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Interventional Oncology · Intra-arterial Therapy

Neuroendocrine Tumor (NET) / Carcinoid — Liver-Directed Therapy

Intra-arterial embolization (TAE, cTACE, DEB-TACE) and radioembolization (Y-90) for hepatic metastases from gastroenteropancreatic NETs, carcinoid tumors, and pancreatic NETs. Mandatory octreotide pretreatment to prevent carcinoid crisis.

Sedation
Moderate / MAC
Key Risk
Carcinoid Crisis · PES · Liver Failure
Antibiotics
Prophylactic (gram-neg / anaerobe)
Follow-up
Chromogranin A · CT/MRI 4–6 wks · Contralateral lobe
1

Indications & Patient Selection

GEP-NET, carcinoid, pNET — hepatic-dominant disease criteria

Indications for Liver-Directed Therapy

  • NET types: gastroenteropancreatic (GEP-NET), carcinoid (ileum/appendix primary), pancreatic NET (pNET) — all frequently metastasize to liver
  • Hepatic-dominant disease — liver mets as primary disease burden
  • Tumor burden ≤75% liver replacement by tumor
  • Well-differentiated (Ki-67 <20%) — G1 or G2 NET
  • Progressive on somatostatin analogs (SSAs) — octreotide LAR, lanreotide
  • Unresectable disease — bilobar, multifocal, or medically inoperable
  • Symptomatic hormonal syndrome — carcinoid syndrome (flushing, diarrhea, bronchospasm) from serotonin/substance P; LDT provides hormonal debulking

Contraindications

  • Ki-67 >20% (G3 NET) — poor response to LDT; systemic therapy preferred
  • Child-Pugh C — inadequate hepatic reserve for embolization
  • >75% liver replacement by tumor — post-embolization liver failure risk
  • Portal vein thrombosis — especially main portal vein (relative for lobar branch PVT)
  • Active biliary infection / cholangitis
  • Prior biliary enteric anastomosis (high hepatic abscess risk post-TACE)

Carcinoid Syndrome — Crisis Risk

  • Classic triad: flushing, diarrhea, bronchospasm from excess serotonin and substance P release
  • Carcinoid crisis: life-threatening hemodynamic collapse triggered by anesthesia, contrast, or tumor manipulation
  • Mandatory pre-treatment: octreotide acetate 250–500 mcg IV 1h before procedure
  • Continue octreotide infusion during procedure and for 12h post-procedure; no exceptions
  • Anesthesia standby strongly recommended for carcinoid patients

Workup / Staging

  • CT chest/abdomen/pelvis — assess hepatic tumor burden, extrahepatic disease, vascular anatomy
  • DOTATATE PET-CT — somatostatin receptor (SSR) status; predicts response to SSA therapy and PRRT; positive scan = favorable LDT candidate
  • Chromogranin A (CgA) — baseline tumor marker; 50% reduction = objective response; rise = progression
  • 24h urine 5-HIAA — baseline for carcinoid; monitor response post-LDT
  • LFTs, INR, Cr, CBC — hepatic reserve assessment
  • Echocardiogram if clinical concern for carcinoid heart disease (right-sided valvulopathy)

Best Response Predictors

Well-differentiated (G1/G2) • Somatostatin receptor positive (DOTATATE PET+) • Hypervascularity on diagnostic angiogram • Lower hepatic tumor burden (<50% liver replacement) • Child-Pugh A/B7

2

Pre-Procedure Checklist

Octreotide mandatory · embolic selection · angio suite prep
!
CARCINOID CRISIS PREVENTION — MANDATORY
Octreotide acetate 250–500 mcg IV must be administered 1 hour before every liver-directed therapy session. Continue as IV infusion (50 mcg/h) during procedure and for 12 hours post-procedure. Failure to pre-treat risks hemodynamic collapse, severe bronchospasm, and death.

