ReviewNeuroendocrinology2013
Signaling pathways as specific pharmacologic targets for neuroendocrine tumor therapy: RET, PI3K, MEK, growth factors, and Notch.
Review in Neuroendocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 22 citations in OpenAlex.
- Targeted therapies in the management of advanced medullary thyroid cancer.The oncologist · 2026Review
- Real-world data analysis of next-generation sequencing and corresponding clinical characteristics in thyroid tumor.Endocrine connections · 2024Article
- An Overview of Altered Pathways Associated with Sensitivity to Platinum-Based Chemotherapy in Neuroendocrine Tumors: Strengths and Prospects.International journal of molecular sciences · 2024Review
- Updates on the Role of Molecular Alterations and NOTCH Signalling in the Development of Neuroendocrine Neoplasms.Journal of clinical medicine · 2019Review
- Targeted therapy of gastroenteropancreatic neuroendocrine tumours: preclinical strategies and future targets.Endocrine connections · 2018Review
- Inhibition of Peripheral Synthesis of Serotonin as a New Target in Neuroendocrine Tumors.The oncologist · 2016Review
- CXCR4/CXCL12/CXCR7 axis is functional in neuroendocrine tumors and signals on mTOR.Oncotarget · 2016Article
- Notch Signaling in Neuroendocrine Tumors.Frontiers in oncology · 2016Review
- Quantitative analysis of receptor tyrosine kinase-effector coupling at functionally relevant stimulus levels.The Journal of biological chemistry · 2015Article
- Aspirin inhibits cell viability and mTOR downstream signaling in gastroenteropancreatic and bronchopulmonary neuroendocrine tumor cells.World journal of gastroenterology · 2014Article
- Specific glycogen synthase kinase-3 inhibition reduces neuroendocrine markers and suppresses neuroblastoma cell growth.Cancer biology & therapy · 2014Article
- Neuroendocrine phenotype alteration and growth suppression through apoptosis by MK-2206, an allosteric inhibitor of AKT, in carcinoid cell lines in vitro.Anti-cancer drugs · 2013Article
- Medullary thyroid cancer: molecular factors, management and treatment.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Neuroendocrine tumors are rare tumors with a common progenitor - the neural crest cell. Included in this category are pulmonary and gastrointestinal tract carcinoid tumors and medullary thyroid cancer. The majority of these tumors are sporadic in nature, however they can be hereditary. Medullary thyroid cancers can present sporadically, with other endocrine tumors, as in the complex of multiple endocrine neoplasias 1, 2A, or 2B, or as familial medullary thyroid cancer. These tumors can become evident at later stages, with metastases already present at the time of diagnosis. Despite the small size and rare incidence of gastrointestinal neuroendocrine (carcinoid) tumors, they can be debilitating when present. Their natural history presents as early lymph node and distant metastases, as well as symptoms of the carcinoid syndrome, which result from the overproduction and secretion of serotonin and somatostatin. As a consequence of their metastases, surgical resection is non-curative and hence there is a need for novel treatment strategies to address tumor burden and symptom control. There are multiple intracellular pathways which can be targeted, either individually or in combination, to address these tumors. Here, we review some of the intracellular pathways, and identify some specific targets, which are vital to the generation and propagation of neuroendocrine tumorigenesis, and thus, can be the foci of novel drug therapies. We also elaborate on present pharmacological strategies and clinical trials involving these intracellular pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.