Transarterial Treatment of Liver Metastatic Neuroendocrine Tumors - Endovascular Today (2023)

Neuroendocrine tumors (NETs) arise from neural and endocrine organs throughout the body, most commonly the gastrointestinal system and pancreas. The World Health Organization classifies well-differentiated gastroenteropancreatic NETs into low grade and intermediate grade, and most poorly differentiated tumors are considered high grade, based on mitotic count/Ki-67 proliferative index.1 Indolent and well-differentiated tumors of the digestive system are traditionally called carcinoid and pancreatic neuroendocrine (islet cell) tumors. Well-differentiated tumors are often indolent, even in the setting of metastatic disease, and thus, are labeled “cancers in slow motion.”2

Clinical presentation of NETs is commonly in the setting of metastatic disease, resulting from tumor biochemical activity or bulk symptoms. Approximately one-third of pancreatic NETs secrete hormones producing a clinical syndrome; additionally, patients with carcinoid tumors may develop carcinoid syndrome, usually after the development of hepatic metastases.3 Symptoms of hormonal excess from pancreatic NETs and carcinoid tumors are often well controlled with somatostatin analogs, specifically, octreotide and lanreotide.3 Moreover, treatment of well-differentiated tumors with these analogs lengthens time-to-tumor progression (TTP) in randomized controlled trials (RCTs).4,5 Newer agents, including sunitinib and everolimus, also improve progression-free survival of pancreatic NETs over placebo in RCTs.6,7

Along with tumor grade, liver metastases are a critical prognostic factor occurring in approximately 40% of patients over the course of their disease.8 Systemic chemotherapy has limited success in treating patients with low-grade liver metastatic neuroendocrine tumors (mNETs), and as such, a variety of local therapy options are employed for controlling symptoms and tumor growth.9 Surgical management of liver mNETs remains the only potentially curative option with 5-year survival rates of 60% to 80%; however, only approximately 10% of patients are candidates for curative resection.10-12 Interestingly, recurrence after surgical management, including the use of intraoperative ablation, is nearly universal, as 94% of patients developed recurrent disease at 5 years in a recent multi-institutional study.10 Given this high recurrence rate, the true curative role of surgery is debatable.

Transarterial therapy is a potent local therapeutic option for liver mNET, especially for low-grade tumors with hormonal symptoms or tumor progression on long-acting octreotide. These tumors are typically hypervascular with predominant hepatic arterial supply, as compared to the background liver, which is mostly supplied by the portal vein. Therefore, transarterial therapy is concentrated in the tumor, which can greatly limit hepatic and systemic toxicities. Intra-arterial therapy options are transarterial embolization (TAE), transarterial chemoembolization (TACE), and radioembolization (yttrium-90 [Y-90]). These catheter-based therapies demonstrate effectiveness in both tumor control and symptom relief. A case example of each is presented, with review of salient patient selection considerations and outcomes data, followed by a brief discussion of special considerations.


Targeted embolization of the hepatic artery, with a variety of particulate embolics, produces tumoral ischemic necrosis while the surrounding liver is perfused by the portal vein (case 1). Treatment is typically followed by an overnight hospital stay for managing postembolization syndrome (self-limiting pain, fever, and nausea/vomiting).

The use of TAE for treatment of liver mNET is institution-specific, as there is no level 1 evidence guiding patient selection or timing of treatment. It is, however, a recognized treatment option by the National Comprehensive Cancer Network (NCCN).13 Contraindications to TAE include > 75% replacement of liver parenchyma with tumor, predominant extrahepatic tumor burden, asymptomatic indolent tumors, and hepatic dysfunction.

