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When should you scan to assess Lu-PSMA response?

A sourced clinical guide to imaging response assessment after Lu-177 PSMA-617 therapy — when re-staging PET is done, how PCWG3 and RECIST 1.1 frame the question, what PROMISE and aPROMISE add for PSMA PET interpretation, what discordant PSA / imaging patterns mean, and how individual response is measured against trial outcomes.

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

Patients and referring clinicians often ask the same question after starting Lu-177 PSMA-617 therapy: when, exactly, should we re-scan to know whether it's working? The honest answer requires distinguishing several different imaging modalities (Ga-68 PSMA PET, conventional CT, bone scan, sometimes FDG PET), several different timing windows (mid-treatment, end-of-treatment, post-treatment surveillance), and several different response frameworks (PCWG3, RECIST 1.1, PROMISE, aPROMISE). This article walks through each, with primary-literature sourcing, and sets out the practical re-staging timeline used at experienced centres.

What ‘assess success’ actually means

AI Overview · short answer

Response assessment after Lu-177 PSMA-617 therapy uses a combination of PSA trajectory (measured pre-each-cycle), conventional imaging (CT and bone scan per PCWG3 framework, typically at mid-treatment and end-of-treatment), and Ga-68 PSMA PET-CT re-staging (typically at end-of-treatment or at clinical or biochemical suggestion of progression)[1]. The Prostate Cancer Working Group 3 (PCWG3) framework is the standard for clinical-trial response assessment in advanced prostate cancer; PROMISE and aPROMISE are PSMA PET-specific frameworks for response and progression classification[2][3]. The VISION trial used PCWG3 imaging response criteria and reported median radiographic progression-free survival of 8.7 months with Lu-177 PSMA-617 versus 3.4 months with standard of care[4].

“Success” in Lu-177 PSMA-617 therapy is not a single endpoint. The clinical question breaks into several different measurable elements[2]:

  • Biochemical response — change in PSA from baseline. A PSA50 response (≥50% decline from baseline confirmed at ≥4 weeks) is the most-used biochemical endpoint.
  • Radiographic response — change on conventional CT and bone scan, classified per PCWG3 (soft-tissue lesions per RECIST 1.1; bone progression per PCWG3 bone-scan criteria).
  • PSMA PET response — change in PSMA SUVmean / SUVmax and lesion count on Ga-68 PSMA PET-CT, classified using PROMISE or aPROMISE.
  • Symptom and quality-of-life response — change in pain, performance status, and patient-reported outcomes.

Each measures a different aspect of the response, and they do not always move together. The right re-staging strategy uses each at the appropriate time.

PCWG3 — the standard response framework

The Prostate Cancer Working Group 3 framework (Scher et al., JCO 2016) is the consensus standard for clinical-trial response assessment in advanced prostate cancer[2]. It defines:

  • Soft-tissue lesion assessment per RECIST 1.1 — measurable lesions on CT or MRI sized at baseline, with response (complete response / partial response / stable disease / progression) classified by change at follow-up.
  • Bone lesion assessment per PCWG3 bone-scan criteria — progression on bone scan requires ≥2 new lesions at first re-staging that are subsequently confirmed (the “2+2” rule), distinguishing true progression from flare phenomena.
  • PSA response criteria — PSA50 (≥50% decline from baseline) and PSA progression criteria (≥25% increase and ≥2 ng/mL above nadir, confirmed at ≥3 weeks).
  • Recommended response-assessment timeline — baseline, mid-treatment (typically 8-12 weeks), and end-of-treatment, with continued surveillance.

PCWG3 was the framework used in the VISION trial and is the standard against which clinical Lu-177 PSMA-617 responses are interpreted[4].

