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PI3K-AKT-mTOR-signaling and beyond: the complex network in gastroenteropancreatic neuroendocrine neoplasms
Franziska Briest1, Patricia Grabowski2
11. Medizinische Klinik 1 CBF, Dept. of Gastroenterology, Infectious Diseases, Rheumatology CC13, Charité Berlin, Germany; ; 2. Freie Universität Berlin, Institute for Chemistry and Biochemistry, Berlin, Germany;
Abstract:
Gastroenteropancreatic neuroendocrine neoplasms are heterogeneous in their clinical behavior and require therapies specially tailored according to staging, grading, origin and expression of peptide receptors. Despite extensive scientific efforts, the therapy options are still not satisfactory. The main reasons are due to the lack of a broad mechanistic knowledge, an insufficient classification of specific diagnostic sub-groups, and predictive markers. GEP-NEN tumors evade early diagnosis because of slow asymptomatic growth behavior and are frequently not detected until metastasized. How signaling networks contribute to tumor progression and how these networks interact remains unclear in large parts. In this review we summarize the knowledge on the growth factor responsive non-angiogenetic pathways in sporadic GEP-NENs, highlight promising mechanistic research approaches, and describe important therapy targets.
Insights
Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) have varied behaviors, needing tailored therapies. Current treatment options are limited by poor mechanistic understanding and diagnostic challenges, hindering effective GEP-NEN management.
Area of Science:
- Oncology
- Molecular Biology
- Gastroenterology
Background:
- Gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) exhibit diverse clinical behaviors.
- Current therapeutic strategies for GEP-NENs are often unsatisfactory due to incomplete mechanistic knowledge and diagnostic limitations.
- GEP-NENs frequently present at advanced stages due to slow, asymptomatic growth, complicating early intervention.
Purpose of the Study:
- To review current knowledge on growth factor-responsive, non-angiogenetic pathways in sporadic GEP-NENs.
- To highlight emerging mechanistic research approaches for understanding GEP-NEN progression.
- To identify and discuss significant therapeutic targets for GEP-NENs.
Main Methods:
- Literature review focusing on signaling networks in sporadic GEP-NENs.
- Analysis of growth factor-responsive pathways and non-angiogenetic mechanisms.
- Synthesis of current research on diagnostic sub-groups and predictive markers.
Main Results:
- Signaling networks' roles in GEP-NEN progression and interactions remain incompletely understood.
- Growth factor-responsive, non-angiogenetic pathways are key areas of investigation.
- Lack of broad mechanistic insight and predictive markers limits therapeutic efficacy.
Conclusions:
- Further research into signaling networks is crucial for advancing GEP-NEN treatment.
- Improved classification and identification of predictive markers are needed for personalized GEP-NEN therapy.
- Targeting specific pathways offers promising avenues for novel GEP-NEN therapies.
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