Standard Setup

  • Biplane or single-plane angiography suite with CBCT capability
  • 2.4 Fr microcatheter system (e.g., Progreat, Renegade) + 4–5 Fr guiding catheter (Cobra, SIM1)
  • Nonionic iodinated contrast for hepatic arteriogram and CBCT
  • Prophylactic antibiotics: ciprofloxacin 400 mg IV or ampicillin-sulbactam (cover gram-neg / anaerobes)
  • Antiemetics: ondansetron 4 mg IV + dexamethasone 8 mg IV pre-procedure
  • Anesthesia on standby (carcinoid crisis); establish IV access ×2

Embolic Options by Tumor Type

  • Bland TAE (carcinoid): Embosphere 100–300 µm — TAE = TACE for carcinoid; chemo does not add benefit over embolization alone for midgut carcinoid
  • cTACE (pNET): Lipiodol + doxorubicin 50 mg (or mitomycin C + cisplatin cocktail)
  • DEB-TACE (pNET): LC Bead 100–300 µm loaded with doxorubicin 50 mg; more relevant for pNET than midgut carcinoid
  • TARE (Y-90): preferred for bilobar or large-burden disease (G1/G2); TheraSphere glass microspheres 120–150 Gy preferred for NET
  • pNET specialty: streptozocin-based TACE protocols at specialized centers
  • Do not hold SSAs (octreotide LAR, lanreotide) perioperatively
Octreotide 250–500 mcg IV given 1h before procedure. IV infusion running at 50 mcg/h. Continuation plan for 12h post-procedure confirmed.
DOTATATE PET-CT reviewed. SSR status confirmed; tumor burden quantified; bilobar vs unilobar involvement noted.
Chromogranin A and 24h urine 5-HIAA documented for baseline response monitoring.
LFTs, INR, CBC, Cr reviewed. Child-Pugh A or B confirmed. Bilirubin <3 mg/dL. No active biliary obstruction.
Embolic strategy selected and confirmed (TAE vs DEB-TACE vs Y-90). One-lobe-at-a-time plan for bilobar disease.
Prophylactic antibiotics administered. Antiemetics given. Anesthesia/MAC notified of carcinoid crisis risk.
Consent obtained. Risks discussed: carcinoid crisis, post-embolization syndrome, hepatic abscess, liver failure, cholecystitis. Sequential lobar treatment plan explained to patient.
3

Relevant Anatomy

Hypervascular NET mets · hepatic artery variants · carcinoid heart disease

NET Hepatic Vascular Physiology

  • NETs are HYPERVASCULAR — tumor blood supply is 100% arterial; normal hepatic parenchyma is 75–80% portal venous supply
  • This differential vascular supply enables selective intra-arterial therapy: embolizing arterial supply preferentially targets tumor while sparing normal parenchyma
  • Intense tumor blush on hepatic arteriogram; "sunburst" or "spoke-wheel" pattern on DSA — highly characteristic of NET mets
  • Bilobar disease in 70–80% of patients with NET liver metastases; sequential lobar treatment required

Hepatic Artery Variants

  • Standard anatomy (55–60%): proper hepatic artery from celiac trunk → right + left hepatic arteries
  • Replaced right hepatic artery (rRHA) from SMA (15–20%): always perform SMA injection to identify and exclude; can be missed on celiac arteriogram alone
  • Replaced left hepatic artery from left gastric artery (10–15%): identify on celiac arteriogram
  • Cystic artery: typically arises from right hepatic artery; must identify and protect before right lobe embolization to prevent acute cholecystitis
  • Right gastric artery: may arise from proper hepatic or LHA; identify and protect before embolization

CBCT for Treatment Planning

  • Cone beam CT (CBCT) identifies lesions not seen on 2D DSA; essential for complete treatment planning
  • Reveals tumor supply from multiple feeding arteries; guides superselective catheterization
  • Confirms cystic artery and non-target vessel location before embolization
  • Post-treatment CBCT confirms Lipiodol deposition (cTACE) or microbead distribution (DEB-TACE)

Carcinoid Heart Disease

  • Right-sided valvular disease (tricuspid regurgitation, pulmonary stenosis) from chronic hepatic serotonin output
  • Serotonin inactivated in lung → left heart spared; right heart exposed from portal/hepatic venous drainage
  • Obtain echocardiogram pre-procedure if clinical concern (murmur, right heart failure symptoms, elevated 5-HIAA)
  • Carcinoid heart disease increases anesthetic and hemodynamic risk; coordinate with cardiology for high-risk cases
4

Step-by-Step Technique

Bland TAE / DEB-TACE for carcinoid · Y-90 for NET · modality comparison

Part A: Bland TAE or DEB-TACE for Carcinoid

1

Octreotide Pretreatment & Anesthesia Prep

Confirm octreotide 500 mcg IV administered 1h prior. Anesthesia on standby or actively present (carcinoid crisis can cause sudden hemodynamic collapse). Establish two large-bore IV lines. Baseline BP, HR documented. Antiemetics and antibiotics administered.
2