A retrospective study utilizing small particle polyvinyl alcohol (PVA) reported symptomatic and morphologic responses to embolization for treatment-refractory unresectable liver mNETs. Eighty-nine percent of patients treated for hormonal symptoms responded to embolization, and all patients treated for pain responded with a cumulative 5-year survival of 54%. Postembolization syndrome occurred in most patients, with an 11% major complication rate. The authors concluded that TAE is a simple and effective treatment for symptomatic liver mNETs.14


TACE combines intra-arterial delivery of chemotherapy with particulate embolization. Advantages of this combination include an improved chemotherapy pharmacokinetic profile, with increased intratumoral drug concentration and dwell time, as compared to systemic drug administration, together with intratumoral ischemia (case 2).

TACE is performed either as oily emulsion of chemotherapy, together with an embolic material (cTACE), or as a drug-loaded bead, where the chemotherapeutic material is integral to the embolic bead (DEB-TACE).

Patient selection for chemoembolization is guided by opinion without level 1 evidence. Contraindications parallel those mentioned with TAE, and TACE is recognized by the NCCN as a treatment option for liver mNET.13

Numerous retrospective reviews detail the performance of adding intra-arterial chemotherapy to hepatic artery embolization (hence cTACE vs TAE). Ruutiainen et al demonstrated trends that favor cTACE over TAE, with improvements in TTP, symptom control, and survival; however, this study lacked statistical power to definitely resolve these differences. Notably, the safety profile of the two techniques was similar; therefore, the addition of chemotherapy was not associated with a higher degree of toxicity compared to TAE.15 A large, multicenter, retrospective, follow-up review compared cTACE to TAE, with the hypothesis that cTACE would result in better symptom control and overall survival than TAE, without increased toxicity. Nevertheless, they observed no statistically significant difference in the symptom control, overall survival, or toxicity associated with these techniques.16 Taken together, these results suggest that the addition of chemotherapy to transarterial embolization does not provide a benefit for symptom control or survival, yet this addition does not increase toxicity.

(Video) Treatment of Liver Metastases in patients with Neuroendocrine Tumors

DEB-TACE is an alternative method of chemoembolization, yet data regarding its use for liver mNETs are limited. A prospective study by de Baere et al reported an 80% imaging partial-response rate at 3 months and median TTP of 15 months for low-grade liver mNETs, with symptom control in 81% of patients.17 These efficacy data compare favorably with TAE and cTACE; however, evidence suggests a higher rate of biliary complications when DEB-TACE is utilized. Guiu et al found that DEB-TACE and mNET were independent risk factors for biloma/liver infarct.18 Additionally, a phase 2 trial was interrupted when 54% of patients treated with DEB-TACE for liver mNET developed a biloma.19 The increased risk of biliary injury may be secondary to the high local chemotherapy concentrations achieved by DEB-TACE, coupled with the absence of a hypertrophied peribiliary plexus, which is found in cirrhotic livers and is believed to be protective against ischemic and chemical insults.18


Radioembolization delivers high-dose internal radiation to liver tumors via the hepatic artery (case 3). This technique differs from external beam radiation therapy, where hepatic radiosensitivity limits the amount of activity that can be prescribed before the development of radiation-induced liver disease.20

Radioembolization is usually performed with microspheres loaded with Y-90, a beta-emitting isotope.21 These microspheres emit high-energy, low-penetration radiation (~ 2.5 mm) within the tumor. There are two commercially available Y-90 devices: glass-based TheraSphere (BTG Interventional Medicine) and resin-based SIR-Spheres (Sirtex Medical Limited). Despite technical product differences, response rates between devices for liver mNETs appear equivalent.22 In distinction to TACE, hepatic artery occlusion is not intended with radioembolization.23 Instead, microspheres lodge in the tumor microenvironment and emit lethal beta radiation over an approximate 2-week period.24 The lack of macroscopic vessel occlusion limits postembolization syndrome, and therapy is administered as an outpatient.23,25

Similar to other arterial therapies, Y-90 device selection for treatment of liver mNETs is institution-specific, without level 1 evidence guiding patient selection and timing of treatment. It is, however, a recently recognized treatment option by the NCCN.13 Absolute contraindications include significant hepatopulmonary shunting and uncorrectable hepatoenteric arterial communications, which yield nontarget radiation (specifically, radiation pneumonitis and gut ulceration). Notably, portal vein thrombosis is not a contraindication, given the minimally embolic nature of this therapy, as compared to TAE and TACE, thus limiting the risk of ischemic hepatitis.

