Pancreatic NETs: where do we stand now?

The systemic management of patients with pancreatic neuroendocrine tumors includes chemotherapy and targeted agents such as everolimus and sunitinib. Which treatment to favor in a particular patient is not known. The most commonly used chemotherapy agents are streptozocin and temozolamide, often pre...

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Bibliographic Details
Published in:Cancer and metastasis reviews 2014-03, Vol.33 (1), p.361-366
Main Authors: Faivre, S., Castellano, D., Strosberg, J., González, E., Salazar, R.
Format: Article
Language:English
Subjects:
Antineoplastic Combined Chemotherapy Protocols - therapeutic use
Biomarkers, Tumor - metabolism
Biomedical and Life Sciences
Biomedicine
Cancer
Cancer Research
Chemotherapy
Disease-Free Survival
DNA Modification Methylases - metabolism
DNA Repair Enzymes - metabolism
Everolimus
Humans
Indoles - therapeutic use
Neuroendocrine Tumors - diagnosis
Neuroendocrine Tumors - drug therapy
Neuroendocrine Tumors - enzymology
Oncology
Pancreatic Neoplasms - diagnosis
Pancreatic Neoplasms - drug therapy
Pancreatic Neoplasms - enzymology
Pyrroles - therapeutic use
Sirolimus - analogs & derivatives
Sirolimus - therapeutic use
Treatment Outcome
Tumor Suppressor Proteins - metabolism
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Summary:The systemic management of patients with pancreatic neuroendocrine tumors includes chemotherapy and targeted agents such as everolimus and sunitinib. Which treatment to favor in a particular patient is not known. The most commonly used chemotherapy agents are streptozocin and temozolamide, often prescribed in combination with fluoropyrimidines. A potential biomarker for selection of temozolomide-based chemotherapy is O-6-methylguanine-DNA-methyltrasferase expression. Chemotherapy yields higher response rates and may be preferable in patients with higher-grade tumors and those who are symptomatic. The mammalian target of rapamycin inhibitor everolimus has shown improvement in progression-free survival (PFS) in a robust, well-conducted phase III study. Everolimus, however, can induce limiting toxicities that may result in treatment discontinuation and does not improve survival. However, the objective response rate is very low. Sunitinib, likewise, increases PFS but the data comes from a smaller trial which was terminated early. Sunitinib displays a different toxicity profile and is associated with a trend towards improved overall survival. It is clear that biomarkers to properly select the most effective agents in an individual patient are needed.
ISSN:0167-7659
1573-7233
DOI:10.1007/s10555-013-9466-0