Patient Guide · Lung NETs

PRRT for lung neuroendocrine tumors.

Q: Can lung cancer patients have PRRT?

Yes — but only for the SSTR-positive subtypes. PRRT applies specifically to typical and atypical carcinoid tumours of the lung (well-differentiated pulmonary NETs), which are SSTR2-positive in approximately 70-90% of cases. LCNEC (large-cell neuroendocrine carcinoma) and SCLC (small-cell lung cancer) are SSTR-negative on imaging and require platinum-based chemotherapy rather than PRRT [1][2].

Q: How well does PRRT work for lung carcinoid tumors?

Published cohort data show disease control rate of 73-80% and median progression-free survival of approximately 27-28 months for metastatic lung carcinoid treated with Lu-177 DOTATATE PRRT. The Sabet German cohort (n=22) reported 73% DCR, 27% partial response, 27-month median PFS, 42-month median OS. The Mariniello Italian cohort (n=34) reported 80% DCR, 27% partial response, 28-month median PFS [5][6].

Q: What is the difference between typical and atypical carcinoid?

Typical carcinoid (WHO 2021): <2 mitoses per 10 high-power fields and no necrosis; SSTR2-positive in ~80-90% of cases; 5-year overall survival ~85-90%. Atypical carcinoid: 2-10 mitoses per 10HPF and/or focal necrosis; SSTR2-positive in ~70-80%; more aggressive; 5-year OS ~50-70%. Both are PRRT candidates if SSTR-positive on imaging, but atypical carcinoid may show shorter response duration and may benefit from combination approaches [1][4].

Q: Can SCLC patients have PRRT?

No — small-cell lung cancer (SCLC) is typically SSTR-negative on imaging (<10% SSTR2-positive) and does not respond to PRRT. SCLC is treated with platinum-based chemotherapy (carboplatin + etoposide standardly) as first-line, with limited later-line options. Recent immune checkpoint inhibitor combinations and targeted approaches are areas of active investigation [2][3]. PRRT is not appropriate for SCLC.

Q: Can LCNEC patients have PRRT?

Generally no — large-cell neuroendocrine carcinoma (LCNEC) is typically SSTR-negative on imaging (~10-20% SSTR2-positive) and is treated like small-cell lung cancer with platinum-based chemotherapy. Rare exceptions exist where LCNEC shows meaningful SSTR uptake on Ga-68 DOTATATE PET-CT and PRRT has been considered on individual basis at experienced centres, but this is uncommon and remains investigational [2][3].

Q: What is the role of Ga-68 DOTATATE PET-CT in lung NETs?

Ga-68 DOTATATE PET-CT is essential for: (1) confirming SSTR2 expression in candidate lung carcinoid tumours before PRRT; (2) assessing tumour distribution and identifying lesions not visible on conventional imaging; (3) distinguishing well-differentiated carcinoid (SSTR-positive) from LCNEC/SCLC (SSTR-negative). Sensitivity for detecting lung carcinoid metastases is approximately 90-95% versus 50-60% for older octreotide scintigraphy [10][14].

Q: How does PRRT compare with everolimus for lung NETs?

Both are established options for advanced lung carcinoid tumours. Everolimus is FDA-approved based on RADIANT-4 trial (median PFS 11 vs 3.9 months on placebo). PRRT is supported by cohort data showing median PFS ~28 months in selected patients. The choice depends on: imaging characteristics (DOTATATE uptake favours PRRT; SSTR-negative or low-uptake disease favours everolimus); disease distribution; prior treatments; patient priorities around toxicity profile (PRRT fatigue/nausea/cytopenia vs everolimus mucositis/pneumonitis/hyperglycaemia) [15].

Q: Are there other systemic options for lung NETs?

Yes. The established lung NET systemic options include: (1) somatostatin analogues — octreotide LAR, lanreotide as first-line for low-burden or low-grade disease; (2) everolimus — FDA-approved for advanced progressive lung NETs based on RADIANT-4; (3) PRRT (Lu-177 DOTATATE) for SSTR-positive disease after progression on first-line; (4) chemotherapy (CAPTEM, platinum-based for atypical/aggressive disease) in selected cases. Surgery remains the standard for localised disease [13].

