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
PSMA — prostate-specific membrane antigen — is the molecular target of both PSMA PET-CT imaging and PSMA-directed radioligand therapy (Lu-177 PSMA-617, investigational Ac-225 PSMA-617). For every patient being evaluated for these treatments, the eligibility-defining question is whether the cancer expresses PSMA at sufficient intensity and across enough of the disease burden. Most prostate cancers do — but not all. This article describes what PSMA actually is, how its expression is measured, the recognised PSMA-negative phenotypes, and what PSMA negativity means for treatment choices.
What is PSMA
AI Overview · short answer
PSMA (prostate-specific membrane antigen) is a transmembrane glycoprotein — formally glutamate carboxypeptidase II, encoded by the FOLH1 gene — that is expressed at low levels in normal prostate epithelium and at substantially higher levels in most prostate cancers, with expression typically increasing with disease progression and androgen-deprivation pressure[1]. Most prostate adenocarcinomas (typical estimates around 85–95% of cases) show clinically meaningful PSMA expression on Ga-68 PSMA PET-CT imaging[2]. Recognised PSMA-low or PSMA-negative phenotypes include small-cell neuroendocrine prostate cancer and treatment-emergent neuroendocrine differentiation. Patient eligibility for Lu-177 PSMA-617 therapy is determined by formal PSMA PET-CT criteria modelled on the VISION trial[3].
PSMA stands for prostate-specific membrane antigen. The name is partly misleading on both counts — it is not exclusively in the prostate, and it is not strictly an antigen in the immunological sense[1]. Biochemically, PSMA is a Type II transmembrane glycoprotein with enzymatic activity. Its formal enzymatic name is glutamate carboxypeptidase II (GCPII), and it is encoded by the FOLH1 gene on chromosome 11. The protein has a small intracellular tail, a single transmembrane domain, and a large extracellular catalytic domain — and it is this extracellular domain that PSMA-targeting ligands bind to.
PSMA is expressed at low baseline levels in several tissues — including normal prostate epithelium, salivary glands, lacrimal glands, kidney tubules, small bowel, and certain brain regions[4]. What makes it useful as a prostate-cancer target is that expression is substantially upregulated in most prostate cancers, with expression intensity typically increasing as the disease becomes more advanced and more castration-resistant. The differential between prostate cancer and most normal tissues is what allows PSMA PET-CT imaging to find disease and PSMA-targeted therapy to deliver radiation preferentially to tumour cells[5].
How PSMA expression is measured in clinical practice
In practice, two methods are used to assess PSMA expression — though only one is widely applied for routine clinical eligibility decisions[6]:
- Ga-68 PSMA-11 PET-CT (or F-18 PSMA-1007 PET-CT) — the dominant method. A small amount of radioactive PSMA-binding tracer is injected, and PET imaging identifies all sites of PSMA expression in the body. Tumour uptake is quantified as SUVmax. Patient eligibility for Lu-177 PSMA-617 therapy under VISION-derived criteria requires that all disease lesions show SUVmax greater than that of the liver, with no large discordant non-PSMA-avid lesions on conventional imaging.
- Immunohistochemistry (IHC) on biopsy tissue — quantifies PSMA expression at the protein level on a specific tissue specimen. Used in research and selected complex cases, less commonly for routine eligibility decisions.
The Ga-68 PSMA PET-CT-based approach has the advantage of assessing PSMA expression across the entire disease burden — not just a single biopsy site. Heterogeneity of PSMA expression across lesions, which is a real clinical phenomenon, is therefore captured directly by the imaging eligibility assessment[7].
What proportion of prostate cancers express PSMA
The short answer: most do[2]. Across published Ga-68 PSMA PET-CT cohorts, clinically meaningful PSMA expression is reported in approximately 85–95% of typical prostate adenocarcinomas. Expression patterns vary by disease stage:
| Setting | Typical PSMA expression pattern |
|---|
| Primary localised prostate cancer | Variable; depends on grade and biology. Higher Gleason grade typically associates with higher PSMA expression |
| Hormone-sensitive metastatic disease | Most cases show clinically meaningful PSMA expression |
| Castration-resistant disease (mCRPC) | Majority show high PSMA expression; expression often increases under androgen-deprivation pressure |
| Late-line CRPC after multiple lines | Most retain PSMA expression; small but recognised proportion develop low-PSMA or neuroendocrine phenotypes |
The clinically relevant statement is: most prostate cancers — including most castration-resistant cases — express PSMA at intensity sufficient for both imaging and therapy. But "most" is not "all", and identifying the minority of patients with PSMA-low or PSMA-negative disease is one of the central clinical roles of the Ga-68 PSMA PET-CT scan itself[3].
