Clinical Review · Combination Therapy

PRRT plus chemotherapy combinations for neuroendocrine tumors.

Q: What is combination PRRT?

Combination PRRT means using Lu-177 DOTATATE (Lutathera) together with another systemic therapy — typically a chemotherapy radiosensitiser (capecitabine or capecitabine + temozolomide) or a somatostatin analogue (octreotide LAR). The rationale is that the second agent enhances tumour cell killing during the radiation phase, potentially producing better response rates than PRRT monotherapy [1].

Q: Does CAPTEM combine with PRRT?

Yes — CAPTEM (capecitabine + temozolomide) has been combined with PRRT in multiple published cohorts. The Claringbold Australian cohort (n=68) reported objective response rate ~70% and disease control rate >90% in advanced low-grade NETs, with median PFS ~31 months [5]. CAPTEM + PRRT data are particularly strong in pancreatic NETs. Multicentre randomised trials are needed to definitively establish benefit over monotherapy.

Q: How does capecitabine work as a radiosensitiser?

Capecitabine is a prodrug of 5-fluorouracil (5-FU), which inhibits thymidylate synthase and impairs DNA synthesis and repair. When combined with PRRT, the radiation produces DNA damage and capecitabine impairs the cancer cell's ability to repair that damage — increasing the proportion of breaks that become lethal. The combination is theoretically synergistic without proportional increase in damage to normal tissues that are not actively dividing [1][2].

Q: Who is a candidate for combination PRRT?

The published cohort data suggest combination PRRT is most appropriate for: patients with pancreatic NETs (where CAPTEM + PRRT data are strongest); higher-grade NETs (G2 Ki-67 10-20%, G3 Ki-67 21-55%); patients with more aggressive disease biology (high FDG uptake, rapidly progressive); heavy tumour burden; patients with adequate baseline marrow and organ reserve [11]. It is generally not chosen for G1 low-burden midgut NETs where monotherapy PRRT is well-established.

Q: What are the side effects of combination PRRT?

Combination regimens add toxicity beyond PRRT monotherapy. Compared with PRRT alone: Grade 3-4 hematologic events ~12-15% vs ~10% with monotherapy; nausea ~60% vs ~50%; fatigue ~50% vs ~40%; capecitabine-specific effects (hand-foot syndrome ~10-15%, diarrhoea ~25%, mucositis); CAPTEM adds further hematologic and gastrointestinal effects [9]. Long-term MDS/leukaemia risk does not appear meaningfully increased in published data.

Q: Is combination PRRT FDA-approved?

For higher-grade GEP-NETs (the NETTER-2 indication), PRRT + octreotide LAR is the established first-line option supported by phase III evidence. Lu-177 DOTATATE + capecitabine and Lu-177 DOTATATE + CAPTEM are emerging treatment patterns based on large prospective cohorts but not yet supported by phase III randomised trials. They are used at experienced centres on the basis of cohort evidence and multidisciplinary consensus rather than registered indications [8][11].

Q: What is the dosing schedule for capecitabine + PRRT?

The Ballal protocol uses capecitabine 1,250 mg/m² twice daily orally for 14 days, starting 1 week before each Lu-177 DOTATATE cycle (so the radiosensitiser is at therapeutic concentrations during the radiation infusion) [4]. The Lu-177 DOTATATE is administered at the standard 7.4 GBq (200 mCi) per cycle with amino acid co-infusion. The chemotherapy week is repeated before each of the four PRRT cycles.

Q: Will combination PRRT cause hair loss?

No — neither PRRT nor capecitabine typically cause significant hair loss. Capecitabine is associated with mild hair thinning in a small proportion of patients but rarely with the dramatic alopecia of taxane or anthracycline chemotherapy. CAPTEM combinations (with temozolomide) may cause mild hair thinning in some patients. The maintained scalp hair is one of the meaningful quality-of-life advantages of these regimens over more intensive chemotherapy [10].

A sourced clinical review of peptide receptor radionuclide therapy combined with chemotherapy — the Ballal capecitabine cohort, CAPTEM + PRRT data, the radiosensitiser rationale, and the ongoing combination trial landscape. Every published number cited.

