy (triplet) for high-volume metastatic hormone-sensitive disease, and Lu-177 PSMA-617 radioligand therapy now integrated into standard mCRPC care across multiple lines. Decisions are individualised and multidisciplinary."
Dr. Ishita B. Sen, MD · Director & Chief, Nuclear Medicine, FMRI
Prostate cancer treatment review · FMRI
At FMRI Gurugram, prostate cancer treatment review follows shared-decision-making frameworks aligned with AUA, EAU, NCCN, and ESMO guidelines. Multidisciplinary tumour board review covers risk stratification (NCCN groups), Ga-68 PSMA PET-CT staging where indicated, and eligibility for Lu-177 PSMA-617 or Ra-223 therapy where clinically appropriate.
Request treatment review · WhatsApp +91 8800 988936
For patients & referring clinicians
Frequently asked questions
Q01
What are the main treatment options for prostate cancer?
Treatment depends on disease stage and risk. For localised disease: active surveillance (low-risk Grade Group 1), radical prostatectomy, external-beam radiation (IMRT/VMAT/SBRT), brachytherapy, or focal therapy. For metastatic hormone-sensitive disease: androgen-deprivation therapy combined with a second-generation androgen-pathway inhibitor (abiraterone, enzalutamide, apalutamide, darolutamide) or docetaxel, with triplet therapy for high-volume disease. For metastatic castration-resistant disease: docetaxel, cabazitaxel, abiraterone, enzalutamide, Ra-223, Lu-177 PSMA-617, PARP inhibitors. Decisions are individualised at multidisciplinary review [1][14].
Q02
What does it mean if my prostate cancer is 'low risk'?
Low-risk prostate cancer is defined by NCCN as: clinical T1-T2a (organ-confined), Grade Group 1 (Gleason 3+3=6), and PSA below 10 ng/mL. Very-low-risk adds requirements for low percentage of cores positive and low core-burden disease. For low-risk Grade Group 1 disease, active surveillance — structured monitoring with PSA, MRI, and periodic repeat biopsy — is the preferred initial management strategy per AUA 2023, NCCN, and EAU guidelines. The Klotz Toronto cohort showed 10-year prostate-cancer-specific survival of 98.1% on active surveillance, and the ProtecT trial showed similar prostate-cancer-specific mortality across active monitoring, surgery, and radiotherapy at 15 years [6][7].
Q03
What is triplet therapy for metastatic prostate cancer?
Triplet therapy is the combination of three agents for de novo metastatic hormone-sensitive prostate cancer (mHSPC): ADT + docetaxel chemotherapy + a second-generation androgen-pathway inhibitor (darolutamide in ARASENS, abiraterone in PEACE-1). ARASENS (NEJM 2022) showed OS HR 0.68 vs ADT + docetaxel alone; PEACE-1 showed OS HR 0.75 in de novo mHSPC with rPFS HR 0.50. Triplet therapy is now standard for high-volume de novo mHSPC; for low-volume mHSPC or patients unfit for docetaxel, ADT + ARPI is the standard [11][12].
Q04
What is metastatic castration-resistant prostate cancer (mCRPC)?
mCRPC is defined as radiographically evident metastatic prostate cancer that has progressed (PSA rise, radiographic progression, or symptomatic deterioration) despite castrate testosterone levels (typically below 50 ng/dL). It marks a clinical transition because the treatment landscape changes — options include docetaxel and cabazitaxel chemotherapy, abiraterone and enzalutamide if not used in mHSPC, Ra-223 for symptomatic bone-metastatic disease, Lu-177 PSMA-617 for PSMA-positive disease, and PARP inhibitors for HRR-mutated disease. The optimal sequence depends on prior treatment, biomarker status, and patient factors [13][14].
Q05
When is Lu-177 PSMA-617 (Pluvicto) used?
Lu-177 PSMA-617 (Pluvicto) is FDA-approved (2022) and EMA-approved (2023) for PSMA-positive mCRPC. Original VISION trial setting: post-taxane and post-androgen-pathway-inhibitor (ARPI) mCRPC, with PSMA expression confirmed on Ga-68 PSMA PET-CT. 2025 FDA label expansion: pre-chemotherapy setting in PSMA-positive mCRPC after ARPI progression, based on the PSMAfore trial. Standard protocol: six cycles of 7.4 GBq at 6-8 week intervals. Eligibility requires PSMA expression on imaging, adequate organ reserve, and multidisciplinary review. For full coverage see our Lu-177 PSMA outcomes article [4][15].
Q06
When is Ra-223 used?
Ra-223 dichloride (Xofigo) is FDA and EMA approved (2013) for symptomatic bone-metastatic castration-resistant prostate cancer. ALSYMPCA randomised 921 patients to Ra-223 vs placebo plus best supportive care: median overall survival 14.9 vs 11.3 months (HR 0.70), time-to-first-symptomatic-skeletal-event 15.6 vs 9.8 months. Standard regimen: six monthly intravenous infusions. Eligibility requires symptomatic bone-dominant disease, absence of visceral metastases (or minimal), and adequate marrow reserve. Sequencing with Lu-177 PSMA-617 is individualised; both target bone-dominant disease [16][17].