PSMA-low and PSMA-negative phenotypes
Several recognised phenotypes are associated with reduced or absent PSMA expression[8]:
- Small-cell neuroendocrine prostate cancer (SCNC) — an aggressive subtype that may arise de novo (rare) or as a treatment-emergent transformation under sustained androgen-deprivation pressure. Characterised by loss of androgen-receptor signalling, loss of PSA production, and frequently low or absent PSMA expression. Typically more avid on FDG PET than on Ga-68 PSMA PET[9].
- Treatment-emergent neuroendocrine differentiation — partial transformation in tumours that retain adenocarcinoma features but develop neuroendocrine programmes after multiple lines of androgen-axis-targeted therapy. Disease may show mixed FDG-avid and PSMA-avid lesions.
- Poorly differentiated adenocarcinoma with loss of luminal differentiation — some cases show reduced PSMA expression and may have heterogeneous patterns on PSMA PET.
- Very rare congenital low-PSMA phenotypes — described in case reports; not a common clinical issue.
The clinical signal that suggests neuroendocrine or low-PSMA disease often includes a discordant pattern between PSA, disease burden on conventional imaging, and Ga-68 PSMA PET findings — for example, large-volume disease on CT or bone scan with low PSMA avidity, or rapidly progressing disease with relatively flat PSA[10].
VISION-derived PSMA PET eligibility criteria for Lu-177 PSMA therapy
The VISION trial established the regulatory criteria for PSMA PET-CT-based eligibility for Lu-177 PSMA-617 therapy[11]:
- PSMA-positive disease on Ga-68 PSMA-11 PET-CT — at least one PSMA-positive metastatic lesion with SUVmax greater than the SUVmax of the liver parenchyma.
- No PSMA-negative discordant disease — no measurable lesion (e.g., on conventional CT) larger than 2.5 cm in short-axis diameter for a lymph node, larger than 1.0 cm in short-axis for a visceral metastasis, or with a large lytic bone lesion lacking PSMA uptake.
- Disease burden distributed sufficiently for PSMA-directed therapy to address — patients with predominantly PSMA-negative disease alongside small PSMA-positive lesions are not considered appropriate candidates.
These criteria are now standard for clinical eligibility decisions in regulated jurisdictions and are followed at experienced Indian centres including FMRI Gurugram for Lu-177 PSMA therapy planning[12].
What PSMA-negative disease means for treatment selection
A patient identified as PSMA-low or PSMA-negative on Ga-68 PSMA PET-CT is not eligible for Lu-177 PSMA-617 therapy under VISION-derived criteria. The treatment landscape for these patients includes[13]:
- Platinum-based chemotherapy — particularly for small-cell or neuroendocrine phenotypes, which often retain platinum sensitivity.
- Standard mCRPC systemic therapy — taxane chemotherapy (docetaxel, cabazitaxel) where androgen-axis options have been exhausted.
- Combination approaches — combinations of chemotherapy with continued androgen-deprivation or investigational agents in clinical trial settings.
- FDG PET-guided assessment — patients with neuroendocrine differentiation often have FDG-avid disease that can be tracked and used to guide treatment selection alongside Ga-68 PSMA PET findings.
- Clinical-trial enrolment — for novel agents targeting alternative pathways (DLL3 antibody-drug conjugates and others in development).
The clinical message is: a Ga-68 PSMA PET-CT that shows low or absent uptake should not be read as a treatment failure — it is diagnostic information that redirects treatment toward different mechanisms of action that are more likely to work for that specific tumour biology.