Y-90 radioembolization is a safe and efficacious therapy for mNETs.26 A recent meta-analysis of resin Y-90 for liver mNETs demonstrated a pooled response rate of 50%, a disease control rate of 86%, and improved overall survival for patients responding to therapy, as compared to nonresponders. These rates compare favorably with somatostatin analogs, cytotoxic chemotherapy, and newer biologic therapies.27 A comparative review of Y-90, TAE, and TACE for unresectable liver mNETs was reported by Yang et al. The authors indicate that the aforementioned transarterial therapies showed comparable efficacy in terms of tumor response, symptom palliation, and lengthening patient survival. Distinctions between the techniques occurred in their side effect profiles with no difference in major complication rates.12


Although the technique for TAE, TACE, and Y-90 is typically unchanged when treating NETs, compared to other primary and secondary liver malignancies, certain disease-specific considerations and complications are either unique or encountered more frequently in this patient population, requiring modification to periprocedural care.

A unique consideration is the potential for carcinoid crisis (a more severe form of carcinoid syndrome that includes profound hypotension or hypertension, confusion, and bronchospasm) resulting from surgical manipulation or general anesthesia. This rare but well-known complication can similarly occur during or after transarterial embolization treatment, even in patients not previously demonstrating carcinoid syndrome. In most cases, carcinoid crisis can be prevented by periprocedural administration of short-acting somatostatin analogs.

Although not unique to the treatment of NET, special consideration should be made for patients lacking a competent sphincter of Oddi, often due to previous pancreaticoduodenectomy. Hepatic artery embolization in the setting of a bilioenteric anastomosis is well known to markedly increase the risk of hepatic abscess, ranging from 33% to 86%, despite aggressive antibiotics.28,29 Recently, there is evidence that radioembolization, along with antibiotic prophylaxis, may lower this risk. Cholapranee et al retrospectively reported that zero of 16 patients undergoing radioembolization developed a hepatic abscess, compared to three of 13 patients who underwent cTACE, despite identical periprocedural antibiotic and bowel regimens.30 Additionally, a prolonged course of oral moxifloxacin for 21 days (beginning 3 days before the procedure) without bowel preparation, retrospectively demonstrated no hepatic abscess in 10 patients undergoing 25 embolization procedures.31


Managing liver mNET is complex and requires a multidisciplinary approach that takes into account the extent and biology of disease. Treatment of liver mNET is undertaken in both curative and palliative settings with the goal of improving survival and quality of life. Catheter-based interventions provide a diverse platform of palliative treatment options, ranging from embolization with resultant tumor ischemia, to intratumoral delivery of high-dose cytotoxic chemotherapy, or lethal internal radiation. These transarterial therapies are effective in controlling tumor burden and related symptoms with a low risk of adverse events. Special considerations include prevention of carcinoid crisis and mitigating risk of postembolization biloma and hepatic abscess. No intra-arterial technique has shown superiority in an RCT, and an evidenced-based treatment algorithm is awaited. In the meantime, a rational approach should recognize catheter-based therapies as a powerful targeted option for liver mNETs.