Q: Does lung carcinoid syndrome happen?

Yes, but less commonly than in midgut NETs. Carcinoid syndrome occurs in approximately 5-10% of lung carcinoid patients (versus 20-30% in midgut NETs). The lower incidence reflects the different biology — lung carcinoid tumours bypass the hepatic first-pass effect less often than midgut NETs with liver metastases [11]. Atypical lung carcinoid tumours may also produce ACTH (causing Cushing's syndrome) or growth hormone-releasing hormone in occasional patients [12].

Q: Can patients have surgery and PRRT for lung NETs?

Yes — many patients have both at different points in the disease trajectory. Surgical resection is the standard for localised lung carcinoid with excellent long-term outcomes. If disease later recurs or progresses to metastatic stage, PRRT becomes an option for SSTR-positive recurrence. Surgical resection and PRRT are not mutually exclusive — they fit into different phases of the lung NET treatment pathway [13].

Lu-177 DOTATATE PRRT for pulmonary neuroendocrine tumors — including typical and atypical carcinoid — published response rates, the critical distinction between SSTR-positive carcinoid and SCLC/LCNEC, patient selection, and where PRRT fits in the broader lung NET treatment pathway. Every clinical number sourced.

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

Published 13 May 2026

Reviewed by Dr. Dharmender Malik

13 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

Pulmonary neuroendocrine tumors (lung NETs) are a heterogeneous spectrum of tumours arising from the diffuse neuroendocrine system in the lung. They account for approximately 25 percent of all neuroendocrine tumours and span four pathological subtypes that differ dramatically in biology, treatment, and prognosis: typical carcinoid (most indolent), atypical carcinoid, large-cell neuroendocrine carcinoma (LCNEC), and small-cell lung cancer (SCLC)^[1]. PRRT applies specifically to the SSTR-positive end of this spectrum — typical and atypical carcinoid tumours — and not to LCNEC or SCLC, which require platinum-based chemotherapy^[2]. This article covers what PRRT can do for lung carcinoid tumours, what the published evidence shows, and how patient selection works.

The four pulmonary NET subtypes — and which respond to PRRT

AI Overview · short answer

The WHO 2021 classification distinguishes four pulmonary NET subtypes by mitotic count and necrosis: typical carcinoid (<2 mitoses/10HPF, no necrosis); atypical carcinoid (2-10 mitoses/10HPF and/or focal necrosis); LCNEC (>10 mitoses/10HPF, large cells); SCLC (>10 mitoses/10HPF, small cells). Typical and atypical carcinoid are SSTR2-positive in approximately 80% of cases — making them PRRT candidates. LCNEC and SCLC are SSTR-negative on imaging and require platinum-based chemotherapy^[1]^[3].

Subtype	Mitoses/10HPF	SSTR2-positive	PRRT candidate	5-year OS
Typical carcinoid	<2, no necrosis	~80-90%	Yes (after progression)	~85-90%
Atypical carcinoid	2-10 and/or focal necrosis	~70-80%	Yes	~50-70%
LCNEC (large-cell NEC)	>10, large cells	~10-20%	No (rare exceptions)	~25-30%
SCLC (small-cell)	>10, small cells	~5-10%	No	~5-10%

The critical clinical distinction is between carcinoid (well-differentiated, SSTR-positive, PRRT-amenable) and LCNEC/SCLC (poorly-differentiated, SSTR-negative, requires chemotherapy). Histopathology with WHO 2021 grading + SSTR-PET imaging makes this distinction definitively^[4].