Common Femoral Artery Access & Diagnostic Arteriogram

Standard CFA access via Seldinger technique; 5 Fr sheath. Celiac arteriogram with 5 Fr Cobra or SIM1 catheter to identify main hepatic artery anatomy, tumor supply, and presence of replaced vessels. Perform SMA injection to exclude replaced right hepatic artery. Note the intense tumor blush characteristic of NET metastases.
3

CBCT for Tumor Mapping

Perform cone beam CT (DynaCT or equivalent) from proper hepatic artery position. Map tumor blush, identify non-target arteries (cystic artery, right gastric artery, falciform artery). Identify lesions not visible on 2D DSA. Use CBCT findings to plan superselective catheterization strategy. Document all tumor-supplying segmental vessels.
4

Superselective Catheterization

Advance 2.4 Fr microcatheter (Progreat, Renegade, Cantata) coaxially through guiding catheter to the tumor-supplying artery. Target the most distal selective position achievable that encompasses tumor supply while protecting uninvolved parenchyma. For right lobe: confirm cystic artery is NOT in the planned embolization field (reposition if needed). Repeat DSA from microcatheter position to confirm superselective tumor supply.
5A

Bland TAE (for midgut carcinoid)

Inject Embosphere microspheres 100–300 µm (or equivalent calibrated microspheres) slowly under fluoroscopic guidance until stasis in the tumor-supplying artery. Inject in 0.5–1 mL aliquots with small-volume contrast to assess flow. Endpoint: stasis of contrast in the feeding artery with cessation of tumor blush. Do not embolize to stasis in main hepatic artery — superselective position protects liver parenchyma.
5B

DEB-TACE (for pNET or selected NET)

Inject doxorubicin-loaded LC Bead 100–300 µm (50 mg doxorubicin loaded) slowly under fluoroscopy. Inject in 1 mL aliquots. Endpoint: stasis or near-stasis in tumor-supplying artery. Flush catheter with 5 mL normal saline post-injection. Post-treatment CBCT to confirm bead distribution within tumor. DEB-TACE provides sustained drug release; chemotherapy adds benefit over embolization alone for pNET but not carcinoid.
6

One-Lobe-at-a-Time Protocol

Treat one hepatic lobe per session. For bilobar disease: treat the dominant lobe at the first session. Schedule contralateral lobe embolization 4–6 weeks later after confirming hepatic recovery (LFTs normalized, patient tolerating first treatment). Simultaneous bilobar embolization significantly increases post-embolization liver failure risk and is generally avoided except in Y-90.
7

Post-Procedure Admission & Monitoring

Admit for 1 night minimum. Continue octreotide infusion overnight (prevents delayed carcinoid crisis). Monitor LFTs, BMP, CBC at 6h and morning. Antiemetics scheduled. Pain management with NSAIDs (post-embolization syndrome). Discharge day 1–2 if afebrile, tolerating PO, pain controlled.

Part B: Y-90 Radioembolization for NET

1

Pre-Treatment Mapping Arteriogram + MAA Dose Planning

Separate session (1–2 weeks before treatment): diagnostic hepatic arteriogram + MAA (macroaggregated albumin) injection from planned treatment position. Nuclear medicine: technetium-99m MAA SPECT/CT to calculate lung shunt fraction (LSF). LSF >20% requires dose reduction or contraindication. Document extrahepatic shunting (GI, gastric). Mark prophylactic coil embolization of gastroduodenal or other non-target vessels as needed.
2

Y-90 Dose Calculation — NET Protocol

Well-differentiated G1/G2 NETs tolerate and respond to higher absorbed doses. TheraSphere glass microspheres preferred for NET (120–150 Gy target dose) per Kennedy et al. and institutional protocols. Calculate dose using MIRD or partition model based on tumor-to-normal liver ratio on MAA SPECT. For bilobar disease: Y-90 allows whole-liver treatment in a single session or staged lobar dosing — advantage over TACE.
3

Y-90 Treatment Day

Octreotide pre-treatment as for TACE. Repeat arteriogram to confirm no interval vascular changes. Advance microcatheter to treatment position (lobar or segmental per plan). Administer Y-90 microsphere vial per institutional radiation safety protocol. Flush catheter per protocol. Post-treatment Bremsstrahlung SPECT/CT (or PET if glass microspheres for 90Y PET) to confirm distribution within target and absence of extrahepatic deposition.
4

Post-Y-90 Follow-up

Same-day or next-morning discharge if no complications. LFTs at 2–4 weeks. Imaging response (CT or MRI) at 3 months. Chromogranin A at 4–6 weeks. Contralateral lobe Y-90 or observation per response. PRRT (peptide receptor radionuclide therapy, Lu-177 DOTATATE) remains a complementary or sequential systemic option for DOTATATE-positive patients.