Christopher Molvar, MD, is Assistant Professor of Radiology in the Section of Vascular and Interventional Radiology at Loyola University Medical Center in Maywood, Illinois. He has stated that he has no financial interests related to this article. Dr. Molvar may be reached at (708) 216-5306;

Andrew Lipnik, MD, is Assistant Professor of Radiology and Radiological Sciences in the Section of Vascular and Interventional Radiology at Vanderbilt University School of Medicine in Nashville, Tennessee. He has stated that he has no financial interests related to this article. Dr. Lipnik may be reached at

(Video) Current Management of Neuroendocrine Tumors at Mount Sinai

Daniel Brown, MD, is Professor of Radiology and Radiological Sciences and Director of Interventional Oncology at Vanderbilt University School of Medicine in Nashville, Tennessee. He has stated that he has no financial interests related to this article. Dr. Brown may be reached at

Robert Lewandowski, MD, is Associate Professor in Radiology and Director of Interventional Oncology at Northwestern University Feinberg School of Medicine in Chicago, Illinois. He has stated that he has no financial interests related to this article. Dr. Lewandowski may be reached at

1. Bosman FT, Carneiro F, Hruban RH, et al. WHO classification of tumours of the digestive system. vol. 3. Lyon, France: IARC Press; 2010.

2. Moertel CG. Karnofsky memorial lecture. An odyssey in the land of small tumors. J Clin Oncol. 1987;5:1502-1522.

3. Rindi G, Wiedenmann B. Neuroendocrine neoplasms of the gut and pancreas: new insights. Nat Rev Endocrinol. 2012;8:54-64.

4. Caplin ME, Pavel M, Cwikla JB, et al. Lanreotide in metastatic enteropancreatic neuroendocrine tumors. N Engl J Med. 2014;371:224-233.

5. Rinke A, Muller HH, Schade-Brittinger C, et al. Placebo-controlled, double-blind, prospective, randomized study on the effect of octreotide LAR in the control of tumor growth in patients with metastatic neuroendocrine midgut tumors: a report from the PROMID Study Group. J Clin Oncol. 2009;27:4656-4663.

6. Yao JC, Shah MH, Ito T, et al. Everolimus for advanced pancreatic neuroendocrine tumors. N Engl J Med. 2011;364:514-523.

7. Raymond E, Dahan L, Raoul JL, et al. Sunitinib malate for the treatment of pancreatic neuroendocrine tumors. N Engl J Med. 2011;364:501-513.

8. Modlin IM, Lye KD, Kidd M. A 5-decade analysis of 13,715 carcinoid tumors. Cancer. 2003;97:934-959.

9. O’Toole D, Hentic O, Corcos O, et al. Chemotherapy for gastro-enteropancreatic endocrine tumours. Neuroendocrinology. 2004;80(suppl 1):79-84.

(Video) Liver Resections and Liver Transplants for Neuroendocrine Tumor Patients - Dr. Brendan Visser

10. Mayo SC, de Jong MC, Pulitano C, et al. Surgical management of hepatic neuroendocrine tumor metastasis: results from an international multi-institutional analysis. Ann Surg Oncol. 2010;17:3129-3136.

11. Mayo SC, de Jong MC, Bloomston M, et al. Surgery versus intra-arterial therapy for neuroendocrine liver metastasis: a multicenter international analysis. Ann Surg Oncol. 2011;18:3657-3665.

12. Yang TX, Chua TC, Morris DL. Radioembolization and chemoembolization for unresectable neuroendocrine liver metastases - a systematic review. Surg Oncol. 2012;21:299-308.

13. NCCN Guidelines Version 1.2015, Neuroendocrine Tumors. 2015. Accessed August 4th, 2015.

14. Brown KT, Koh BY, Brody LA, et al. Particle embolization of hepatic neuroendocrine metastases for control of pain and hormonal symptoms. J Vasc Interv Radiol. 1999;10:397-403.

15. Ruutiainen AT, Soulen MC, Tuite CM, et al. Chemoembolization and bland embolization of neuroendocrine tumor metastases to the liver. J Vasc Interv Radiol. 2007;18:847-855.

16. Pitt SC, Knuth J, Keily JM, et al. Hepatic neuroendocrine metastases: chemo- or bland embolization? J Gastrointest Surg. 2008;12:1951-1960.

17. de Baere T, Deschamps F, Teriitheau C, et al. Transarterial chemoembolization of liver metastases from well differentiated gastroenteropancreatic endocrine tumors with doxorubicin-eluting beads: preliminary results. J Vasc Interv Radiol. 2008;19:855-861.

