Evidence map›Paper›PMID 38709422›Full record

ReviewCurrent oncology reports2024

Past, Present, and Future Therapeutic Strategies for NF-1-Associated Tumors.

Brian Na, Shilp R Shah, Harish N Vasudevan

Erratum issuedAbstract readReview
In one paragraph

Review in Current oncology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. A transcriptomic, proteomic, and functional genetic atlas dissects neurofibromin function in the peripheral nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Neuroendocrine Tumors: Germline Genetics and Hereditary Syndromes.Current treatment options in oncology · 2025
    Review
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Brian NaDepartment of Neurology, UCLA Neuro-Oncology Program, University of California Los Angeles, Los Angeles, CA, 90095, USA.
Shilp R ShahSamueli School of Engineering, University of California Los Angeles, Los Angeles, CA, 90095, USA.
Harish N VasudevanDepartment of Radiation Oncology, University of California San Francisco, San Francisco, CA, 94143, USA. harish.vasudevan@ucsf.edu.

Funding

Project 4: Secondary Cancers Among NF1 Cancer SurvivorsU54CA196519 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KEVIN M. SHANNON · 2015 to 2026
$26.9M
NCI NIH HHS U54 CA196519
6 · The paper itself

Abstract

purpose of reviewNeurofibromatosis type 1 (NF-1) is a cancer predisposition syndrome caused by mutations in the NF1 tumor suppressor gene that encodes the neurofibromin protein, which functions as a negative regulator of Ras signaling. We review the past, current, and future state of therapeutic strategies for tumors associated with NF-1. RECENT

findingsTherapeutic efforts for NF-1-associated tumors have centered around inhibiting Ras output, leading to the clinical success of downstream MEK inhibition for plexiform neurofibromas and low-grade gliomas. However, MEK inhibition and similar molecular monotherapy approaches that block Ras signaling do not work for all patients and show limited efficacy for more aggressive cancers such as malignant peripheral nerve sheath tumors and high-grade gliomas, motivating novel treatment approaches. We highlight the current therapeutic landscape for NF-1-associated tumors, broadly categorizing treatment into past strategies for serial Ras pathway blockade, current approaches targeting parallel oncogenic and tumor suppressor pathways, and future avenues of investigation leveraging biologic and technical innovations in immunotherapy, pharmacology, and gene delivery.

Indexed as

Neurofibromatosis 1Neurofibromin 1HumansImmunotherapyMolecular Targeted TherapyMutationras ProteinsSignal TransductionNeurofibromin 1ras ProteinsCell signalingMEK inhibitionNeurofibromatosis type 1Targeted therapy

Identifiers

PMID38709422
PMCPMC11169015

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.