PSMA expression heterogeneity within a single patient
Within a single patient with metastatic prostate cancer, PSMA expression is not always uniform across all lesions. Heterogeneous patterns are recognised and clinically relevant[14]:
- Lesion-to-lesion heterogeneity — most lesions may be highly PSMA-avid while one or two are weakly avid or non-avid, reflecting clonal evolution and possibly differential treatment response.
- Discordant PSMA / FDG patterns — using both Ga-68 PSMA PET and FDG PET, distinct lesion patterns may be identified (PSMA-positive/FDG-negative; PSMA-positive/FDG-positive; PSMA-negative/FDG-positive). The PSMA-negative/FDG-positive pattern is the strongest signal of neuroendocrine differentiation or de-differentiation.
- Response heterogeneity — during a course of Lu-177 PSMA therapy, response is sometimes heterogeneous — some lesions respond well while others progress, reflecting underlying expression and biology differences.
This heterogeneity is one reason for incorporating mid-treatment imaging into Lu-177 PSMA protocols at experienced centres — to identify patients whose disease pattern is shifting and where treatment plan should be revised[15].
How PSMA expression changes with disease progression
PSMA expression generally increases as prostate cancer progresses through hormone-sensitive disease into castration-resistant disease, particularly under sustained androgen-deprivation pressure[16]. This is one reason PSMA-targeted therapy is most established and most evidence-supported in the mCRPC setting. The relationship between androgen-receptor signalling and PSMA expression is bidirectional and complex: AR signalling generally suppresses PSMA in normal prostate epithelium, but in cancer the relationship is altered, and inhibition of AR signalling under ADT often increases PSMA expression. This biological feature is what makes mCRPC a particularly favourable setting for PSMA-targeted therapy.
Conversely, in the late-line setting after multiple lines of ARPI therapy, a subset of patients develops AR-independent or neuroendocrine programmes. In these patients, PSMA expression may fall — and the patient who was previously a candidate for PSMA-targeted therapy may not remain a candidate. Re-staging with Ga-68 PSMA PET-CT — and sometimes a second FDG PET — at progression on PSMA-targeted therapy is therefore part of well-conducted care[17].
Implications for PET imaging and staging
The fact that not all prostate cancers express PSMA — and that expression patterns evolve — has implications for PSMA PET-CT use across the disease course[18]:
- At diagnosis and primary staging — Ga-68 PSMA PET-CT has high sensitivity for nodal and distant disease in intermediate-to-high-risk prostate cancer. Most cases will show clinically meaningful uptake.
- At biochemical recurrence after primary treatment — Ga-68 PSMA PET-CT has substantially higher detection rates than conventional imaging, particularly at low PSA levels.
- At mCRPC eligibility assessment — Ga-68 PSMA PET-CT is the gateway investigation for Lu-177 PSMA-617 eligibility under VISION criteria.
- At progression on PSMA-targeted therapy — re-staging with PSMA PET (and possibly FDG PET) is appropriate to identify whether progression is on PSMA-positive disease (where a different PSMA-directed approach may help) or PSMA-negative disease (where the treatment paradigm must change).
The PSMA PET-CT is, in this sense, not just an imaging study — it is a real-time biology readout that informs treatment-selection decisions throughout the prostate cancer journey.
The bottom line
- PSMA (prostate-specific membrane antigen) is a transmembrane glycoprotein — formally glutamate carboxypeptidase II, encoded by FOLH1 — expressed at low levels in normal tissues and upregulated in most prostate cancers[1].
- Most prostate cancers (approximately 85–95% in typical published cohorts) show clinically meaningful PSMA expression, with intensity typically increasing through hormone-sensitive disease into castration-resistant disease[2].
- Recognised PSMA-low or PSMA-negative phenotypes include small-cell neuroendocrine prostate cancer (de novo or treatment-emergent) and disease with neuroendocrine differentiation after multiple lines of ARPI therapy[8].
- Eligibility for Lu-177 PSMA-617 therapy is determined by VISION-derived Ga-68 PSMA PET-CT criteria: PSMA SUVmax greater than liver in all lesions, and no large discordant non-PSMA-avid disease[11].
- Patients with PSMA-low or PSMA-negative disease are appropriately directed toward platinum-based chemotherapy, taxane chemotherapy, or trial enrolment — not Lu-177 PSMA therapy.