How VISION did response assessment

VISION (Sartor et al., NEJM 2021) randomised 831 patients with mCRPC to Lu-177 PSMA-617 plus standard of care versus standard of care alone, and used a structured imaging timeline that is now widely adopted clinically[4]:

  • Baseline — Ga-68 PSMA-11 PET-CT for eligibility, baseline CT chest/abdomen/pelvis and bone scan for measurable disease and PCWG3-classifiable burden, baseline PSA.
  • Every 8 weeks — CT and bone scan during therapy (mid-treatment re-staging).
  • End-of-treatment — at completion of up to six cycles, full re-staging.
  • Surveillance — every 12 weeks until protocol progression.

VISION reported median radiographic progression-free survival (rPFS) of 8.7 months with Lu-177 PSMA-617 vs 3.4 months with standard of care (HR 0.40, p<0.001) and median OS of 15.3 vs 11.3 months (HR 0.62, p<0.001)[4]. The trial confirmed that PCWG3-framework imaging response assessment is the appropriate clinical tool for evaluating Lu-PSMA therapy.

When the Ga-68 PSMA PET-CT is repeated

Ga-68 PSMA-11 PET-CT is the eligibility-defining scan before Lu-PSMA therapy. Whether and when to repeat it is a separate question[5]:

  • Mid-treatment Ga-68 PSMA PET — typically performed at some centres around cycle 3 or cycle 4. It can identify discordant patterns (e.g., new PSMA-negative / FDG-positive lesions suggesting neuroendocrine transformation) and inform treatment-modification decisions. Routine mid-treatment PSMA PET is not mandatory under the VISION protocol but is used at experienced centres for response biomarker tracking.
  • End-of-treatment Ga-68 PSMA PET — performed at completion of the planned therapy course to characterise residual PSMA-positive disease and document response.
  • At biochemical or clinical suggestion of progression — Ga-68 PSMA PET-CT is the preferred restaging study to characterise the pattern of progression (PSMA-positive vs PSMA-negative, sites of new disease) and to guide subsequent therapy selection.
  • For consideration of re-treatment — if additional Lu-PSMA cycles are being considered after the initial course, a current Ga-68 PSMA PET is essential to confirm continued PSMA expression.

PROMISE and aPROMISE — PSMA PET-specific frameworks

RECIST 1.1 and PCWG3 predate the routine use of PSMA PET in prostate cancer and do not directly handle PSMA PET response. Two PSMA-specific frameworks have emerged[6][7]:

  • PROMISE (Prostate Cancer Molecular Imaging Standardized Evaluation; Eiber et al.) — a structured framework for reporting PSMA PET findings, with miTNM staging language and graded PSMA expression levels relative to liver, parotid, and blood pool.
  • aPROMISE (automated PROMISE; Buteau, Gafita, and colleagues) — software-supported quantitative version that provides automated lesion segmentation, PSMA-VOL (whole-body PSMA volume), and PSMA-MEAN (mean SUV). The TheraP trial used aPROMISE-derived biomarkers and showed that baseline PSMA-MEAN strongly predicted Lu-177 PSMA-617 benefit[8].

For routine clinical use today, PCWG3 + RECIST 1.1 + PROMISE-style PSMA PET reporting together cover the principal response-assessment elements. Automated aPROMISE quantitation is used in selected centres and research protocols.

How PSA trajectory fits in

PSA is the most accessible and least expensive response signal — but it should not be used alone[9]:

  • PSA flare — a transient PSA rise in the first 2-4 weeks after the first Lu-PSMA cycle has been documented and should not be interpreted as progression. PCWG3 specifically requires PSA progression to be confirmed at ≥3 weeks above nadir.
  • PSA50 response — VISION reported PSA50 response in 46% of Lu-177 PSMA-617 patients vs 7.1% with standard of care; TheraP reported 66% vs 37% with cabazitaxel comparison[4][10].
  • PSA-only progression — should not, by itself, trigger treatment change. Imaging progression on conventional CT and bone scan, or PSMA PET, is required to define disease progression under PCWG3.
  • PSA-imaging discordance — when PSA suggests one direction and imaging another, the structured framework is to weigh imaging more heavily for treatment decisions while continuing to track PSA for trajectory.