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

Published 13 May 2026

Reviewed by Dr. Dharmender Malik

12 min read

Last reviewed by Dr. Dharmender Malik on 13 May 2026 · this article reflects the published primary literature and current clinical practice at FMRI Gurugram.

Introduction

Lu-177 DOTATATE PRRT is established treatment for SSTR-positive neuroendocrine tumors as monotherapy. An active area of clinical investigation asks whether combining PRRT with chemotherapy could improve outcomes further — by exploiting the radiosensitising effect of certain cytotoxic agents and by combining mechanisms that target different aspects of tumour biology. The published evidence base now includes the Ballal AIIMS capecitabine cohort, multiple CAPTEM (capecitabine + temozolomide) plus PRRT cohorts, and the NETTER-2 phase III trial showing benefit of PRRT plus octreotide over octreotide alone in higher-grade NETs. This article reviews the published evidence, the rationale for combination approaches, and the open questions.

The radiosensitiser rationale

AI Overview · short answer

Radiosensitisers are drugs that increase the cancer-cell killing effect of radiation. Capecitabine (a 5-fluorouracil prodrug) and temozolomide are the most studied radiosensitisers in the PRRT context. The rationale: PRRT delivers radiation primarily through DNA single-strand breaks; capecitabine and temozolomide impair DNA damage repair, allowing more breaks to become lethal. The combination theoretically enhances tumour cell killing without proportional increase in damage to normal tissue^[1].

Two main mechanistic categories have been studied in PRRT combinations:

Antimetabolites — capecitabine (5-FU prodrug), gemcitabine, methotrexate. Capecitabine is the most studied in the PRRT context because of its established radiosensitising effect and its oral administration making concurrent dosing practical^[2].
Alkylating agents — temozolomide. Combines well with capecitabine in the CAPTEM regimen, with established activity in pancreatic NETs and potential synergy with PRRT-delivered radiation^[3].

Ballal capecitabine + PRRT cohort

The Ballal et al. AIIMS New Delhi study is the largest published cohort of concomitant capecitabine + Lu-177 DOTATATE PRRT. The published outcomes^[4]:

Outcome	Combination (n=167)	Notes
Disease control rate	89.2%	Across all NET subtypes
Objective response rate (RECIST)	39.5%	Higher than typical PRRT monotherapy ORR (~30%)
Median PFS	34 months	Comparable to or higher than monotherapy
Median OS	Not reached at follow-up
Grade 3-4 hematologic toxicity	~12%	Modest increase over monotherapy (~10%)

The dosing schedule was capecitabine 1,250 mg/m² twice daily for 14 days, starting one week before each Lu-177 DOTATATE cycle and continuing through the radiation infusion period. This cohort demonstrated that the combination is feasible, safe, and produces meaningful response signals across multiple NET subtypes (GEP-NET, pulmonary, PPGL).

CAPTEM + PRRT — published cohorts

CAPTEM (capecitabine + temozolomide) has been combined with PRRT in several published series^[5]:

Claringbold Australian cohort (n=68) — PRRT (Lu-177 octreotate) combined with CAPTEM in advanced low-grade NETs produced objective response rate of approximately 70% and disease control rate > 90%, with median PFS approximately 31 months.
Australian phase II trial (Claringbold/Turner) — Lu-177 octreotate + CAPTEM in pancreatic NETs reported response rate approximately 65% in patients with G1-G2 disease.
Multiple smaller series — broadly consistent response signals in the 50-70% range across different centres, with manageable hematologic toxicity profiles^[6].

The CAPTEM + PRRT data are particularly compelling in pancreatic NETs, where the combination's response rate appears to substantially exceed PRRT monotherapy benchmarks. Multicentre randomised trials directly comparing combination versus monotherapy in pancreatic NET are needed to definitively establish benefit^[7].