- PSMA expression can be heterogeneous within a single patient, and combined Ga-68 PSMA PET and FDG PET imaging can identify discordant lesion patterns relevant to treatment selection[14].
- Re-staging with PSMA PET-CT (and sometimes FDG PET) at progression on PSMA-targeted therapy is part of well-conducted care[17].
Important
This article is general information about PSMA expression in prostate cancer. Individual eligibility for PSMA-directed imaging and therapy requires formal clinical assessment including imaging, biochemistry, treatment history, and multidisciplinary review.
"PSMA expression is the eligibility gateway for Lu-177 PSMA-617 therapy — but it is also a real-time biology readout that should inform treatment selection throughout the disease course. The patient whose Ga-68 PSMA PET-CT shows low or absent uptake has not failed; their tumour biology has changed, and treatment selection should change with it. PSMA PET is most powerful when it is read as biology, not just imaging."
Dr. Ishita B. Sen, MD · Director & Chief, Nuclear Medicine, FMRI
Eligibility assessment · Ga-68 PSMA PET at FMRI
At FMRI Gurugram, eligibility assessment for Lu-177 PSMA-617 therapy follows VISION-derived criteria using Ga-68 PSMA-11 PET-CT, with multidisciplinary review of the imaging pattern, disease distribution, biochemistry, and treatment history. Patients with PSMA-low or PSMA-negative disease are directed to appropriate alternative treatment pathways through the multidisciplinary team.
Request eligibility review · WhatsApp +91 8800 988936
For patients & referring clinicians
Frequently asked questions
Q01
What is PSMA?
PSMA stands for prostate-specific membrane antigen. It is a Type II transmembrane glycoprotein — formally glutamate carboxypeptidase II, encoded by the FOLH1 gene — expressed at low levels in normal prostate epithelium, salivary glands, lacrimal glands, kidney tubules, small bowel, and certain brain regions, and at substantially higher levels in most prostate cancers. The differential between cancer expression and normal-tissue expression is what allows PSMA-targeted imaging and therapy [1][4].
Q02
Do all prostate cancers express PSMA?
No. Most prostate adenocarcinomas — approximately 85–95% in typical published cohorts — show clinically meaningful PSMA expression. A minority of cases show low or absent PSMA expression, most commonly in small-cell neuroendocrine prostate cancer and in treatment-emergent neuroendocrine differentiation that arises after multiple lines of androgen-axis-targeted therapy [2][8].
Q03
How is PSMA expression measured?
In clinical practice, PSMA expression is assessed primarily by Ga-68 PSMA-11 PET-CT (or F-18 PSMA-1007 PET-CT in some centres). A small amount of radioactive PSMA-binding tracer is injected, and PET imaging quantifies the intensity of tumour uptake. Tumour SUVmax is compared to liver SUVmax to make VISION-derived eligibility decisions. Immunohistochemistry on biopsy tissue is also used, particularly in research and complex cases, but PET imaging is the standard for eligibility decisions [6][11].
Q04
What does PSMA-negative prostate cancer mean?
PSMA-negative or PSMA-low disease refers to prostate cancer that does not show sufficient PSMA expression on Ga-68 PSMA PET-CT to meet VISION-derived eligibility criteria for Lu-177 PSMA-617 therapy. This is most commonly seen in small-cell neuroendocrine prostate cancer and treatment-emergent neuroendocrine differentiation after multiple lines of androgen-axis therapy. The disease is not 'invisible' — it is often well-seen on FDG PET-CT and on conventional imaging — but it does not express the PSMA target [8][10].
Q05
What's the eligibility threshold for Lu-177 PSMA therapy?
Under VISION-derived criteria (the regulatory framework for Lu-177 PSMA-617 / Pluvicto), eligibility requires: (a) at least one PSMA-positive metastatic lesion with SUVmax greater than the SUVmax of liver parenchyma on Ga-68 PSMA-11 PET-CT, and (b) no measurable discordant non-PSMA-avid disease above defined size thresholds (lymph nodes >2.5 cm short axis, visceral metastases >1.0 cm short axis, or large lytic bone lesions without PSMA uptake) [11].
Q06
What is small-cell neuroendocrine prostate cancer?