18. Guiu B, Deschamps F, Aho S, et al. Liver/biliary injuries following chemoembolisation of endocrine tumours and hepatocellular carcinoma: lipiodol vs. drug-eluting beads. J Hepatol. 2012;56:609-617.

19. Bhagat N, Reyes DK, Lin M, et al. Phase II study of chemoembolization with drug-eluting beads in patients with hepatic neuroendocrine metastases: high incidence of biliary injury. Cardiovasc Intervent Radiol. 2013;36:449-459.

20. Gil-Alzugaray B, Chopitea A, Inarrairaegui M, et al. Prognostic factors and prevention of radioembolization-induced liver disease. Hepatology. 2013;57:1078-1087.

(Video) Treatment with radioembolisation of liver tumours

21. Salem R, Mazzaferro V, Sangro B. Yttrium 90 radioembolization for the treatment of hepatocellular carcinoma: biological lessons, current challenges, and clinical perspectives. Hepatology. 2013;58:2188-2197.

22. 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;247:1029-1035.

23. Salem R, Lewandowski RJ. Chemoembolization and radioembolization for hepatocellular carcinoma. Clin Gastroenterol Hepatol. 2013;11:604-611; quiz e43-4.

24. Sato K, Lewandowski RJ, Bui JT, et al. Treatment of unresectable primary and metastatic liver cancer with yttrium-90 microspheres (TheraSphere): assessment of hepatic arterial embolization. Cardiovasc Intervent Radiol. 2006;29:522-529.

25. Geschwind JF, Salem R, Carr BI, et al. Yttrium-90 microspheres for the treatment of hepatocellular carcinoma. Gastroenterology. 2004;127:S194-205.

26. Memon K, Lewandowski RJ, Mulcahy MF, et al. Radioembolization for neuroendocrine liver metastases: safety, imaging, and long-term outcomes. Int J Radiat Oncol Biol Phys. 2012;83:887-894.

27. Devcic Z, Rosenberg J, Braat AJ, et al. The efficacy of hepatic 90Y resin radioembolization for metastatic neuroendocrine tumors: a meta-analysis. J Nucl Med. 2014;55:1404-1410.

28. Kim W, Clark TW, Baum RA, et al. Risk factors for liver abscess formation after hepatic chemoembolization. J Vasc Interv Radiol. 2001;12:965-968.

29. Mezhir JJ, Fong Y, Fleischer D, et al. Pyogenic abscess after hepatic artery embolization: a rare but potentially lethal complication. J Vasc Interv Radiol. 2011;22:177-182.

30. Cholapranee A, van Houten D, Deitrick G, et al. Risk of liver abscess formation in patients with prior biliary intervention following yttrium-90 radioembolization. Cardiovasc Intervent Radiol. 2015;38:397-400.

31. Khan W, Sullivan KL, McCann JW, et al. Moxifloxacin prophylaxis for chemoembolization or embolization in patients with previous biliary interventions: a pilot study. AJR Am J Roentgenol. 2011;197:W343-345.

(Video) Liver-Directed Therapies in Pancreatic Neuroendocrine Tumors


Are there any new treatments for neuroendocrine cancer? ›

Lutetium Lu 177 dotatate is the first radioactive drug approved to treat these rare cancers. Patients with GEP-NETs have limited treatment options if initial therapy fails to keep the cancer from growing or progressing.

How long can you live with metastatic neuroendocrine cancer? ›

The 5-year survival rate for people with a GI tract NET that has not spread to other parts of the body from where it started is 97%. If the tumor has spread to nearby tissue or the regional lymph nodes, the 5-year survival rate is 95%. If the tumor has spread to distant areas of the body, the survival rate is 67%.

What is the best treatment for neuroendocrine cancer? ›

Completely removing the entire tumor is the standard treatment, when possible. Most localized NETs are successfully treated with surgery alone. The surgeon will usually remove some tissue surrounding the tumor, called a margin, in an effort to leave no traces of cancer in the body.