Q07
What is biochemical recurrence after prostatectomy or radiation?
Biochemical recurrence (BCR) is a rising PSA after definitive treatment without yet-detectable disease on conventional imaging. After radical prostatectomy, BCR is typically defined as PSA above 0.2 ng/mL on two consecutive measurements. After radiation, the Phoenix criteria (PSA nadir + 2 ng/mL) are standard. The modern management pathway uses Ga-68 PSMA PET-CT to localise recurrence — local salvage (radiotherapy after prostatectomy; salvage prostatectomy or local ablation after radiation) for local recurrence; ADT-based systemic therapy for nodal or distant disease [10].
Q08
Are PARP inhibitors used for prostate cancer?
Yes — PARP inhibitors are approved for selected mCRPC patients with homologous-recombination-repair (HRR) pathway mutations. Olaparib (PROfound), rucaparib (TRITON3), talazoparib + enzalutamide (TALAPRO-2), and niraparib + abiraterone (MAGNITUDE) are approved in defined populations. BRCA1/2 mutations confer the largest benefit; ATM, CHEK2, PALB2, and other HRR genes have varied responses. Germline and somatic testing is recommended for all metastatic prostate cancer patients (NCCN, AUA). Genetic counselling is part of the testing pathway because germline findings have family-screening implications [14][24].
Q09
What is the prognosis for metastatic prostate cancer?
5-year prostate-cancer-specific survival for metastatic disease at diagnosis is approximately 30% per SEER 2020-2024 data. However, this figure substantially improved over the past decade with modern systemic therapy: ADT + ARPI, triplet therapy (ARASENS, PEACE-1), Lu-177 PSMA-617, PARP inhibitors. Individual prognosis depends on disease volume and pattern (visceral vs nodal vs bone-dominant), biomarker status, response to first-line therapy, and patient factors. Modern multimodal therapy has substantially extended median overall survival across the metastatic-disease cohort, though metastatic disease remains non-curative with current treatments [11][14].
Q10
Should I get genetic testing if I have prostate cancer?
Yes — germline and somatic genetic testing is now recommended for all men with metastatic prostate cancer per NCCN and AUA guidelines, and is increasingly recommended for selected localised high-risk disease. The principal targets are homologous-recombination-repair genes (BRCA1, BRCA2, ATM, CHEK2, PALB2, HOXB13). Findings can guide therapy (PARP inhibitor eligibility), inform prognosis, and trigger family screening if a germline pathogenic variant is identified. Testing is typically combined with genetic counselling, which is part of the comprehensive evaluation [24].
Q11
Is prostate cancer treatment available in India at international standards?
Yes — major Indian oncology centres including FMRI Gurugram deliver prostate cancer treatment in alignment with international guidelines (AUA, EAU, NCCN, ESMO). The full treatment portfolio is available: robotic prostatectomy, modern external-beam radiation (IMRT/VMAT/SBRT), brachytherapy, the full systemic-therapy portfolio (abiraterone, enzalutamide, apalutamide, darolutamide, docetaxel, cabazitaxel), Ra-223, Lu-177 PSMA-617, and PARP inhibitors with biomarker-guided eligibility. Imaging is delivered on modern digital PET-CT scanners including Ga-68 PSMA PET-CT. The regulatory framework operates under AERB, DCGI, BRIT, and NABH oversight [20].
Q12
How do I arrange a prostate cancer treatment review at FMRI?
At FMRI Gurugram, prostate cancer treatment review follows shared-decision-making frameworks aligned with AUA, EAU, NCCN, and ESMO guidelines. Multidisciplinary tumour board review covers risk stratification (NCCN groups), Ga-68 PSMA PET-CT staging where indicated, and eligibility for Lu-177 PSMA-617, Ra-223, or PARP inhibitor therapy where clinically appropriate. WhatsApp +91 8800 988936 to begin a confidential review.
Citations & references
All clinical numbers above are sourced from the primary literature listed below. Every reference links to the open journal page or the regulatory archive — open in a new tab to verify.
[1] NCCN Clinical Practice Guidelines in Oncology: Prostate Cancer. National Comprehensive Cancer Network.
View source ↗[2] Eastham JA, Auffenberg GB, Barocas DA, et al. Clinically Localized Prostate Cancer: AUA / ASTRO Guideline (2022).
View source ↗[3] Mottet N, van den Bergh RCN, Briers E, et al. EAU-EANM-ESTRO-ESUR-SIOG Guidelines on Prostate Cancer. European Association of Urology, 2024.
View source ↗[4] U.S. Food and Drug Administration. FDA approves Pluvicto for metastatic castration-resistant prostate cancer. March 23, 2022; label expanded March 2025.
View source ↗[5] Epstein JI, Egevad L, Amin MB, et al. The 2014 International Society of Urological Pathology (ISUP) Consensus Conference on Gleason Grading.
Am J Surg Pathol. 2016;40(2):244-252.