Discordant patterns and FDG PET

One specific re-staging question deserves its own attention: when the PSMA PET pattern looks different from the PSA pattern or from conventional imaging, what does it mean?[11]

  • Falling PSA, stable / improving PSMA PET, stable conventional imaging — concordant response. Continue treatment course.
  • Rising PSA, increasing PSMA PET, increasing conventional imaging — concordant progression. Re-stage and reconsider treatment.
  • Rising PSA with new PSMA-negative lesions on conventional imaging — concerning for neuroendocrine differentiation or PSMA-negative phenotype. Adding an FDG PET often confirms FDG-avid PSMA-negative disease, redirecting treatment toward platinum-based chemotherapy.
  • Stable / falling PSA with new PSMA-positive lesions — uncommon; requires individualised review with the multidisciplinary team.

The PSMA-negative / FDG-positive pattern, in particular, is the strongest signal of neuroendocrine transformation and is one reason combined PSMA + FDG imaging is increasingly used at experienced centres for late-line prostate cancer[11].

The practical re-staging timeline

For a typical patient on a six-cycle Lu-177 PSMA-617 protocol, the imaging timeline used at experienced centres looks like this[12]:

TimepointImagingDecision-making
Baseline (pre-cycle 1)Ga-68 PSMA-11 PET-CT (eligibility); CT chest/abdomen/pelvis; bone scan; baseline PSAConfirm eligibility per VISION criteria; document baseline burden
Pre each cyclePSA, kidney function, marrow countsConfirm cycle eligibility; flag emerging toxicity
After cycle 1 (24-48h)Post-administration SPECT/CTConfirm intended Lu-PSMA distribution
Mid-treatment (after cycle 2-3, ~12 weeks)CT chest/abdomen/pelvis; bone scan; ± Ga-68 PSMA PET at selected centresPCWG3 response classification; identify early discordance
End-of-treatmentCT chest/abdomen/pelvis; bone scan; Ga-68 PSMA PET-CTDocument end-of-course response; plan surveillance or next-line therapy
Surveillance (every 12 weeks)PSA, periodic CT and bone scan, Ga-68 PSMA PET at clinical or biochemical changeTrack for progression; plan next intervention

The exact intervals can be modified by clinical circumstance — for example, more frequent imaging in patients with high-burden disease or rapid biochemical changes; less frequent imaging in stable patients with established response[13].

How individual response relates to trial endpoints

An individual patient's response cannot be predicted simply from VISION median figures. Several factors shift individual probability of response in published subgroup analyses[14]:

  • Baseline PSMA SUVmean on Ga-68 PSMA PET — higher PSMA expression is associated with greater Lu-PSMA benefit. The TheraP trial documented this as a prospectively measured biomarker using aPROMISE quantitation[8].
  • Disease burden and pattern — extensive marrow disease, visceral involvement, or large-volume disease often portends a more difficult course.
  • Prior treatment history — patients earlier in the treatment sequence (e.g., post-ARPI but pre-chemotherapy, per PSMAfore) generally show better PFS than heavily pre-treated patients.
  • Discordant FDG-positive / PSMA-negative disease — even small components of FDG-avid PSMA-negative disease can drive overall progression and limit Lu-PSMA benefit[11].

This is why response-assessment timing is not a fixed rule for every patient. The multidisciplinary team integrates these factors and tailors imaging frequency and re-staging-trigger thresholds accordingly.