Sabet cohort — the foundational PRRT lung carcinoid data

The Sabet et al. German cohort is one of the foundational PRRT lung carcinoid studies, providing the most cited response data^[5]:

Population — 22 patients with metastatic or unresectable lung carcinoid tumours (mostly typical, some atypical) who had progressed on prior therapy.
Treatment — Lu-177 DOTATATE at 7.4 GBq per cycle, up to 4 cycles.
Disease control rate — 73% (PR + SD at first response assessment).
Partial response (RECIST) — 27%.
Median progression-free survival — 27 months.
Median overall survival — 42 months.

The Sabet data established that PRRT produces meaningful response in metastatic lung carcinoid — disease control in nearly three-quarters of patients, with median PFS of more than two years.

Mariniello and other supporting cohorts

Subsequent studies have confirmed and extended the Sabet data^[6]^[7]:

Cohort	n	Disease control rate	Partial response	Median PFS
Sabet (Germany, 2017)	22	73%	27%	27 mo
Mariniello (Italy, 2016)	34	80%	27%	28 mo
Brabander (Erasmus subset, 2017)	~50 lung NETs	~75%	~30%	~30 mo
Ianniello (Italy, 2016)	34 lung carcinoid	~70%	23%	~28 mo

Across cohorts, response rates and PFS are remarkably consistent in the 70-80% disease control rate range with PFS of approximately 28 months. The aggregated evidence supports PRRT as an established second-line option for SSTR-positive metastatic lung carcinoid after progression on somatostatin analogues^[8].

How lung NETs differ from gut NETs for PRRT

Several biological and clinical features distinguish lung NETs from gut NETs in the PRRT context^[9]:

SSTR expression heterogeneity — Lung carcinoid tumours show somewhat more variable SSTR2 expression than midgut NETs. Approximately 80-90% of typical carcinoid and 70-80% of atypical carcinoid are SSTR2-positive on Ga-68 DOTATATE PET-CT versus ~95% of midgut NETs^[10].
Carcinoid syndrome less common — Lung carcinoid tumours produce carcinoid syndrome in only approximately 5-10% of cases (versus 20-30% in midgut NETs), because they bypass the hepatic first-pass effect less often^[11].
Atypical carcinoid biology — More aggressive than typical carcinoid; intermediate response patterns to PRRT; often benefits from combination approaches with everolimus or platinum chemotherapy in selected cases.
Lung-specific clinical features — cough, recurrent post-obstructive pneumonia, haemoptysis. Atypical carcinoid may produce ACTH (causing Cushing's syndrome) or growth hormone-releasing hormone in occasional patients^[12].
Treatment pathway — Surgical resection is standard for localised lung carcinoid; PRRT is for unresectable or metastatic disease after progression on somatostatin analogues^[13].

Patient selection for lung NET PRRT

Selection criteria for PRRT in lung carcinoid tumours^[14]:

Histology — confirmed typical or atypical carcinoid (well-differentiated lung NET) on biopsy with WHO 2021 grading. LCNEC and SCLC are excluded.
Imaging — Ga-68 DOTATATE PET-CT showing Krenning score ≥ 2 in target lesions; FDG PET-CT helpful for assessing tumour heterogeneity (high FDG uptake may indicate more aggressive subset).
Disease status — metastatic or unresectable disease with documented progression on prior therapy (typically somatostatin analogues; selected patients also after everolimus).
Organ function — same standard requirements as for GEP-NET PRRT (eGFR ≥ 50, marrow reserve, ECOG 0-2).
Multidisciplinary review — confirms PRRT is the appropriate next step versus surgical resection (for limited disease), everolimus (an established option in lung NETs), platinum chemotherapy (for high-grade atypical), or clinical trial enrolment.

Clinical note · everolimus in lung NETs

Everolimus is FDA-approved for advanced, progressive, non-functional lung carcinoid tumours based on the RADIANT-4 trial, which reported median PFS 11 months versus 3.9 months on placebo (HR 0.50; p<0.001) [Yao Lancet 2016]. The choice between PRRT and everolimus in lung carcinoid depends on imaging characteristics (DOTATATE uptake favours PRRT; SSTR-negative or low-uptake disease favours everolimus), disease distribution, prior treatments, and patient priorities around toxicity profile^[15].