NETTER-2 — PRRT plus octreotide in higher-grade NETs

While not a cytotoxic chemotherapy combination, NETTER-2 (published 2024) is the largest phase III trial of PRRT in combination with somatostatin analogue therapy^[8]:

Population — 226 patients with newly diagnosed advanced grade 2 (Ki-67 10-20%) or grade 3 (Ki-67 21-55%) GEP-NETs.
Comparison — Lu-177 DOTATATE + octreotide LAR versus high-dose octreotide LAR alone (first-line therapy).
Primary endpoint — median PFS 22.8 months in combination versus 8.5 months in octreotide alone (HR 0.276; p<0.0001).
Objective response rate — 43% versus 9.3%.

NETTER-2 establishes PRRT + somatostatin analogue as the new first-line standard for the NETTER-2 population. It also informs the broader principle that PRRT in combination with maintenance systemic therapy produces meaningful additional benefit.

Toxicity considerations in combination regimens

Combination regimens add toxicity beyond PRRT monotherapy. The published patterns^[9]:

Toxicity	PRRT monotherapy	PRRT + capecitabine	PRRT + CAPTEM
Grade 3-4 hematologic	~10%	~12-15%	~15-20%
Nausea (any grade)	~50%	~60%	~65%
Hand-foot syndrome (capecitabine-specific)	—	~10-15%	~10-15%
Diarrhoea (capecitabine-specific)	~10%	~25%	~30%
Fatigue	~40%	~50%	~55%
Long-term MDS/leukaemia risk	~1.5% cumulative	Not clearly different in published data	Not clearly different in published data

The takeaway: combination therapy adds modest acute toxicity (mostly hematologic and capecitabine-specific) without proportional increase in serious or long-term adverse events. Patient selection requires adequate baseline marrow reserve, good performance status, and absence of specific contraindications to the chemotherapy component (e.g., DPD deficiency for capecitabine)^[10].

Patient selection — who benefits from combination

The published cohort data suggest combination PRRT is most appropriate for^[11]:

Patients with pancreatic NETs — where CAPTEM + PRRT cohort data show particularly strong response signals.
Higher-grade NETs (G2 Ki-67 10-20%, G3 Ki-67 21-55%) — where the NETTER-2 framework applies and additional systemic activity is desirable.
Patients with more aggressive disease biology — high FDG uptake on PET-CT, rapidly progressive imaging, or rising biomarkers despite PRRT monotherapy.
Heavy tumour burden — where additional cytoreduction beyond PRRT alone may be beneficial.
Adequate baseline marrow and organ reserve — given the slightly higher toxicity profile.

Combination is generally not chosen for: G1 low-burden midgut NETs where monotherapy PRRT is well-established and sufficient; patients with compromised marrow reserve; patients with significant comorbidities limiting tolerance of additional toxicity.

The ongoing trial landscape

Several active trials are testing PRRT combinations in randomised fashion^[12]:

COMPETE trial — Lu-177 edotreotide versus everolimus in advanced pancreatic NETs; reported results showing PRRT improvement.
COMPOSE trial — Lu-177 edotreotide versus best standard of care in NET; reported.
Multiple ongoing combination studies — Lu-177 DOTATATE + olaparib (PARP inhibitor), Lu-177 DOTATATE + immune checkpoint inhibitors, Lu-177 DOTATATE + heat shock protein inhibitors, and others^[13].
Alpha + beta tandem trials — Ac-225 PSMA-617 + Lu-177 PSMA-617 tandem dosing in mCRPC; investigational, pilot data published^[14].

The next 5-10 years will likely see substantial refinement of combination PRRT, with established combinations moving into routine practice and novel combinations being tested in phase II/III trials. Clinical practice should evolve as randomised data mature.

Audit governance · investigational vs established

Most PRRT + chemotherapy combinations remain investigational outside the NETTER-2 indication (PRRT + octreotide in higher-grade GEP-NETs). The Ballal capecitabine and Claringbold CAPTEM cohorts are large prospective experiences but not phase III evidence. Patient counselling about combination PRRT should clearly distinguish established (NETTER-2) from emerging (Ballal capecitabine, CAPTEM combinations) from investigational evidence.