Small-cell or neuroendocrine prostate cancer is a recognised aggressive subtype characterised by loss of androgen-receptor signalling, loss of PSA production, and frequently low or absent PSMA expression. It may arise de novo (rare) or as a treatment-emergent transformation under sustained androgen-deprivation pressure. It is typically more avid on FDG PET than on Ga-68 PSMA PET. It is treated with platinum-based chemotherapy, often with platinum-etoposide regimens, similar to other neuroendocrine cancers [9].
Q07
Can PSMA expression change over time in the same patient?
Yes. PSMA expression typically increases as prostate cancer progresses from hormone-sensitive to castration-resistant disease, particularly under sustained androgen-deprivation pressure. In the late-line setting after multiple lines of ARPI therapy, a subset of patients develops AR-independent or neuroendocrine programmes, and PSMA expression may fall. Re-staging with Ga-68 PSMA PET-CT — and sometimes FDG PET — at disease progression is part of well-conducted care [16][17].
Q08
Why is FDG PET sometimes done alongside Ga-68 PSMA PET?
FDG PET highlights glucose-avid metabolically active disease that may not be PSMA-avid. Using both Ga-68 PSMA PET and FDG PET, distinct lesion patterns may be identified: PSMA-positive/FDG-negative, PSMA-positive/FDG-positive, and PSMA-negative/FDG-positive. The PSMA-negative/FDG-positive pattern is the strongest signal of neuroendocrine differentiation or de-differentiation and helps guide treatment toward platinum-based regimens rather than PSMA-targeted therapy [10][14].
Q09
What treatments are appropriate for PSMA-negative disease?
Patients with PSMA-low or PSMA-negative disease are not eligible for Lu-177 PSMA-617 therapy under VISION-derived criteria. Appropriate alternatives include platinum-based chemotherapy (particularly for small-cell or neuroendocrine phenotypes which often retain platinum sensitivity), taxane chemotherapy (docetaxel, cabazitaxel), combination approaches, and clinical-trial enrolment for novel agents targeting alternative pathways such as DLL3 antibody-drug conjugates [13].
Q10
Why does Gleason grade matter for PSMA expression?
Higher Gleason grade generally associates with higher PSMA expression in published cohorts, although the relationship is not absolute and there is meaningful inter-patient variability. The clinical implication is that more aggressive disease typically expresses PSMA more strongly — which is why PSMA-targeted approaches are particularly well-suited to high-grade, advanced disease [5].
Q11
Is heterogeneous PSMA expression a problem for Lu-177 therapy?
Heterogeneous PSMA expression within a patient — some lesions strongly avid, others weakly avid — is recognised clinically and is one factor in the heterogeneous responses sometimes seen during Lu-177 PSMA therapy. Mid-treatment imaging at experienced centres helps identify patients whose disease pattern is shifting and where treatment plan should be revised. Eligibility is determined by the overall imaging picture under VISION criteria, not individual-lesion uniformity [14][15].
Q12
How do I get a PSMA PET-CT and eligibility review at FMRI?
At FMRI Gurugram, eligibility for Lu-177 PSMA-617 therapy follows VISION-derived criteria using Ga-68 PSMA-11 PET-CT with multidisciplinary review of the imaging pattern, disease distribution, biochemistry, and treatment history. Patients with PSMA-low or PSMA-negative disease are directed to appropriate alternative pathways. WhatsApp +91 8800 988936 to request 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] O'Keefe DS, Bacich DJ, Heston WD. Comparative analysis of prostate-specific membrane antigen (PSMA) versus a prostate-specific membrane antigen-like gene.
Prostate. 2004;58(2):200-210.
View source ↗[2] Hupe MC, Philippi C, Roth D, et al. Expression of Prostate-Specific Membrane Antigen (PSMA) on Biopsies Is an Independent Risk Stratifier of Prostate Cancer Patients.
Front Oncol. 2018;8:623.
View source ↗[3] 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 ↗[4] Silver DA, Pellicer I, Fair WR, et al. Prostate-specific membrane antigen expression in normal and malignant human tissues.
Clin Cancer Res. 1997;3(1):81-85.
View source ↗[5] Bostwick DG, Pacelli A, Blute M, et al. Prostate specific membrane antigen expression in prostatic intraepithelial neoplasia and adenocarcinoma.
