Evidence map›Paper›PMID 34680266›Full record

ReviewCancers2021

Pancreatic Neuroendocrine Tumors: Molecular Mechanisms and Therapeutic Targets.

Chandra K Maharjan, Po Hien Ear, Catherine G Tran, James R Howe, Chandrikha Chandrasekharan, Dawn E Quelle

Open access · goldAbstract readReview
In one paragraph

Review in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
6.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Chandra K MaharjanDepartment of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0003-0673-9888
Po Hien EarDepartment of Surgery, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Catherine G TranDepartment of Surgery, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
James R HoweDepartment of Surgery, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Chandrikha ChandrasekharanDepartment of Internal Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Dawn E QuelleDepartment of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0001-8776-0122
University of Iowa · US

Funding

Viral VectorP30CA086862 · NCI · UNIVERSITY OF IOWA · PI Jon C.D. Houtman · 2000 to 2026
$70.0M
Project 4: New Approaches to Improving the Effectiveness of Radionuclide Targeted Treatments in Neuroendocrine TumorsP50CA174521 · NCI · UNIVERSITY OF IOWA · PI MENDA, YUSUF · 2015 to 2021
$13.2M
Role of RABL6A-PP2A in neuroendocrine tumorsR01CA260200 · NCI · UNIVERSITY OF IOWA · PI NARLA, GOUTHAM, QUELLE, DAWN E · 2021 to 2025
$2.6M
NCI NIH HHS P30 CA086862NCI NIH HHS P50 CA174521NCI NIH HHS R01 CA260200
6 · The paper itself

Abstract

Pancreatic neuroendocrine tumors (pNETs) are unique, slow-growing malignancies whose molecular pathogenesis is incompletely understood. With rising incidence of pNETs over the last four decades, larger and more comprehensive 'omic' analyses of patient tumors have led to a clearer picture of the pNET genomic landscape and transcriptional profiles for both primary and metastatic lesions. In pNET patients with advanced disease, those insights have guided the use of targeted therapies that inhibit activated mTOR and receptor tyrosine kinase (RTK) pathways or stimulate somatostatin receptor signaling. Such treatments have significantly benefited patients, but intrinsic or acquired drug resistance in the tumors remains a major problem that leaves few to no effective treatment options for advanced cases. This demands a better understanding of essential molecular and biological events underlying pNET growth, metastasis, and drug resistance. This review examines the known molecular alterations associated with pNET pathogenesis, identifying which changes may be drivers of the disease and, as such, relevant therapeutic targets. We also highlight areas that warrant further investigation at the biological level and discuss available model systems for pNET research. The paucity of pNET models has hampered research efforts over the years, although recently developed cell line, animal, patient-derived xenograft, and patient-derived organoid models have significantly expanded the available platforms for pNET investigations. Advancements in pNET research and understanding are expected to guide improved patient treatments.

Indexed as

molecular mechanismspancreatic neuroendocrine tumorspNET models

Identifiers

PMID34680266
PMCPMC8533967
OpenAlexW3205531691

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.