Atypical carcinoid — specific considerations

Atypical carcinoid is more aggressive than typical carcinoid and presents distinct challenges^[16]:

Higher Ki-67 and mitotic rate means more rapid disease progression and shorter response duration on most therapies.
FDG uptake often more intense than typical carcinoid; SSTR-positive + FDG-positive pattern indicates more aggressive disease behaviour.
Combination approaches — Some experienced centres consider PRRT + capecitabine or PRRT + CAPTEM in atypical carcinoid based on extrapolation from GEP-NET combination data. See our combination PRRT review.
Response durability — response to PRRT may be shorter in atypical carcinoid than in typical carcinoid; the published cohorts do not always separate these subgroups cleanly. Salvage approaches and switch to alternative systemic therapy may be considered earlier^[17].
Multidisciplinary review is particularly important — atypical carcinoid often benefits from intensified management combining systemic therapy, locoregional therapy (such as radiofrequency ablation or stereotactic radiotherapy for individual lesions), and consideration of repeat surgical resection in selected oligometastatic cases.

The broader lung NET treatment pathway

PRRT fits into the lung carcinoid treatment pathway as follows^[13]:

Localised typical carcinoid — surgical resection is the standard, with excellent long-term outcomes (5-year OS 85-90%).
Localised atypical carcinoid — surgical resection, often with mediastinal lymphadenectomy; adjuvant therapy considered in some cases.
Metastatic / unresectable, low-burden disease — somatostatin analogues (octreotide LAR or lanreotide) as first-line systemic therapy.
Progressive disease on somatostatin analogues, SSTR-positive on Ga-68 DOTATATE PET-CT — PRRT or everolimus, depending on imaging characteristics and disease distribution.
Progressive atypical carcinoid with aggressive features — consideration of platinum-based chemotherapy (cisplatin/carboplatin + etoposide), or combination PRRT approaches in experienced centres.
LCNEC and SCLC — platinum-based chemotherapy is standard; PRRT not appropriate.

The bottom line

PRRT is established treatment for SSTR-positive metastatic lung carcinoid tumours (typical and atypical) — disease control rate 73-80% and median PFS approximately 28 months in published cohorts (Sabet, Mariniello)^[5]^[6].
The critical distinction is between SSTR-positive carcinoid (PRRT candidate) and SSTR-negative LCNEC/SCLC (requires platinum chemotherapy)^[2].
Lung NETs show somewhat more variable SSTR2 expression than midgut NETs (80-90% positive for typical carcinoid, 70-80% for atypical), making Ga-68 DOTATATE PET-CT particularly important for eligibility assessment^[10].
Everolimus is an alternative established systemic option for advanced lung carcinoid (RADIANT-4: 11.0 vs 3.9 month median PFS); the choice between PRRT and everolimus depends on imaging, disease distribution, and patient factors^[15].
Atypical carcinoid is more aggressive than typical carcinoid; multidisciplinary review of combination approaches (PRRT + chemotherapy, PRRT + everolimus) may be appropriate for selected patients.
Surgical resection remains the standard for localised lung carcinoid; PRRT is for unresectable or metastatic disease after progression on first-line systemic therapy^[13].

Important

This article is general patient education. Whether PRRT is appropriate for a specific lung neuroendocrine tumour depends on histology (typical vs atypical carcinoid vs LCNEC/SCLC), Ga-68 DOTATATE PET-CT findings, disease distribution, prior treatments, and overall clinical context. Decisions require multidisciplinary review by thoracic oncology, nuclear medicine, and pulmonology specialists familiar with your specific case.

"The most important question in any conversation about PRRT for a lung tumour is — is this carcinoid, or is this LCNEC or SCLC? The biology is genuinely different. PRRT works very well for SSTR-positive typical and atypical carcinoid; it does not work for small-cell or large-cell neuroendocrine carcinoma of the lung. The Ga-68 DOTATATE PET-CT, combined with definitive histopathology grading, answers this question definitively — and it has to be answered before any meaningful PRRT discussion."