What the evidence does and does not say about timing

Several statements about response-assessment timing are well-supported; others remain open[15]:

StatementEvidence support
PCWG3 framework with mid-treatment imaging is the standard for Lu-PSMA response assessmentStrong — used in VISION and TheraP; consensus framework
End-of-treatment Ga-68 PSMA PET should be performed to characterise residual diseaseStrong — standard practice; informs subsequent therapy
Routine mid-treatment Ga-68 PSMA PET (every 2 cycles) improves outcomesUncertain — not mandated by VISION; used at selected centres for early identification of discordance
PSA alone is sufficient for treatment-modification decisionsNo — PCWG3 requires confirmed imaging progression for treatment change
Adding FDG PET to PSMA PET at progression is informativeStrong — particularly to identify neuroendocrine transformation
The optimal interval between cycles for response-driven dosing modification is establishedOpen research question — dose-response adaptation is an active area of investigation

The bottom line

  • Response assessment after Lu-177 PSMA-617 therapy combines PSA trajectory, PCWG3-framework conventional imaging (CT + bone scan), and Ga-68 PSMA PET-CT — not any one in isolation[2].
  • VISION used PCWG3 framework with imaging at baseline, every 8 weeks during therapy, end-of-treatment, and every 12 weeks in surveillance — the de facto standard for clinical practice[4].
  • Ga-68 PSMA PET-CT is repeated at end-of-treatment routinely, at biochemical or clinical suggestion of progression, and before any consideration of re-treatment[5].
  • PROMISE and aPROMISE provide PSMA PET-specific reporting frameworks; aPROMISE-derived PSMA-VOL and PSMA-MEAN have been validated as response biomarkers in TheraP[8].
  • PSA-imaging discordance is real and clinically relevant; the PSMA-negative / FDG-positive pattern at progression signals neuroendocrine transformation and redirects treatment toward platinum-based regimens[11].
  • PSA alone is not sufficient for treatment-modification decisions under PCWG3; imaging progression must be confirmed[2].
  • Individual response varies with baseline PSMA SUVmean, disease burden and pattern, prior treatment history, and presence of FDG-positive PSMA-negative disease — imaging timing should be tailored to these factors by the multidisciplinary team[14].
Important

This article is general information about response assessment timing after Lu-177 PSMA-617 therapy. Individual imaging schedules and re-staging decisions require formal clinical assessment by the treating nuclear medicine and oncology team, integrating baseline burden, prior treatment history, and clinical trajectory.

"Response assessment after Lu-PSMA therapy is not a single scan at a single time. It is a structured protocol — PSA before every cycle, PCWG3 imaging at mid-treatment and end-of-treatment, Ga-68 PSMA PET to characterise residual disease, and FDG PET when the pattern looks discordant. The right timing is the one defined by the multidisciplinary team using the trial framework — not by a calendar rule."

Dr. Ishita B. Sen, MD · Director & Chief, Nuclear Medicine, FMRI

Lu-PSMA response review · structured imaging timeline at FMRI

At FMRI Gurugram, Lu-177 PSMA-617 response review follows PCWG3 + RECIST 1.1 + PROMISE-style reporting, with structured imaging at baseline, mid-treatment, end-of-treatment, and surveillance. Ga-68 PSMA PET re-staging is integrated with PSA trajectory and conventional imaging, with FDG PET added when the pattern suggests neuroendocrine transformation.

Request response review · WhatsApp +91 8800 988936
For patients & referring clinicians

Frequently asked questions

Q01 When should the first scan be done after starting Lu-177 PSMA-617 therapy?

Under the VISION trial protocol, conventional imaging (CT chest/abdomen/pelvis + bone scan) is repeated every 8 weeks during therapy. PSA is checked before each cycle. A post-administration Lu-177 SPECT/CT is performed within 24-48 hours of cycle 1 to confirm intended distribution. Whether Ga-68 PSMA PET is repeated mid-treatment varies by centre — it is not mandated by VISION but is used at experienced centres for early identification of discordance [4][12].

Q02 What is a PSMA PET scan?

A PSMA PET scan is a positron emission tomography scan using a radioactive tracer (most commonly Ga-68 PSMA-11 or F-18 PSMA-1007) that binds prostate-specific membrane antigen on prostate cancer cells. It shows the body-wide distribution and intensity of PSMA-expressing disease. For Lu-PSMA therapy, the Ga-68 PSMA-11 PET-CT is used to confirm eligibility (per VISION criteria), characterise disease distribution, and assess response on re-staging [5].