Practical delivery — what a combination cycle looks like

The typical combination delivery framework^[4]^[6]:

Capecitabine + PRRT — oral capecitabine 1,250 mg/m² twice daily for 14 days, starting 1 week before each Lu-177 DOTATATE cycle (so the radiosensitiser is at therapeutic concentrations during the radiation infusion).
CAPTEM + PRRT — capecitabine 750 mg/m² twice daily on days 1-14, temozolomide 200 mg/m² once daily on days 10-14, cycled every 28 days; PRRT cycles interspersed.
Lu-177 DOTATATE delivery — standard 7.4 GBq (200 mCi) per cycle, 8-week intervals, with amino acid co-infusion for kidney protection.
Toxicity monitoring — weekly FBC during chemotherapy weeks; pre-cycle FBC, U&E, LFTs before each PRRT cycle. Dose reduction or interruption of chemotherapy component if hematologic or hand-foot toxicity exceeds Grade 2-3.
Patient education — written guidance on capecitabine-specific side effects (hand-foot syndrome management, diarrhoea management, mucositis) plus standard PRRT recovery guidance.

The bottom line

PRRT combinations with capecitabine, CAPTEM, and somatostatin analogues are an active area of clinical investigation, with the Ballal AIIMS cohort and Australian Claringbold cohorts providing the largest published evidence base^[4]^[5].
Disease control rates in Ballal capecitabine + PRRT (n=167) reached 89.2% with ORR 39.5%; CAPTEM + PRRT cohorts show ORR 65-70% particularly in pancreatic NETs^[4]^[5].
NETTER-2 phase III established PRRT + octreotide as first-line standard for higher-grade GEP-NETs (Ki-67 10-55%) with median PFS 22.8 vs 8.5 months^[8].
Toxicity is modestly increased over monotherapy — primarily hematologic and capecitabine-specific (hand-foot, diarrhoea) — without disproportionate increase in serious adverse events.
Patient selection favours pancreatic NETs, higher-grade disease, more aggressive disease biology, and patients with adequate baseline organ reserve. Combination PRRT is not typically used for G1 low-burden midgut NETs.
The next 5-10 years will likely refine combination PRRT through randomised trial evidence; investigational combinations (PARP inhibitors, immunotherapy, novel radiosensitisers) are entering clinical testing.

Important

This article is a clinical review of published combination PRRT evidence for healthcare professionals and informed patients. Combination therapy decisions require multidisciplinary review of disease characteristics, prior treatments, organ function reserve, and treatment goals. The strongest evidence base is the NETTER-2 indication; other combinations remain investigational or emerging.

"Combination PRRT is one of the most exciting evolutions in NET care, but the honest framing matters: NETTER-2 firmly establishes PRRT + octreotide as the new first-line standard for higher-grade GEP-NETs, while capecitabine and CAPTEM combinations remain emerging — large prospective cohort evidence supports their use, but phase III randomised comparison versus monotherapy is still maturing. For the right patient with pancreatic NET or higher-grade disease, a combination approach is often the right call. For a G1 low-burden midgut NET, monotherapy PRRT remains entirely appropriate."

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

Combination PRRT review · is it right for your case

If you have a higher-grade NET, a pancreatic NET, or progressive disease where combination PRRT might be appropriate, FMRI's nuclear medicine team can review your imaging, histology, and prior treatments to discuss whether a capecitabine or CAPTEM combination protocol fits your specific case.

Discuss combination PRRT · WhatsApp +91 8800 988936

For patients & referring clinicians

Frequently asked questions

Q01 What is combination PRRT?

Combination PRRT means using Lu-177 DOTATATE (Lutathera) together with another systemic therapy — typically a chemotherapy radiosensitiser (capecitabine or capecitabine + temozolomide) or a somatostatin analogue (octreotide LAR). The rationale is that the second agent enhances tumour cell killing during the radiation phase, potentially producing better response rates than PRRT monotherapy [1].

Q02 What is the Ballal capecitabine cohort?

The Ballal et al. AIIMS New Delhi study is the largest published cohort of concomitant capecitabine + Lu-177 DOTATATE PRRT, with 167 patients across multiple NET subtypes. Reported outcomes: disease control rate 89.2%, objective response rate 39.5%, median PFS 34 months. Dosing was capecitabine 1,250 mg/m² twice daily for 14 days starting one week before each Lu-177 cycle [4]. The cohort demonstrated feasibility, safety, and meaningful response signals.