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

Lung NET PRRT consultation · candidacy review

If you have a lung neuroendocrine tumour and want to know whether PRRT is an option, FMRI's nuclear medicine team can review your histology (typical vs atypical carcinoid, vs LCNEC/SCLC), Ga-68 DOTATATE PET-CT findings, and prior treatments to give you a clear answer about candidacy.

Discuss lung NET PRRT · WhatsApp +91 8800 988936

For patients & referring clinicians

Frequently asked questions

Q01 Can lung cancer patients have PRRT?

Yes — but only for the SSTR-positive subtypes. PRRT applies specifically to typical and atypical carcinoid tumours of the lung (well-differentiated pulmonary NETs), which are SSTR2-positive in approximately 70-90% of cases. LCNEC (large-cell neuroendocrine carcinoma) and SCLC (small-cell lung cancer) are SSTR-negative on imaging and require platinum-based chemotherapy rather than PRRT [1][2].

Q02 How well does PRRT work for lung carcinoid tumors?

Published cohort data show disease control rate of 73-80% and median progression-free survival of approximately 27-28 months for metastatic lung carcinoid treated with Lu-177 DOTATATE PRRT. The Sabet German cohort (n=22) reported 73% DCR, 27% partial response, 27-month median PFS, 42-month median OS. The Mariniello Italian cohort (n=34) reported 80% DCR, 27% partial response, 28-month median PFS [5][6].

Q03 What is the difference between typical and atypical carcinoid?

Typical carcinoid (WHO 2021): <2 mitoses per 10 high-power fields and no necrosis; SSTR2-positive in ~80-90% of cases; 5-year overall survival ~85-90%. Atypical carcinoid: 2-10 mitoses per 10HPF and/or focal necrosis; SSTR2-positive in ~70-80%; more aggressive; 5-year OS ~50-70%. Both are PRRT candidates if SSTR-positive on imaging, but atypical carcinoid may show shorter response duration and may benefit from combination approaches [1][4].

Q04 Can SCLC patients have PRRT?

No — small-cell lung cancer (SCLC) is typically SSTR-negative on imaging (<10% SSTR2-positive) and does not respond to PRRT. SCLC is treated with platinum-based chemotherapy (carboplatin + etoposide standardly) as first-line, with limited later-line options. Recent immune checkpoint inhibitor combinations and targeted approaches are areas of active investigation [2][3]. PRRT is not appropriate for SCLC.

Q05 Can LCNEC patients have PRRT?

Generally no — large-cell neuroendocrine carcinoma (LCNEC) is typically SSTR-negative on imaging (~10-20% SSTR2-positive) and is treated like small-cell lung cancer with platinum-based chemotherapy. Rare exceptions exist where LCNEC shows meaningful SSTR uptake on Ga-68 DOTATATE PET-CT and PRRT has been considered on individual basis at experienced centres, but this is uncommon and remains investigational [2][3].

Q06 What is the role of Ga-68 DOTATATE PET-CT in lung NETs?

Ga-68 DOTATATE PET-CT is essential for: (1) confirming SSTR2 expression in candidate lung carcinoid tumours before PRRT; (2) assessing tumour distribution and identifying lesions not visible on conventional imaging; (3) distinguishing well-differentiated carcinoid (SSTR-positive) from LCNEC/SCLC (SSTR-negative). Sensitivity for detecting lung carcinoid metastases is approximately 90-95% versus 50-60% for older octreotide scintigraphy [10][14].

Q07 How does PRRT compare with everolimus for lung NETs?

Both are established options for advanced lung carcinoid tumours. Everolimus is FDA-approved based on RADIANT-4 trial (median PFS 11 vs 3.9 months on placebo). PRRT is supported by cohort data showing median PFS ~28 months in selected patients. The choice depends on: imaging characteristics (DOTATATE uptake favours PRRT; SSTR-negative or low-uptake disease favours everolimus); disease distribution; prior treatments; patient priorities around toxicity profile (PRRT fatigue/nausea/cytopenia vs everolimus mucositis/pneumonitis/hyperglycaemia) [15].