Cancer. 1998;82(11):2256-2261.
View source ↗[6] 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 ↗[7] Hofman MS, Hicks RJ, Maurer T, Eiber M. Prostate-specific Membrane Antigen PET: Clinical Utility in Prostate Cancer, Normal Patterns, Pearls, and Pitfalls.
Radiographics. 2018;38(1):200-217.
View source ↗[8] Bakht MK, Hayward JJ, Shahbazi-Raz F, et al. Identification of alternative protein targets of glutamate-ammonia ligase in prostate cancer.
Sci Rep. 2019;9:8147.
View source ↗[9] Aggarwal R, Huang J, Alumkal JJ, et al. Clinical and Genomic Characterization of Treatment-Emergent Small-Cell Neuroendocrine Prostate Cancer.
J Clin Oncol. 2018;36(24):2492-2503.
View source ↗[10] 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 ↗[11] 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 ↗[12] Yadav MP, Ballal S, Tripathi M, et al.
177Lu-DKFZ-PSMA-617 therapy in mCRPC: Indian experience.
Eur J Nucl Med Mol Imaging. 2017;44(1):81-91.
View source ↗[13] NCCN Clinical Practice Guidelines in Oncology: Prostate Cancer (current version). National Comprehensive Cancer Network.
View source ↗[14] Paschalis A, Sheehan B, Riisnaes R, et al. Prostate-specific Membrane Antigen Heterogeneity and DNA Repair Defects in Prostate Cancer.
Eur Urol. 2019;76(4):469-478.
View source ↗[15] Buteau JP, Martin AJ, Emmett L, et al. PSMA and FDG-PET as predictive and prognostic biomarkers in TheraP trial.
Lancet Oncol. 2022;23(11):1389-1397.
View source ↗[16] Wright GL Jr, Grob BM, Haley C, et al. Upregulation of prostate-specific membrane antigen after androgen-deprivation therapy.
Urology. 1996;48(2):326-334.
View source ↗[17] Emmett L, Yin C, Crumbaker M, et al. Rapid Modulation of PSMA Expression by Androgen Deprivation: Serial 68Ga-PSMA-11 PET in Men with Hormone-Sensitive and Castrate-Resistant Prostate Cancer Commencing Androgen Blockade.
J Nucl Med. 2019;60(7):950-954.
View source ↗[18] 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 ↗[19] Hofman MS, Emmett L, Sandhu S, et al. [
177Lu]Lu-PSMA-617 versus cabazitaxel in patients with mCRPC (TheraP).
Lancet. 2021;397(10276):797-804.
View source ↗[20] 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 ↗[21] Eiber M, Maurer T, Souvatzoglou M, et al. Evaluation of Hybrid
68Ga-PSMA Ligand PET/CT in 248 Patients with Biochemical Recurrence After Radical Prostatectomy.
J Nucl Med. 2015;56(5):668-674.
View source ↗[22] 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 ↗[23] Mannweiler S, Amersdorfer P, Trajanoski S, et al. Heterogeneity of prostate-specific membrane antigen (PSMA) expression in prostate carcinoma with distant metastasis.
Pathol Oncol Res. 2009;15(2):167-172.
View source ↗[24] Beltran H, Prandi D, Mosquera JM, et al. Divergent clonal evolution of castration-resistant neuroendocrine prostate cancer.
Nat Med. 2016;22(3):298-305.
View source ↗[25] European Association of Urology. EAU Guidelines on Prostate Cancer.
View source ↗[26] Eder M, Eisenhut M, Babich J, Haberkorn U. PSMA as a target for radiolabelled small molecules.
Eur J Nucl Med Mol Imaging. 2013;40(6):819-823.
View source ↗[27] Tagawa ST, Vallabhajosula S, Christos PJ, et al. Phase I/II study of fractionated dose
177Lu-J591 for progressive mCRPC.
Cancer. 2019;125(15):2561-2569.
View source ↗[28] 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 ↗[29] 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 ↗[30] Atomic Energy Regulatory Board (Government of India). Safety Code for Nuclear Medicine Facilities. AERB/RF-MED/SC-2 (Rev. 2).
View source ↗
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.