Evidence map›Paper›PMID 36734615›Full record

ReviewJournal of the American Chemical Society2023

Demystifying the Druggability of the MYC Family of Oncogenes.

Nishant M Karadkhelkar, Mingliang Lin, Lisa M Eubanks, Kim D Janda

Open access · greenAbstract readReview
In one paragraph

Review in Journal of the American Chemical Society, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 42 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

4 authors at 1 institution in 1 country.

Nishant M KaradkhelkarDepartment of Chemistry, Department of Immunology and Microbial Science, The Skaggs Institute for Chemical Biology, and WIRM Institute for Research and Medicine, The Scripps Research Institute, La Jolla, California 92037, United States.
Mingliang LinDepartment of Chemistry, Department of Immunology and Microbial Science, The Skaggs Institute for Chemical Biology, and WIRM Institute for Research and Medicine, The Scripps Research Institute, La Jolla, California 92037, United States.ORCID 0000-0002-3325-4539
Lisa M EubanksDepartment of Chemistry, Department of Immunology and Microbial Science, The Skaggs Institute for Chemical Biology, and WIRM Institute for Research and Medicine, The Scripps Research Institute, La Jolla, California 92037, United States.ORCID 0000-0001-5288-6294
Kim D JandaDepartment of Chemistry, Department of Immunology and Microbial Science, The Skaggs Institute for Chemical Biology, and WIRM Institute for Research and Medicine, The Scripps Research Institute, La Jolla, California 92037, United States.ORCID 0000-0001-6759-4227
Scripps Research Institute · US

Funding

High-Throughput Screen for the Oncoprotein MYCR01CA262290 · NCI · SCRIPPS RESEARCH INSTITUTE, THE · PI JANDA, KIM · 2021 to 2024
$1.6M
NCI NIH HHS R01 CA262290
6 · The paper itself

Abstract

The MYC family of oncogenes (MYC, MYCN, and MYCL) encodes a basic helix-loop-helix leucine zipper (bHLHLZ) transcriptional regulator that is responsible for moving the cell through the restriction point. Through the HLHZIP domain, MYC heterodimerizes with the bHLHLZ protein MAX, which enables this MYC-MAX complex to bind to E-box regulatory DNA elements thereby controlling transcription of a large group of genes and their proteins. Translationally, MYC is one of the foremost oncogenic targets, and deregulation of expression of the MYC family gene/proteins occurs in over half of all human tumors and is recognized as a hallmark of cancer initiation and maintenance. Additionally, unexpected roles for this oncoprotein have been found in cancers that nominally have a non-MYC etiology. Although MYC is rarely mutated, its gain of function in cancer results from overexpression or from amplification. Moreover, MYC is a pleiotropic transcription factor possessing broad pathogenic prominence making it a coveted cancer target. A widely held notion within the biomedical research community is that the reliable modulation of MYC represents a tremendous therapeutic opportunity given its role in directly potentiating oncogenesis. However, the MYC-MAX heterodimer interaction contains a large surface area with a lack of well-defined binding sites creating the perception that targeting of MYC-MAX is forbidding. Here, we discuss the biochemistry behind MYC and MYC-MAX as it relates to cancer progression associated with these transcription factors. We also discuss the notion that MYC should no longer be regarded as undruggable, providing examples that a therapeutic window is achievable despite global MYC inhibition.

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsNeoplasmsHumansOncogenesProto-Oncogene Proteins c-mycTranscription FactorsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsProto-Oncogene Proteins c-mycTranscription Factors

Identifiers

PMID36734615
PMCPMC10182829
OpenAlexW4319063558

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.