Modality Comparison: TAE vs DEB-TACE vs Y-90 for NET Liver Metastases

FeatureBland TAEDEB-TACEY-90 Radioembolization
Best forMidgut carcinoid; hypervascular NETpNET; where chemo adds benefitBilobar / large-burden G1–G2 NET
Radiologic response rate50–90% (hypervascular)50–80%50–60% (Rhee et al. AJR 2008)
Carcinoid syndrome controlExcellent (70–90%)ExcellentGood (60–70%)
Bilobar treatmentSequential; 4–6 wk apartSequential; 4–6 wk apartPossible same session or sequential
Post-embolization syndromeCommon; 1–3 day admissionCommon; 1–3 day admissionMild; often outpatient
Parenchymal preservationModerate (ischemic)Moderate (ischemic)Superior (radiation effect)
Repeat treatmentsYes; re-treat at progressionYes; re-treat at progressionLimited by cumulative radiation dose
Key referenceKress O et al. Gut 2003Petre EN et al. Thieme 2016Kennedy AS et al. IJROBP 2008; Rhee TK et al. AJR 2008

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5

Angiographic Landmarks

DSA patterns · CBCT planning · non-target vessel identification

NET / Carcinoid DSA Appearance

  • Intense hypervascularity — NET metastases are among the most hypervascular hepatic tumors on DSA; strong arterial blush visible even on non-selective celiac arteriogram
  • "Sunburst" or "spoke-wheel" pattern — radiating feeding vessels converging on a hypervascular tumor nodule; pathognomonic of NET mets on DSA
  • Multiple discrete tumor nodules with individual arterial pedicles; each requires superselective targeting for complete treatment
  • Early venous opacification (arteriovenous shunting) in highly vascular lesions; accounts for risk of Y-90 lung shunting

Non-Target Vessel Identification

  • Cystic artery: arises from right hepatic artery in 90% of cases; identify on DSA as small vessel to gallbladder before right lobe embolization; ensure microcatheter is distal to takeoff; inadvertent embolization causes acute cholecystitis (5–10%); consider prophylactic cholecystectomy if repeated right lobe TACE planned
  • Right gastric artery: may arise from LHA or proper hepatic artery; identify on initial arteriogram; protect from non-target embolization (gastric mucosal injury)
  • Falciform artery: from segment 3/4 supply; can be non-target for left lobe embolization; identify on CBCT
  • Phrenic arteries: hepatophrenic anastomoses may supply dome lesions; evaluate on CBCT

CBCT Role in NET Treatment Planning

Cone beam CT performed from the treatment catheter position before embolization is essential for NET liver-directed therapy. CBCT reveals NET lesions that are occult on 2D DSA due to overlapping vessels or suboptimal 2D projections. It confirms the tumor supply map from the current catheter position, identifies non-target vessels (particularly the cystic artery) relative to the embolization territory, and serves as the definitive roadmap for the treatment session. Post-treatment CBCT confirms Lipiodol uptake (cTACE) or microsphere distribution (DEB-TACE) within the target zone.

6

Troubleshooting

Intraoperative problems and solutions
EMERGENCY

Carcinoid Crisis (Intraoperative)

Severe bronchospasm, hemodynamic instability (hypotension, flushing, tachycardia or bradycardia) during or immediately after embolization. Immediate management: (1) Stop procedure; (2) Octreotide 500 mcg IV bolus immediately; (3) Call anesthesia if not present; (4) IV fluid bolus 500 mL; (5) Vasopressors (norepinephrine or phenylephrine) for refractory hypotension; (6) Bronchodilators (albuterol) for bronchospasm; supportive care. Resume procedure only after stabilization if octreotide infusion confirmed running. Prevention is far superior to rescue.

Hepatic

Biliary Injury / Bile Duct Stricture

Bile duct stricture from TACE (particularly cTACE or DEB-TACE) results from ischemia of peribiliary capillary plexus. Risk is significantly increased with bilobar simultaneous embolization. Prevention: strict one-lobe-at-a-time protocol; superselective technique to limit normal parenchyma ischemia; avoid embolization in patients with prior biliary enteric anastomosis (extremely high abscess/biloma risk). Management: PTBD if biliary obstruction develops; MRCP to characterize stricture.