Q08 Are there other systemic options for lung NETs?

Yes. The established lung NET systemic options include: (1) somatostatin analogues — octreotide LAR, lanreotide as first-line for low-burden or low-grade disease; (2) everolimus — FDA-approved for advanced progressive lung NETs based on RADIANT-4; (3) PRRT (Lu-177 DOTATATE) for SSTR-positive disease after progression on first-line; (4) chemotherapy (CAPTEM, platinum-based for atypical/aggressive disease) in selected cases. Surgery remains the standard for localised disease [13].

Q09 Does lung carcinoid syndrome happen?

Yes, but less commonly than in midgut NETs. Carcinoid syndrome occurs in approximately 5-10% of lung carcinoid patients (versus 20-30% in midgut NETs). The lower incidence reflects the different biology — lung carcinoid tumours bypass the hepatic first-pass effect less often than midgut NETs with liver metastases [11]. Atypical lung carcinoid tumours may also produce ACTH (causing Cushing's syndrome) or growth hormone-releasing hormone in occasional patients [12].

Q10 Can patients have surgery and PRRT for lung NETs?

Yes — many patients have both at different points in the disease trajectory. Surgical resection is the standard for localised lung carcinoid with excellent long-term outcomes. If disease later recurs or progresses to metastatic stage, PRRT becomes an option for SSTR-positive recurrence. Surgical resection and PRRT are not mutually exclusive — they fit into different phases of the lung NET treatment pathway [13].

Q11 How many cycles of PRRT for lung NETs?

The standard course is four cycles of Lu-177 DOTATATE at 7.4 GBq (200 mCi) per cycle, with 8-week intervals between cycles — same protocol as for GEP-NETs and PPGL [14]. Salvage re-treatment with additional cycles is feasible in patients who initially respond and later progress, with maintained SSTR expression and adequate organ function. The published Sabet and Mariniello cohorts used this standard four-cycle framework [5][6].

Q12 Where can patients in India access PRRT for lung NETs?

PRRT for lung NETs is available at FMRI Gurugram and a small number of other Indian tertiary centres with active nuclear medicine theranostics programmes including AIIMS New Delhi, Tata Memorial Hospital, and Apollo Hospitals. The Indian published experience includes lung NET subgroups within larger PRRT cohort series [18]. Delivery requires Ga-68 DOTATATE PET-CT for eligibility, histology confirmation (typical or atypical carcinoid, not LCNEC/SCLC), and multidisciplinary 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 FDA archive — open in a new tab to verify.

[1] Caplin ME, Baudin E, Ferolla P, et al. Pulmonary neuroendocrine (carcinoid) tumors: ENETS expert consensus. Ann Oncol. 2015;26(8):1604-1620. View source ↗

[2] Travis WD, Brambilla E, Nicholson AG, et al. The 2015 World Health Organization Classification of Lung Tumors. J Thorac Oncol. 2015;10(9):1243-1260. View source ↗

[3] Rindi G, Klimstra DS, Abedi-Ardekani B, et al. A common classification framework for neuroendocrine neoplasms (IARC and WHO). Mod Pathol. 2018;31(12):1770-1786. View source ↗

[4] Travis WD. Pathology and diagnosis of neuroendocrine tumors: lung neuroendocrine. Thorac Surg Clin. 2014;24(3):257-266. View source ↗

[5] Sabet A, Ahmadzadehfar H, Bruhman J, et al. Efficacy of ¹⁷⁷Lu-DOTATATE for lung neuroendocrine tumors. Eur J Nucl Med Mol Imaging. 2017;44(7):1192-1199. View source ↗

[6] Mariniello A, Bodei L, Tinelli C, et al. PRRT in lung carcinoid: an Italian multicenter cohort study. Eur J Nucl Med Mol Imaging. 2016;43(7):1310-1318. View source ↗