Q03 How is response classified — PCWG3 or RECIST?

For advanced prostate cancer, the standard framework is PCWG3 (Prostate Cancer Working Group 3; Scher et al., JCO 2016). PCWG3 uses RECIST 1.1 for soft-tissue lesions and PCWG3-specific criteria for bone-scan progression (the '2+2' rule for bone progression). PCWG3 was used in VISION and is the reference framework for Lu-PSMA response interpretation. PSMA PET-specific reporting uses PROMISE/aPROMISE [2][6][7].

Q04 Can PSA alone tell us if the therapy is working?

PSA is the most accessible and least expensive response signal but should not be used alone for treatment-modification decisions. PCWG3 requires confirmed imaging progression (not PSA alone) to define disease progression. A PSA flare in the first 2-4 weeks after the first Lu-PSMA cycle is recognised and should not be misread as progression. PSA-imaging discordance is common; structured PCWG3 framework weighs imaging more heavily for treatment decisions [2][9].

Q05 When is the Ga-68 PSMA PET scan repeated?

Ga-68 PSMA PET-CT is routinely repeated at end-of-treatment to characterise residual disease and inform subsequent therapy. It is also repeated at biochemical or clinical suggestion of progression to characterise the pattern (PSMA-positive vs PSMA-negative). At some centres, a mid-treatment Ga-68 PSMA PET (around cycle 3-4) is added for early identification of discordance, though this is not mandated by VISION [5][12].

Q06 What is the PSA flare phenomenon after the first Lu-PSMA cycle?

A transient PSA rise in the first 2-4 weeks after the first Lu-PSMA cycle is recognised and should not be interpreted as treatment failure. It may reflect tumour cell turnover and release of PSA. PCWG3 specifically requires PSA progression to be confirmed at ≥3 weeks above nadir to differentiate flare from true progression. Persisting or progressive PSA rise after the flare window does warrant assessment [2][9].

Q07 What if my PSMA PET shows mixed response?

Heterogeneous response — some lesions responding, others stable or progressing — is recognised on Ga-68 PSMA PET. The clinical interpretation depends on the overall pattern: predominantly responding disease with isolated progressing lesions may warrant continued Lu-PSMA with focal management (SBRT, surgery) of the dominant resistant lesion; predominantly progressing disease typically prompts treatment change. New PSMA-negative / FDG-positive lesions specifically suggest neuroendocrine transformation [11].

Q08 When should an FDG PET be added?

FDG PET is added when the clinical picture suggests possible neuroendocrine transformation or de-differentiation — typically when there is rising PSA with new disease that doesn't show PSMA avidity, when conventional imaging shows progression discordant with PSMA findings, or when the baseline Ga-68 PSMA PET showed low or heterogeneous uptake. The PSMA-negative / FDG-positive pattern is the strongest signal of neuroendocrine transformation and redirects treatment toward platinum-based chemotherapy [11].

Q09 What are PROMISE and aPROMISE?

PROMISE (Prostate Cancer Molecular Imaging Standardized Evaluation; Eiber et al.) is a structured framework for reporting PSMA PET findings using miTNM staging and graded PSMA expression levels. aPROMISE is the software-supported quantitative version that provides automated lesion segmentation, PSMA-VOL (whole-body PSMA volume), and PSMA-MEAN. TheraP trial used aPROMISE-derived biomarkers and showed baseline PSMA-MEAN predicted Lu-PSMA benefit [6][7][8].

Q10 How does my baseline PSMA expression predict response?

Higher baseline PSMA SUVmean on Ga-68 PSMA PET is associated with greater Lu-PSMA benefit in published prospective data. The TheraP trial showed that baseline PSMA-MEAN (a quantitative aPROMISE metric) predicted PSA response and PFS benefit from Lu-PSMA-617 vs cabazitaxel. Conversely, low baseline PSMA expression, particularly in the presence of FDG-positive disease, is associated with poorer response and shorter PFS [8][14].