Hepatic

Post-Embolization Liver Failure

Acute hepatic decompensation following LDT: rising bilirubin, coagulopathy, encephalopathy. Risk factors: Child-Pugh B8+ or C, >50% tumor replacement, bilobar simultaneous treatment, prior hepatic surgery. Management: IV albumin, fresh frozen plasma, lactulose for encephalopathy; ICU monitoring; hepatology consult. Prevention: strict patient selection (Child-Pugh A–B7 only), one-lobe-at-a-time, adequate pre-treatment LFTs confirmed.

Oncologic

Inadequate Tumor Response

G3 NET (Ki-67 >20%) responds poorly to liver-directed embolization. If treatment was performed for G3 NET and response is inadequate, transition to systemic therapy: everolimus (mTOR inhibitor) + SSA, temozolomide-capecitabine, or platinum-based chemotherapy. For G1/G2 NET with inadequate response to TACE, consider switching to Y-90 (different mechanism) or PRRT if DOTATATE PET positive. Rising chromogranin A at 4–6 weeks without improvement in symptoms or imaging = progression; reassess treatment strategy with multidisciplinary tumor board.

Technical

Cystic Artery Included in Embolization Field

If post-embolization DSA or CBCT demonstrates cystic artery territory was included in the embolization field, monitor closely for acute cholecystitis (RUQ pain, fever, leukocytosis, elevated alk phos within 24–72h). Obtain RUQ ultrasound if symptoms develop. Mild cases: supportive management, antibiotics. Severe / gangrenous: surgery consult. Note: prophylactic cholecystectomy may be considered before a planned repeat right lobe TACE program to eliminate this risk.

7

Complications

NET-specific risks · post-embolization syndrome · hepatic complications

NET-Specific Complications

  • Carcinoid crisis (1–5%) — life-threatening; hemodynamic collapse, severe bronchospasm; almost entirely preventable with octreotide pretreatment; treat with octreotide 500 mcg IV bolus + vasopressors
  • Post-embolization syndrome — nearly universal; nausea, fever, fatigue, RUQ pain, malaise; expect 2–5 days; manage with antiemetics, NSAIDs, adequate IV hydration; discharge day 1–2
  • Hormonal flare — transient worsening of carcinoid symptoms (flushing, diarrhea) in first 24–48h post-embolization from tumor lysis and serotonin release; managed with octreotide infusion continuation

General TACE Complications

  • Hepatic abscess (1–2%) — especially after prior biliary interventions (sphincterotomy, stenting, biliary enteric anastomosis); fever, leukocytosis, LFT rise at 1–2 weeks; CT diagnosis; prophylactic antibiotics peri-procedure; drain if >4 cm or septated; high morbidity in this population
  • Cholecystitis (5–10%) — if cystic artery inadvertently embolized; RUQ pain + fever + ultrasound findings; antibiotics for mild cases; surgery if gangrenous or no response; plan prophylactic cholecystectomy before repeat right lobe TACE program
  • Biliary stricture / biloma (rare) — peribiliary ischemia; PTBD if obstruction develops; more common with non-selective or repeated embolization
  • Liver failure (rare with proper selection) — avoid bilobar simultaneous embolization; respect Child-Pugh selection criteria
  • Non-target embolization — gastric ulceration (right gastric); pneumonitis (phrenic); prevented by careful DSA review and superselective catheterization
8

