Evidence map›Paper›PMID 35199090›Full record

ReviewJID innovations : skin science from molecules to population health2022

Drugging the Epigenome: Overcoming Resistance to Targeted and Immunotherapies in Melanoma.

Ailish Hanly, Frederick Gibson, Sarah Nocco, Samantha Rogers, Muzhou Wu, Rhoda M Alani

Open access · goldAbstract readReview
In one paragraph

Review in JID innovations : skin science from molecules to population health, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
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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.

Ailish HanlyDepartment of Dermatology, Boston University School of Medicine|Boston Medical Center, Boston, Massachusetts, USA.
Frederick GibsonDepartment of Dermatology, Boston University School of Medicine|Boston Medical Center, Boston, Massachusetts, USA.
Sarah NoccoDepartment of Dermatology, Boston University School of Medicine|Boston Medical Center, Boston, Massachusetts, USA.
Samantha RogersDepartment of Dermatology, Boston University School of Medicine|Boston Medical Center, Boston, Massachusetts, USA.
Muzhou WuDepartment of Dermatology, Boston University School of Medicine|Boston Medical Center, Boston, Massachusetts, USA.
Rhoda M AlaniDepartment of Dermatology, Boston University School of Medicine|Boston Medical Center, Boston, Massachusetts, USA.
Boston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This past decade has seen tremendous advances in understanding the molecular pathogenesis of melanoma and the development of novel effective therapies for melanoma. Targeted therapies and immunotherapies that extend survival of patients with advanced disease have been developed; however, the vast majority of patients experience relapse and therapeutic resistance over time. Moreover, cellular plasticity has been demonstrated to be a driver of therapeutic resistance mechanisms in melanoma and other cancers, largely functioning through epigenetic mechanisms, suggesting that targeting of the cancer epigenetic landscape may prove a worthwhile endeavor to ensure durable treatment responses and cures. Here, we review the epigenetic alterations that characterize melanoma development, progression, and resistance to targeted therapies as well as epigenetic therapies currently in use and under development for melanoma and other cancers. We further assess the landscape of epigenetic therapies in clinical trials for melanoma and provide a framework for future advances in epigenetic therapies to circumvent the development of therapeutic resistance in melanoma.

Indexed as

BRAFi, BRAF inhibitorDNMT, DNA methyltransferaseDNMTi, DNA methyltransferase inhibitordsRNA, double-stranded RNAEZH2, enhancer of zeste homolog 2EZH2i, enhancer of zeste homolog 2 inhibitorHAT, histone acetyltransferaseHDAC, histone deacetylaseHDACi, histone deacetylase inhibitorMEKi, MAPK/extracellular signal‒regulated kinase inhibitorPTM, post-translational modificationSIRT, sirtuinTMZ, temozolomide

Identifiers

PMID35199090
PMCPMC8844701
OpenAlexW4212956459

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.