Q11 What if my scans show progression — does that mean Lu-PSMA failed?

Imaging progression on PCWG3 framework defines protocol progression and typically prompts treatment change. It does not mean the cycles administered to that point were without benefit — they may have provided meaningful disease control during the time on therapy. Re-staging Ga-68 PSMA PET (± FDG PET) at progression characterises the pattern and guides next-line therapy: continued PSMA-positive disease may be a candidate for Ac-225 PSMA salvage in experienced centres; PSMA-negative neuroendocrine disease typically prompts platinum-based regimens [11][13].

Q12 How do I get a structured Lu-PSMA response review at FMRI?

At FMRI Gurugram, Lu-177 PSMA-617 response review follows PCWG3 + RECIST 1.1 + PROMISE-style reporting, with structured imaging at baseline, mid-treatment, end-of-treatment, and surveillance. Ga-68 PSMA PET re-staging is integrated with PSA trajectory and conventional imaging, with FDG PET added when the pattern suggests neuroendocrine transformation. 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] Fanti S, Goffin K, Hadaschik BA, et al. Consensus statements on PSMA PET/CT response assessment criteria in prostate cancer. Eur J Nucl Med Mol Imaging. 2021;48(2):469-476. View source ↗
[2] 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 recommendations. J Clin Oncol. 2016;34(12):1402-1418. View source ↗
[3] Eisenhauer EA, Therasse P, Bogaerts J, et al. New response evaluation criteria in solid tumours: revised RECIST guideline (version 1.1). Eur J Cancer. 2009;45(2):228-247. View source ↗
[4] 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 ↗
[5] Kuo PH, Benson T, Messmann R, et al. Why we did what we did: PSMA PET/CT selection criteria for the VISION trial. J Nucl Med. 2022;63(6):816-818. View source ↗
[6] Eiber M, Herrmann K, Calais J, et al. Prostate Cancer Molecular Imaging Standardized Evaluation (PROMISE): Proposed miTNM Classification for the Interpretation of PSMA-Ligand PET/CT. J Nucl Med. 2018;59(3):469-478. View source ↗
[7] Seifert R, Emmett L, Rowe SP, et al. Second Version of the Prostate Cancer Molecular Imaging Standardized Evaluation Framework Including Response Evaluation for Clinical Trials (PROMISE V2). Eur Urol. 2023;83(5):405-412. View source ↗
[8] Buteau JP, Martin AJ, Emmett L, et al. PSMA and FDG-PET as predictive and prognostic biomarkers in patients given [177Lu]Lu-PSMA-617 versus cabazitaxel for metastatic castration-resistant prostate cancer (TheraP). Lancet Oncol. 2022;23(11):1389-1397. View source ↗
[9] Gillessen S, Bossi A, Davis ID, et al. Management of patients with advanced prostate cancer — metastatic and/or castration-resistant prostate cancer: Report of the Advanced Prostate Cancer Consensus Conference. Eur J Cancer. 2023;185:178-215. View source ↗
[10] 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 ↗
[11] Thang SP, Violet J, Sandhu S, et al. Poor Outcomes for Patients with Metastatic Castration-resistant Prostate Cancer with Low PSMA Expression Despite High FDG Uptake on Dual-tracer PET. Eur J Nucl Med Mol Imaging. 2019;46(8):1632-1639. View source ↗
[12] Iravani A, Violet J, Azad A, et al. Lutetium-177 PSMA therapy: practical aspects, dosimetry, and outcomes. Theranostics. 2020;10(20):8854-8866. View source ↗
[13] European Association of Nuclear Medicine. EANM procedure guidelines for radionuclide therapy with 177Lu-labelled PSMA-ligands. Eur J Nucl Med Mol Imaging. 2019;46(12):2536-2544. View source ↗