What is the survival rate for neuroendocrine cancer on liver? ›

In the early stages of disease (I–III A (= N0, M0)] the treatment of choice is radical surgery of the primary and lymph nodes. This treatment is related to an excellent 5-year disease specific survival of 100%. In stage III B and IV patients' 5-year survival rates of 97.1% and 84.8% are reported [2, 7].

What is the best hospital for neuroendocrine tumors? ›

Mayo Clinic doctors have extensive experience diagnosing and treating neuroendocrine tumors. Each year, Mayo Clinic doctors care for more than 1,900 people with neuroendocrine tumors, including people with very rare types. Nationally recognized expertise.

Can metastatic neuroendocrine cancer be cured? ›

Many neuroendocrine tumors have spread at the time of diagnosis or recurred after surgery. Most metastatic tumors (that have spread) are not curable but can be treatable with multiple forms of therapy.

What foods should be avoided with neuroendocrine tumors? ›

Limit or avoid stimulants such as alcohol and caffeine.
  • Include binding foods: applesauce, bananas, tapioca, barley, oats, white rice, noodles, peanut butter, baked potato without the skin.
  • Avoid foods that are natural laxatives, such as prunes, prune juice, rhubarb, and papaya.

Can neuroendocrine cancer go into remission? ›

Peptide receptor radionuclide therapy is a safe and effective therapeutic option for the control of inoperable neuroendocrine tumours, with potential quality of life improvement. Complete remission with lutetium-177 -labeled somatostatin analogues ([177Lu]Lu-DOTA-TATE), although rare, is possible in some cases.

How serious is neuroendocrine cancer? ›

Compared with more common malignant tumors, neuroendocrine tumors are slow-growing but can produce amino acids that cause severe symptoms. Aggressive therapy is recommended to lessen the severity of symptoms or to prevent possible harm to the liver. The portal for UPMC Cole patients receiving inpatient care.

What foods help neuroendocrine tumors? ›

eat regular, smaller meals and snacks every 2 hours or so. choose foods that contain proteins such as meat or meat alternatives (tofu and soya), eggs, beans and other pulses or legumes. use full fat milk and butter. drink nourishing drinks such as full fat milk drinks and smoothies.

Can a neuroendocrine tumor be cured? ›

Many neuroendocrine tumors can be successfully treated with surgery and chemotherapy, especially if the tumor is localized and has not spread to the lymph nodes or other organs in the body.

Does neuroendocrine cancer spread fast? ›

There are many types of neuroendocrine tumors. Some grow slowly and some grow very quickly. Some neuroendocrine tumors produce excess hormones (functional neuroendocrine tumors).

How is neuroendocrine tumor of the liver treated? ›

If neuroendocrine tumours (NETs) spread, they often spread to the liver (called liver metastases). Liver directed therapy directly targets the cancer in the liver and is often used to treat NETs that have spread to the liver. Liver directed therapy is mainly used when surgery can't be done.

How long can you live with liver NETs? ›

The 1-, 3-, 5-, and 10-year overall survival rates for patients with NETs were 72.8%, 52.7%, 39.4%, and 18.1%, respectively.

Can liver metastasis cured? ›

In most cases, cancer that has spread to the liver cannot be cured. People whose cancer has spread to the liver often die of their disease. However, treatments may help shrink tumors, improve life expectancy, and relieve symptoms.

Where do neuroendocrine tumors spread? ›

NETs can spread, or metastasize, to other locations in the body, such as the lymph nodes or the liver. When a tumor spreads it is called metastasis and may also be called advanced or malignant (cancerous).

Does radiation work on neuroendocrine tumors? ›

Radiation therapy uses high-energy rays (such as x-rays) or radioactive particles to kill cancer cells. Surgery is the main treatment for most pancreatic neuroendocrine tumors (NETs), but radiation therapy may be an option for those who can't have surgery for some reason.