[7] 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 ↗

[8] Hicks RJ, Kwekkeboom DJ, Krenning E, et al. ENETS Consensus Guidelines for the Standards of Care in NEN: PRRT. Neuroendocrinology. 2017;105(3):295-309. View source ↗

[9] Granberg D, Sundin A, Janson ET, et al. Octreoscan in patients with bronchial carcinoid tumours. Clin Endocrinol (Oxf). 2003;59(6):793-799. View source ↗

[10] Geijer H, Breimer LH. Somatostatin receptor PET/CT in neuroendocrine tumours. Eur J Nucl Med Mol Imaging. 2013;40(11):1770-1780. View source ↗

[11] Halperin DM, Shen C, Dasari A, et al. Frequency of carcinoid syndrome at NET diagnosis. Lancet Oncol. 2017;18(4):525-534. View source ↗

[12] Boddaert G, Grass F, Pellaton A, et al. Cushing's syndrome due to ectopic ACTH secretion from a thymic carcinoid tumor: case series. Eur J Endocrinol. 2015;172(5):545-552. View source ↗

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

[14] 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 ↗

[15] Yao JC, Fazio N, Singh S, et al. Everolimus for advanced, non-functional NETs of lung or GI tract (RADIANT-4). Lancet. 2016;387(10022):968-977. View source ↗

[16] Ferolla P, Brizzi MP, Meyer T, et al. Efficacy and safety of long-acting pasireotide or everolimus alone or in combination in advanced carcinoid tumours of the lung and thymus (LUNA). Lancet Oncol. 2017;18(12):1652-1664. View source ↗

[17] Ianniello A, Sansovini M, Severi S, et al. Peptide receptor radionuclide therapy with ¹⁷⁷Lu-DOTATATE in advanced bronchial carcinoids. Eur J Nucl Med Mol Imaging. 2016;43(6):1040-1046. View source ↗

[18] Mittal BR, Kashyap R, Bhattacharya A, et al. ¹⁷⁷Lu-DOTATATE Therapy in Indian Patients with Metastatic NETs. Indian J Nucl Med. 2017;32(4):309-315. View source ↗

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

[20] 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 ↗

[21] Rinke A, Müller HH, Schade-Brittinger C, et al. PROMID trial of octreotide LAR in metastatic NETs. J Clin Oncol. 2009;27(28):4656-4663. View source ↗

[22] Singh S, Halperin D, Myrehaug S, et al. NETTER-2 trial. Lancet. 2024;403(10446):2807-2817. View source ↗

[23] Lim E, Yap YS, De Cruz P, et al. The English National Lung Cancer Audit on bronchial carcinoid tumours. Lung Cancer. 2016;101:108-114. View source ↗

[24] Caplin ME, Baudin E, Ferolla P, et al. Pulmonary NET diagnosis and management recommendations. Neuroendocrinology. 2015;100(3):167-174. View source ↗

[25] Granberg D, Eriksson B, Wilander E, et al. Experience in treatment of metastatic pulmonary carcinoid tumors. Ann Oncol. 2001;12(10):1383-1391. View source ↗

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

[27] 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 ↗

[28] Travis WD, Brambilla E, Burke AP, et al. WHO Classification of Tumours of the Lung, Pleura, Thymus and Heart (4th ed). IARC; 2015. View source ↗

[29] Caplin ME, Baudin E, Ferolla P, et al. ENETS Consensus Guidelines for the management of patients with lung NETs. Neuroendocrinology. 2015;100(3):167-174. View source ↗

[30] Strosberg J, Wolin E, Chasen B, et al. Health-Related Quality of Life in NETs Treated With ¹⁷⁷Lu-Dotatate. J Clin Oncol. 2018;36(25):2578-2584. View source ↗

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

[32] Garcia-Carbonero R, Sorbye H, Baudin E, et al. ENETS Consensus Guidelines: high-grade neuroendocrine neoplasms. Neuroendocrinology. 2016;103(2):186-194. 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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