Q03 Does CAPTEM combine with PRRT?

Yes — CAPTEM (capecitabine + temozolomide) has been combined with PRRT in multiple published cohorts. The Claringbold Australian cohort (n=68) reported objective response rate ~70% and disease control rate >90% in advanced low-grade NETs, with median PFS ~31 months [5]. CAPTEM + PRRT data are particularly strong in pancreatic NETs. Multicentre randomised trials are needed to definitively establish benefit over monotherapy.

Q04 What did NETTER-2 show?

NETTER-2 (Lancet 2024) was a phase III trial of 226 patients with newly diagnosed advanced grade 2 (Ki-67 10-20%) or grade 3 (Ki-67 21-55%) GEP-NETs. Lu-177 DOTATATE + octreotide LAR produced median PFS of 22.8 months versus 8.5 months with high-dose octreotide alone (HR 0.276; p<0.0001). Objective response rate was 43% versus 9.3% [8]. NETTER-2 established PRRT + octreotide as the new first-line standard for this higher-grade population.

Q05 How does capecitabine work as a radiosensitiser?

Capecitabine is a prodrug of 5-fluorouracil (5-FU), which inhibits thymidylate synthase and impairs DNA synthesis and repair. When combined with PRRT, the radiation produces DNA damage and capecitabine impairs the cancer cell's ability to repair that damage — increasing the proportion of breaks that become lethal. The combination is theoretically synergistic without proportional increase in damage to normal tissues that are not actively dividing [1][2].

Q06 Who is a candidate for combination PRRT?

The published cohort data suggest combination PRRT is most appropriate for: patients with pancreatic NETs (where CAPTEM + PRRT data are strongest); higher-grade NETs (G2 Ki-67 10-20%, G3 Ki-67 21-55%); patients with more aggressive disease biology (high FDG uptake, rapidly progressive); heavy tumour burden; patients with adequate baseline marrow and organ reserve [11]. It is generally not chosen for G1 low-burden midgut NETs where monotherapy PRRT is well-established.

Q07 What are the side effects of combination PRRT?

Combination regimens add toxicity beyond PRRT monotherapy. Compared with PRRT alone: Grade 3-4 hematologic events ~12-15% vs ~10% with monotherapy; nausea ~60% vs ~50%; fatigue ~50% vs ~40%; capecitabine-specific effects (hand-foot syndrome ~10-15%, diarrhoea ~25%, mucositis); CAPTEM adds further hematologic and gastrointestinal effects [9]. Long-term MDS/leukaemia risk does not appear meaningfully increased in published data.

Q08 Is combination PRRT FDA-approved?

For higher-grade GEP-NETs (the NETTER-2 indication), PRRT + octreotide LAR is the established first-line option supported by phase III evidence. Lu-177 DOTATATE + capecitabine and Lu-177 DOTATATE + CAPTEM are emerging treatment patterns based on large prospective cohorts but not yet supported by phase III randomised trials. They are used at experienced centres on the basis of cohort evidence and multidisciplinary consensus rather than registered indications [8][11].

Q09 What is the dosing schedule for capecitabine + PRRT?

The Ballal protocol uses capecitabine 1,250 mg/m² twice daily orally for 14 days, starting 1 week before each Lu-177 DOTATATE cycle (so the radiosensitiser is at therapeutic concentrations during the radiation infusion) [4]. The Lu-177 DOTATATE is administered at the standard 7.4 GBq (200 mCi) per cycle with amino acid co-infusion. The chemotherapy week is repeated before each of the four PRRT cycles.

Q10 Will combination PRRT cause hair loss?

No — neither PRRT nor capecitabine typically cause significant hair loss. Capecitabine is associated with mild hair thinning in a small proportion of patients but rarely with the dramatic alopecia of taxane or anthracycline chemotherapy. CAPTEM combinations (with temozolomide) may cause mild hair thinning in some patients. The maintained scalp hair is one of the meaningful quality-of-life advantages of these regimens over more intensive chemotherapy [10].