Critical Pearls

High-yield decision points and practice-defining principles
Octreotide before EVERY procedure — no exceptions. Carcinoid crisis is unpredictable and can occur even in patients who have tolerated prior embolizations. Administer octreotide acetate 500 mcg IV 1h before procedure, maintain continuous IV infusion (50 mcg/h) during the procedure, and continue for 12h post-procedure. This protocol applies to ALL liver-directed treatments in patients with carcinoid tumor or functional NET, regardless of symptom status at baseline.
TAE = TACE for carcinoid — chemotherapy does not add benefit. For midgut carcinoid (ileum/appendix primary), bland embolization (TAE with Embosphere 100–300 µm) achieves equivalent tumor response and hormonal control to chemoembolization. This is because carcinoid mets are so hypervascular that ischemia alone is the dominant therapeutic mechanism. Adding doxorubicin or other chemotherapy does not improve outcomes in carcinoid but does increase toxicity. DEB-TACE is more relevant for pNET where cytotoxic benefit has been demonstrated.
DOTATATE PET is essential for treatment strategy planning. DOTATATE PET-CT identifies somatostatin receptor (SSR) expression. SSR-positive lesions (DOTATATE+) respond better to SSA therapy (octreotide LAR, lanreotide) AND to PRRT (Lu-177 DOTATATE = systemic radiotherapy). For DOTATATE-positive patients, coordinate LDT with systemic oncology to determine whether PRRT or LDT should be sequenced first. DOTATATE-negative (dedifferentiated) lesions are often G3 and respond poorly to both SSA and LDT — identify early to avoid futile liver-directed procedures.
Treat one lobe at a time — ablate and protect the other side. Sequential lobar embolization (4–6 weeks apart) vs simultaneous bilobar embolization significantly reduces post-embolization liver failure risk. Treat the dominant (more diseased) lobe first; allow LFTs to normalize before treating the contralateral lobe. This is especially critical for Child-Pugh B patients and those with >50% tumor burden. The liver's regenerative capacity between sessions is a key safety mechanism. Exception: Y-90 can treat both lobes in a single session with lower hepatotoxicity due to its primarily radiobiologic mechanism.
Y-90 is preferred for large-burden or bilobar G1/G2 NET. Well-differentiated (G1/G2) NETs with >25% liver replacement respond better to Y-90 radioembolization than TACE because Y-90 preserves more hepatic parenchyma (radiobiologic effect rather than ischemic necrosis). Rhee et al. (AJR 2008) demonstrated 50–60% radiologic response rates with durable hormonal control. TheraSphere glass microspheres at 120–150 Gy target dose is the preferred Y-90 formulation for NET based on the ability to deliver higher absorbed dose safely. Kennedy et al. (IJROBP 2008) reported 90-day hormonal response in 50% of patients treated with Y-90.
Monitor chromogranin A for treatment response. A 50% or greater reduction in serum chromogranin A (CgA) at 4–6 weeks post-LDT constitutes an objective biochemical response. CgA decline often precedes imaging response by weeks. For carcinoid, 24h urine 5-HIAA is also monitored. Rising CgA at follow-up indicates tumor progression or resistance, and should trigger reassessment of treatment strategy (switch modality, add systemic therapy, PRRT consideration). CgA monitoring is cost-effective and does not require repeat cross-sectional imaging at the 1-month time point.
9

References & Resources

Primary sources and related procedures

Key Concepts

  • PRRT (peptide receptor radionuclide therapy) — Lu-177 DOTATATE (Lutathera); systemic radiolabeled SSA; complements LDT for DOTATATE-positive NET; NETTER-1 trial demonstrated PFS benefit
  • Everolimus + octreotide LAR (RADIANT-3): systemic option for progressive pNET
  • Ki-67 grading: G1 (<3%), G2 (3–20%), G3 (>20%); G3 = poor LDT candidate
  • Child-Pugh score: A (5–6 pts) = best candidates; B7 = acceptable; B8+ / C = avoid LDT

Primary References

  • Petre EN, Brown KT, Sofocleous CT. Chapter 9: Hepatic Artery Embolization for Neuroendocrine Tumor Metastases. In: Faintuch S, Salazar GM, eds. Interventional Oncology: A Practical Guide for the Interventional Radiologist. Thieme; 2016. [Content sourced from Prologo JD, Ray CE Jr., eds. Advanced Pain Management in Interventional Radiology. Thieme; 2024. Ch. 9.]
  • Kress O, Wagner HJ, Wied M, et al. Transarterial chemoembolization of advanced liver metastases of gastroenteropancreatic tumors — a promising palliative approach. Gut. 2003;52(11):1636–1639.
  • Kennedy AS, Dezarn WA, McNeillie P, et al. Radioembolization for unresectable neuroendocrine hepatic metastases using resin 90Y-microspheres: early results with tumor dosimetry. Int J Radiat Oncol Biol Phys. 2008;72(5):1559–1566.
  • Rhee TK, Lewandowski RJ, Liu DM, et al. 90Y radioembolization for metastatic neuroendocrine liver tumors: preliminary results from a multi-institutional experience. Ann Surg. 2008;247(6):1029–1035. / Rhee TK et al. AJR Am J Roentgenol. 2008.
  • Strosberg JR, El-Haddad G, Wolin E, et al. Phase 3 trial of 177Lu-Dotatate for midgut neuroendocrine tumors (NETTER-1). N Engl J Med. 2017;376(2):125–135.
  • Yao JC, Shah MH, Ito T, et al. Everolimus for advanced pancreatic neuroendocrine tumors (RADIANT-3). N Engl J Med. 2011;364(6):514–523.