[14] Gafita A, Calais J, Grogan TR, et al. Nomograms to predict outcomes after 177Lu-PSMA therapy in men with metastatic castration-resistant prostate cancer. Lancet Oncol. 2021;22(8):1115-1125. View source ↗
[15] Pouliot F, Saperia C, Le S, et al. Practical Imaging Recommendations for PSMA-Targeted Therapy: A Multidisciplinary Consensus from the Movember Foundation. Eur Urol Open Sci. 2023;58:39-50. View source ↗
[16] Calais J, Czernin J, Cao M, et al. 68Ga-PSMA-11 PET/CT mapping of prostate cancer biochemical recurrence after radical prostatectomy. J Nucl Med. 2018;59(4):576-585. View source ↗
[17] 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 ↗
[18] Hennrich U, Eder M. 177Lu-PSMA-617 (Pluvicto): The First FDA-Approved Radiotherapeutical for Treatment of Prostate Cancer. Pharmaceuticals (Basel). 2022;15(10):1292. View source ↗
[19] Yadav MP, Ballal S, Tripathi M, et al. 177Lu-DKFZ-PSMA-617 therapy in metastatic castration-resistant prostate cancer: safety, efficacy, and quality of life. Eur J Nucl Med Mol Imaging. 2017;44(1):81-91. View source ↗
[20] Hofman MS, Violet J, Hicks RJ, et al. [177Lu]-PSMA-617 radionuclide treatment in patients with metastatic castration-resistant prostate cancer (LuPSMA). Lancet Oncol. 2018;19(6):825-833. View source ↗
[21] Heck MM, Tauber R, Schwaiger S, et al. Treatment outcome and toxicity for 177Lu-PSMA-I&T in mCRPC. Eur Urol. 2019;75(6):920-926. View source ↗
[22] Rasul S, Hartenbach M, Wadsak W, et al. Clinical outcome with [177Lu]Lu-PSMA-I&T. Eur J Nucl Med Mol Imaging. 2020;47(13):3107-3116. View source ↗
[23] Sartor O. The PSMAfore trial: Lu-177 PSMA-617 in taxane-naive mCRPC. N Engl J Med. 2024;391(16):1500-1510. View source ↗
[24] Maurer T, Eiber M, Schwaiger M, Gschwend JE. Current use of PSMA-PET in prostate cancer management. Nat Rev Urol. 2016;13(4):226-235. View source ↗
[25] Hofman MS, Hicks RJ, Maurer T, Eiber M. Prostate-specific Membrane Antigen PET: Clinical Utility in Prostate Cancer. Radiographics. 2018;38(1):200-217. View source ↗
[26] NCCN Clinical Practice Guidelines in Oncology: Prostate Cancer. National Comprehensive Cancer Network. View source ↗
[27] European Association of Urology. EAU-EANM-ESTRO-ESUR-SIOG Guidelines on Prostate Cancer. View source ↗
[28] Emmett L, Yin C, Crumbaker M, et al. Rapid Modulation of PSMA Expression by Androgen Deprivation: Serial 68Ga-PSMA-11 PET. J Nucl Med. 2019;60(7):950-954. View source ↗
[29] Hofman MS, Emmett L, Sandhu S, et al. Overall survival with Lu-177 PSMA-617 versus cabazitaxel in mCRPC (TheraP) — final results. Lancet Oncol. 2024;25(1):99-107. View source ↗
[30] Atomic Energy Regulatory Board (Government of India). Safety Code for Nuclear Medicine Facilities. AERB/RF-MED/SC-2 (Rev. 2). View source ↗
Dr. Ishita B. Sen
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.

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Medical disclaimer All physicians and researchers profiled on this page hold appointments at the Department of Nuclear Medicine & Molecular Imaging, Fortis Memorial Research Institute, Gurugram. Theranostic Physicians Private Limited (TPPL) is the clinical practice entity through which they consult and treat patients. Treatment outcomes vary by individual case; clinical decisions are made on the basis of complete medical records, current imaging, and a multidisciplinary review.