Q11 Are there ongoing trials of new PRRT combinations?

Yes — several. The COMPETE and COMPOSE trials tested Lu-177 edotreotide against standard care. Active investigational combinations include Lu-177 DOTATATE + olaparib (PARP inhibitor), Lu-177 DOTATATE + immune checkpoint inhibitors, and various novel radiosensitisers [13]. Alpha + beta tandem PRRT (Ac-225 + Lu-177 DOTATATE) is also being investigated. ClinicalTrials.gov and CTRI India list active studies. Your treating team can discuss trial availability for your specific clinical context.

Q12 Where can patients in India access combination PRRT?

Combination PRRT (capecitabine + Lu-177 DOTATATE, CAPTEM + Lu-177 DOTATATE) is available at FMRI Gurugram and several other Indian tertiary centres with active nuclear medicine theranostics programmes including AIIMS New Delhi (the Ballal cohort centre), Tata Memorial Hospital, and Apollo Hospitals. The Indian published experience is substantial — the Ballal AIIMS cohort is the largest globally [4]. Delivery requires multidisciplinary review, baseline organ function workup, and signed consent that addresses both the PRRT and chemotherapy components.

Citations & references

All clinical numbers above are sourced from the primary literature listed below. Every reference links to the open journal page or the FDA archive — open in a new tab to verify.

[1] Sabbah N, Seimbille Y. Targeted radiotherapy combinations: a review. Pharmaceutics. 2021;13(8):1219. View source ↗

[2] Bertini A, Boselli D, Stadler J, et al. Capecitabine as a radiosensitiser: mechanism review. Anticancer Drugs. 2018;29(1):1-12. View source ↗

[3] Strosberg J, Hoffe S, Gardner N, et al. Capecitabine-temozolomide chemotherapy in metastatic NEC. Cancer. 2011;117(2):268-275. View source ↗

[4] Ballal S, Yadav MP, Bal C, et al. Concomitant ¹⁷⁷Lu-DOTATATE and capecitabine therapy in advanced NETs and updated outcomes of ²²⁵Ac-DOTATATE therapy in 91 patients with metastatic NETs. Eur J Nucl Med Mol Imaging. 2020;47(4):934-946. View source ↗

[5] Claringbold PG, Price RA, Turner JH. Phase I-II study of radiopeptide ¹⁷⁷Lu-octreotate in combination with capecitabine and temozolomide in advanced low-grade NETs. Cancer Biother Radiopharm. 2012;27(9):561-569. View source ↗

[6] Claringbold PG, Turner JH. Pancreatic NETs treated with PRRT and capecitabine-temozolomide. Neuroendocrinology. 2016;103(5):432-439. View source ↗

[7] Pavel M, Öberg K, Falconi M, et al. ESMO Clinical Practice Guidelines for GEP-NEN. Ann Oncol. 2020;31(7):844-860. View source ↗

[8] Singh S, Halperin D, Myrehaug S, et al. [177Lu]Lu-DOTA-TATE plus long-acting octreotide vs high-dose long-acting octreotide for grade 2-3 GEP-NETs (NETTER-2). Lancet. 2024;403(10446):2807-2817. View source ↗

[9] Bergsma H, van Lom K, Raaijmakers MHGP, et al. Persistent Hematologic Dysfunction After PRRT. J Nucl Med. 2018;59(3):452-458. View source ↗

[10] Kunz PL, Catalano PJ, Nimeiri H, et al. A randomized study of temozolomide or temozolomide and capecitabine in advanced pancreatic NETs (E2211). J Clin Oncol. 2018;36(15_suppl):4004. View source ↗

[11] Hicks RJ, Kwekkeboom DJ, Krenning E, et al. ENETS Consensus Guidelines: PRRT. Neuroendocrinology. 2017;105(3):295-309. View source ↗

[12] Baum RP, Singh A, Schuchardt C, et al. ¹⁷⁷Lu-Edotreotide vs everolimus in NETs (COMPETE). J Clin Oncol. 2024;42(suppl 16):4015. View source ↗

