Evidence map›Paper›PMID 40280500›Full record

ReviewBiochimica et biophysica acta. Reviews on cancer2025

Myc family proteins: Molecular drivers of tumorigenesis and resistance in neuroendocrine tumors.

Hannah M Hylton-McComas, Alyssa Cordes, Konstantinos V Floros, Anthony C Faber, Benjamin J Drapkin, Wayne O Miles

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta. Reviews on cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. Dual targeting of AMRC12 andTheranostics · 2026
    Article
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.

Hannah M Hylton-McComasDepartment of Cancer Biology and Genetics, The Ohio State University, 460 West 12(th) Avenue, Columbus, OH 43210, USA; The Ohio State University Comprehensive Cancer Center, The Ohio State University, 460 West 12(th) Avenue, Columbus, OH 43210, USA.
Alyssa CordesHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Internal Medicine and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Konstantinos V FlorosVCU Philips Institute, Virginia Commonwealth University School of Dentistry and Massey Comprehensive Cancer Center, Richmond, VA 23298, USA; Department of Pediatrics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.
Anthony C FaberVCU Philips Institute, Virginia Commonwealth University School of Dentistry and Massey Comprehensive Cancer Center, Richmond, VA 23298, USA; Department of Pediatrics, Virginia Commonwealth University School of Medicine, Richmond, VA 23298, USA.
Benjamin J DrapkinHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, TX, USA; Department of Internal Medicine and Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Wayne O MilesDepartment of Cancer Biology and Genetics, The Ohio State University, 460 West 12(th) Avenue, Columbus, OH 43210, USA; The Ohio State University Comprehensive Cancer Center, The Ohio State University, 460 West 12(th) Avenue, Columbus, OH 43210, USA. Electronic address: wayne.miles@osumc.edu.

Funding

The translation regulation of pro-apoptotic genesR01CA251753 · NCI · OHIO STATE UNIVERSITY · PI MILES, WAYNE · 2020 to 2024
$2.0M
Acquired Cross-Resistance through MYC Amplification in Small Cell Lung CancerR01CA286912 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Benjamin J Drapkin · 2025 to 2026
$1.2M
NCI NIH HHS R01 CA251753NCI NIH HHS R01 CA286912
6 · The paper itself

Abstract

Neuroendocrine cancers are a diverse and poorly understood collection of malignancies derived from neuroendocrine cells throughout the body. These cancers uniquely exhibit properties of both the nervous and endocrine systems. Only a limited number of genetic driver mutations have been identified in neuroendocrine cancers, however the mechanisms of how these genetic aberrations alter tumor biology remain elusive. Recent studies have implicated the MYC family of transcription factors as important oncogenic factors in neuroendocrine tumors. We take a systematic approach to understand the roles of the MYC family (c-MYC, n-MYC, l-MYC) in the tumorigenesis of neuroendocrine cancers of the lung, GI tract, pancreas, kidney, prostate, pediatric neuroblastoma, and adrenal glands. Reflecting the complexity of neuroendocrine cancers, we highlight the roles of the MYC family in deregulating the cell cycle and transcriptional networks, invoking cellular plasticity, affecting proliferation capacity, aiding in chromatin remodeling, angiogenesis, metabolic changes, and resistance mechanisms. Depicting the diversity of neuroendocrine cancers, we suggest new approaches in understanding the underlying tumorigenic processes of neuroendocrine cancers from the perspective of MYC.

Indexed as

CarcinogenesisNeuroendocrine TumorsProto-Oncogene Proteins c-mycAnimalsDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticHumansMYC protein, humanProto-Oncogene Proteins c-mycMYCNeuroendocrineOncogeneTranscription factor

Identifiers

PMID40280500
PMCPMC13591539

What OpenQuestion holds

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Registered trials

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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.