View source ↗[6] D'Amico AV, Whittington R, Malkowicz SB, et al. Biochemical outcome after radical prostatectomy, external beam radiation therapy, or interstitial radiation therapy for clinically localized prostate cancer.
JAMA. 1998;280(11):969-974.
View source ↗[7] Klotz L, Vesprini D, Sethukavalan P, et al. Long-term follow-up of a large active surveillance cohort of patients with prostate cancer.
J Clin Oncol. 2015;33(3):272-277.
View source ↗[8] Sanda MG, Cadeddu JA, Kirkby E, et al. Clinically Localized Prostate Cancer: AUA / ASTRO / SUO Guideline. Part II: Recommended Approaches and Details of Specific Care Options.
J Urol. 2018;199(4):990-997.
View source ↗[9] Hamdy FC, Donovan JL, Lane JA, et al. Fifteen-Year Outcomes after Monitoring, Surgery, or Radiotherapy for Prostate Cancer (ProtecT).
N Engl J Med. 2023;388(17):1547-1558.
View source ↗[10] Lowrance W, Dreicer R, Jarrard DF, et al. Updates to Advanced Prostate Cancer: AUA / SUO Guideline (2023).
View source ↗[11] Sweeney CJ, Chen YH, Carducci M, et al. Chemohormonal Therapy in Metastatic Hormone-Sensitive Prostate Cancer (CHAARTED).
N Engl J Med. 2015;373(8):737-746.
View source ↗[12] Smith MR, Hussain M, Saad F, et al. Darolutamide and Survival in Metastatic, Hormone-Sensitive Prostate Cancer (ARASENS).
N Engl J Med. 2022;386(12):1132-1142.
View source ↗[13] Scher HI, Halabi S, Tannock I, et al. Design and end points of clinical trials for patients with progressive prostate cancer and castrate levels of testosterone: PCWG3.
J Clin Oncol. 2016;34(12):1402-1418.
View source ↗[14] Cornford P, van den Bergh RCN, Briers E, et al. EAU-EANM-ESTRO-ESUR-SIOG Guidelines on Prostate Cancer. Part II — 2024 Update: Treatment of Relapsing and Metastatic Prostate Cancer.
Eur Urol. 2024.
View source ↗[15] Sartor O, de Bono J, Chi KN, et al. Lutetium-177-PSMA-617 for Metastatic Castration-Resistant Prostate Cancer (VISION).
N Engl J Med. 2021;385(12):1091-1103.
View source ↗[16] Parker C, Nilsson S, Heinrich D, et al. Alpha emitter radium-223 and survival in metastatic prostate cancer (ALSYMPCA).
N Engl J Med. 2013;369(3):213-223.
View source ↗[17] Hofman MS, Emmett L, Sandhu S, et al. [
177Lu]Lu-PSMA-617 versus cabazitaxel in patients with metastatic castration-resistant prostate cancer (TheraP).
Lancet. 2021;397(10276):797-804.
View source ↗[18] Temel JS, Greer JA, Muzikansky A, et al. Early palliative care for patients with metastatic non-small-cell lung cancer.
N Engl J Med. 2010;363(8):733-742.
View source ↗[19] Memorial Sloan Kettering Cancer Center prostate cancer nomograms.
View source ↗[20] ESMO Clinical Practice Guidelines: Prostate Cancer. European Society for Medical Oncology.
View source ↗[21] James ND, de Bono JS, Spears MR, et al. Abiraterone for Prostate Cancer Not Previously Treated with Hormone Therapy (STAMPEDE).
N Engl J Med. 2017;377(4):338-351.
View source ↗[22] Fizazi K, Tran N, Fein L, et al. Abiraterone plus Prednisone in Metastatic, Castration-Sensitive Prostate Cancer (LATITUDE).
N Engl J Med. 2017;377(4):352-360.
View source ↗[23] Davis ID, Martin AJ, Stockler MR, et al. Enzalutamide with Standard First-Line Therapy in Metastatic Prostate Cancer (ENZAMET).
N Engl J Med. 2019;381(2):121-131.
View source ↗[24] 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(5):443-453.
View source ↗[25] de Bono J, Mateo J, Fizazi K, et al. Olaparib for Metastatic Castration-Resistant Prostate Cancer (PROfound).
N Engl J Med. 2020;382(22):2091-2102.
View source ↗[26] 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).
Lancet. 2020;395(10231):1208-1216.
View source ↗[27] Beer TM, Armstrong AJ, Rathkopf DE, et al. Enzalutamide in Metastatic Prostate Cancer before Chemotherapy (PREVAIL).
N Engl J Med. 2014;371(5):424-433.
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About the Author
Dr. Ishita B. Sen
MBBS · MD (Nuclear Medicine) · DNB · Post-doctoral Fellowship, Memorial Sloan Kettering Cancer Center, New York
Director and Chief of Nuclear Medicine at Fortis Memorial Research Institute. Co-founder of Theranostic Physicians Private Limited (TPPL). Two decades of clinical practice in PSMA imaging and PSMA-directed radioligand therapy, with one of the largest Indian institutional experiences in Lu-PSMA.