Can neuroendocrine tumors disappear? ›

For some people with a pancreatic neuroendocrine tumor (NET), treatment can remove or destroy the cancer.

Can you shrink a neuroendocrine tumor? ›

Results showed that 42 percent of patients with the high-grade form of neuroendocrine carcinomas saw their tumors shrink partially or completely after treatment, while none of the low-grade patients did. For all patients, 70 percent saw their cancer spread within six months.

Does Immunotherapy work for neuroendocrine cancer? ›

The most significant finding was that a subset of patients with neuroendocrine tumors, those with high-grade carcinoma, seem to benefit most from dual immunotherapy, with a response rate approaching 44%. Many of those responses, at least initially, appear to be long-lasting and continuous. [1].

How long does it take a neuroendocrine tumor to grow? ›

In general, it can take 3-5 years and even up to 10 or longer for carcinoid tumors to grow. These are generally very slow-growing tumors.

What causes neuroendocrine tumors to grow? ›

Changes in the NF1 gene cause this disease. The gene normally makes a protein called neurofibromin, which makes cells grow in an orderly way. When the NF1 gene changes, your cells may grow out of control and form cancer. If you have NF1 you're more likely to get NETs such as carcinoid tumors and pheochromocytoma.

What is the most common neuroendocrine tumor? ›

Pancreatic neuroendocrine tumors (PNETs), a group of endocrine tumors arising in the pancreas, are among the most common neuroendocrine tumors (NETs). Functioning PNETs include insulinoma, gastrinoma, VIPoma, glucagonoma, and others that produce specific hormonal hypersecretion syndromes.

What is the difference between neuroendocrine tumor and neuroendocrine carcinoma? ›

There are two fundamentally different groups of NENs: well-differentiated, low-proliferating NENs, called neuroendocrine tumors (NETs) or carcinoids, and poorly differentiated, highly proliferating NENs, called small- or large-cell neuroendocrine carcinomas (NECs).

Is liver cancer a neuroendocrine cancer? ›

The liver could be the primary origin of neuroendocrine tumors, and if the tumors have diagnosed as primary hepatic neuroendocrine tumors, surgical resection must be considered for curative treatment (11).

What is a neuroendocrine tumor of the liver? ›

Neuroendocrine liver metastases are usually multiple and of varying size. In most cases both liver lobes are affected, but miliary seeding throughout the liver is seen only occasionally. The carcinoid is the most common neuroendocrine tumor causing liver metastases, especially when of midgut origin.

What are the stages of neuroendocrine cancer? ›

Neuroendocrine tumors are staged according to the TNM staging system: tumor (T), node (N), metastasis (M). The World Health Organization (WHO) classifies neuroendocrine tumors according to the malignant potential of the tumor: Well-differentiated neuroendocrine tumors (grade 1 and 2)

Where do neuroendocrine tumors come from? ›

A neuroendocrine tumor (NET) begins in the specialized cells of the body's neuroendocrine system. These cells have traits of both hormone-producing endocrine cells and nerve cells. They are found throughout the body's organs and help control many of the body's functions.

What kind of cancer is a neuroendocrine tumor? ›

Some examples of neuroendocrine tumors are carcinoid tumors, islet cell tumors, medullary thyroid cancer, pheochromocytomas, neuroendocrine carcinoma of the skin (Merkel cell cancer), small cell lung cancer, and large cell neuroendocrine carcinoma (a rare type of lung cancer).

Can chemotherapy cure neuroendocrine tumors? ›

Chemotherapy uses anti cancer (cytotoxic) drugs to destroy neuroendocrine tumour (NET) cells. You might have it for a NET that is fast growing and that has spread to other parts of the body. You might have chemotherapy on its own, or together with other treatments such as targeted drugs or radiotherapy.