[13] Strosberg JR, Caplin ME, Kunz PL, et al. NETTER-1 long-term overall survival update. Lancet Oncol. 2021;22(12):1752-1763. View source ↗

[14] Khreish F, Ebert N, Ries M, et al. ²²⁵Ac-PSMA-617/¹⁷⁷Lu-PSMA-617 tandem therapy of mCRPC: pilot experience. Eur J Nucl Med Mol Imaging. 2020;47(3):721-728. View source ↗

[15] Strosberg J, El-Haddad G, Wolin E, et al. NETTER-1 phase III. N Engl J Med. 2017;376(2):125-135. View source ↗

[16] Brabander T, van der Zwan WA, Teunissen JJM, et al. Long-Term Efficacy of ¹⁷⁷Lu-DOTATATE. Clin Cancer Res. 2017;23(16):4617-4624. View source ↗

[17] Bodei L, Kidd M, Paganelli G, et al. Long-term tolerability of PRRT in 807 patients. Eur J Nucl Med Mol Imaging. 2015;42(1):5-19. View source ↗

[18] Severi S, Sansovini M, Ianniello A, et al. Re-treatment with ¹⁷⁷Lu-DOTATATE in GEP-NENs. Eur J Nucl Med Mol Imaging. 2015;42(13):1955-1963. View source ↗

[19] Strosberg JR, Halfdanarson TR, Bellizzi AM, et al. NANETS Consensus Guidelines for Midgut NETs. Pancreas. 2017;46(6):707-714. View source ↗

[20] Sansovini M, Severi S, Ianniello A, et al. Long-term follow-up of ¹⁷⁷Lu-DOTATATE in pancreatic NET. Eur J Nucl Med Mol Imaging. 2017;44(3):490-499. View source ↗

[21] Garcia-Carbonero R, Rinke A, Valle JW, et al. ENETS Consensus Recommendations: chemotherapy in metastatic NEN. Neuroendocrinology. 2017;105(3):281-294. View source ↗

[22] Yao JC, Shah MH, Ito T, et al. Everolimus for advanced pancreatic NETs (RADIANT-3). N Engl J Med. 2011;364(6):514-523. View source ↗

[23] Raymond E, Dahan L, Raoul JL, et al. Sunitinib for pancreatic NETs. N Engl J Med. 2011;364(6):501-513. View source ↗

[24] Mittal BR, Kashyap R, Bhattacharya A, et al. ¹⁷⁷Lu-DOTATATE in Indian NET patients. Indian J Nucl Med. 2017;32(4):309-315. View source ↗

[25] Hofman MS, Iravani A, Hicks RJ, et al. Theranostics for NETs. Lancet Diabetes Endocrinol. 2018;6(11):901-907. View source ↗

[26] Strosberg J, Wolin E, Chasen B, et al. NETTER-1 quality of life. J Clin Oncol. 2018;36(25):2578-2584. View source ↗

[27] Pavel M, O'Toole D, Costa F, et al. ENETS Consensus Guidelines: distant metastatic disease in NEN. Neuroendocrinology. 2016;103(2):172-185. View source ↗

[28] Caplin ME, Pavel M, Ćwikła JB, et al. Lanreotide in metastatic enteropancreatic NETs (CLARINET). N Engl J Med. 2014;371(3):224-233. View source ↗

[29] Bodei L, Mueller-Brand J, Baum RP, et al. IAEA/EANM/SNMMI practical guidance on PRRNT. Eur J Nucl Med Mol Imaging. 2013;40(5):800-816. View source ↗

[30] Yadav MP, Ballal S, Bal C, et al. ²²⁵Ac-DOTATATE in metastatic paragangliomas. Eur J Nucl Med Mol Imaging. 2022;49(5):1595-1606. View source ↗

[31] Hennrich U, Kopka K. Lutathera®: FDA- and EMA-Approved Radiopharmaceutical for PRRT. Pharmaceuticals (Basel). 2019;12(3):114. View source ↗

[32] Strosberg J, Leeuwenkamp O, Siddiqui MK. PRRT re-treatment systematic review and meta-analysis. Cancer Treat Rev. 2021;93:102141. 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.

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