What foods stop tumor growth? ›

12 Foods that Shrink Benign Tumors [Anti-Cancer Diet Guide]
  • Turmeric. ...
  • Green Tea. ...
  • Cruciferous vegetables. ...
  • Walnuts. ...
  • Berries. ...
  • Tomatoes. ...
  • Fatty fish. ...
  • Folate-rich food.

What do neuroendocrine tumors release? ›

About one-third of pancreatic neuroendocrine tumors secrete hormones, including insulin, glucagon, gastrin, or vasoactive intestinal peptide.

Can neuroendocrine tumors spread to the liver? ›

Neuroendocrine tumours frequently metastasize to the liver. Although generally slowly progressing, hepatic metastases are the major cause of carcinoid syndrome and ultimately lead to liver dysfunction, cardiac insufficiency and finally death.

Do neuroendocrine tumors come back? ›

Doctors want to keep track of your recovery in the months and years ahead. This is important because a NET can recur even several years after treatment.

Can stress cause neuroendocrine cancer? ›

Chronic stress produces stress hormones during the activation of the neuroendocrine system (hypothalamus-pituitary-adrenal axis) and the sympathetic nervous system, which can promote tumor development and regulate the tumor microenvironment.

Does neuroendocrine cancer run in families? ›

Endocrine tumor syndromes are caused by genetic mutations that can be passed on in families from generation to generation. Some types of neuroendocrine tumors are found much more frequently in patients with these genetic mutations.

How quickly do liver mets grow? ›

The doubling time of colorectal metastases has been shown from follow-up studies to range from 60–200 days, but occasionally we see much faster growth rates, and in other cases tumours appear indolent over a long period of observation before suddenly exploding into rapid growth.

How long can you live with a tumor on your liver? ›

The general 5-year survival rate for liver cancer in the United States is 20%, compared to 3% 40 years ago. Survival rates depend on several factors, including the stage of the disease. For the 43% of people who are diagnosed with liver cancer at an early stage, the 5-year survival rate is 35%.

How quickly do liver tumors grow? ›

9 In our study, the average time required for an HCC to grow from 1 cm to 2 cm in diameter was 212 days for patients with HBV infection and 328.4 days for patients with HCV infection.

What is the best treatment for liver metastases? ›

Treatment of liver metastases. Surgery to remove the metastases may be an option if there are a small number of tumors in the liver and they are not in areas that would affect normal liver function. A different procedure called ablation might also be an option. In ablation, a thin needle is put into the tumor.

Can liver metastases go into remission? ›

Because liver metastases spread to the liver from another part of the body, they can be very difficult to treat. But with the right approach, remission and even a cure are possible for some patients.

How do you get rid of liver metastasis? ›

Treatments for liver metastasis include surgery to remove the tumor, chemotherapy, biologic drugs, radiation, or a procedure called ablation which destroys cancerous lesions.

Why do people get neuroendocrine tumors? ›

The exact cause of neuroendocrine tumors isn't known. These cancers begin in neuroendocrine cells that have traits similar to those of nerve cells and hormone-producing cells. Neuroendocrine cells are found throughout your body.

What is life expectancy with immunotherapy? ›

A study conducted by UCLA researchers involving patients with non-small cell lung cancer (NSCLC) found that the immunotherapy drug pembrolizumab increased the average 5-year survival rate of these patients from 5.5% to 15%.

How long can a cancer patient live with immunotherapy? ›

In her study, 70% of the patients who were able to complete 2 years on the chemo-immunotherapy combination were still alive at five years. They get infusions every three weeks for those two years, but most can work during treatment. "The quality of life of these patients is quite high," Garassino said.

Can you beat cancer with immunotherapy? ›

Immunotherapy drugs work better in some cancers than others and while they can be a miracle for some, they fail to work for all patients. Overall response rates are about 15 to 20%.

Where do neuroendocrine Tumours spread to? ›

NETs can spread, or metastasize, to other locations in the body, such as the lymph nodes or the liver. When a tumor spreads it is called metastasis and may also be called advanced or malignant (cancerous).


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