Evidence map›Paper›PMID 33800547›Full record

ReviewInternational journal of molecular sciences2021

Targeting Genome Stability in Melanoma-A New Approach to an Old Field.

Marta Osrodek, Michal Wozniak

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 45% 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

8 citing papers in PubMed, 6 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

2 authors at 1 institution in 1 country.

Marta OsrodekDepartment of Molecular Biology of Cancer, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0002-2575-121X
Michal WozniakDepartment of Molecular Biology of Cancer, Medical University of Lodz, 92-215 Lodz, Poland.ORCID 0000-0003-2251-8647
Medical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite recent groundbreaking advances in the treatment of cutaneous melanoma, it remains one of the most treatment-resistant malignancies. Due to resistance to conventional chemotherapy, the therapeutic focus has shifted away from aiming at melanoma genome stability in favor of molecularly targeted therapies. Inhibitors of the RAS/RAF/MEK/ERK (MAPK) pathway significantly slow disease progression. However, long-term clinical benefit is rare due to rapid development of drug resistance. In contrast, immune checkpoint inhibitors provide exceptionally durable responses, but only in a limited number of patients. It has been increasingly recognized that melanoma cells rely on efficient DNA repair for survival upon drug treatment, and that genome instability increases the efficacy of both MAPK inhibitors and immunotherapy. In this review, we discuss recent developments in the field of melanoma research which indicate that targeting genome stability of melanoma cells may serve as a powerful strategy to maximize the efficacy of currently available therapeutics.

Indexed as

Genomic InstabilityAnimalsClinical Trials as TopicCutaneous Malignant MelanomaDNA DamageDNA RepairDrug Resistance, NeoplasmGenome, HumanHumansImmunotherapyMAP Kinase Kinase KinasesMAP Kinase Signaling SystemMelanomaMiceMolecular Targeted TherapyProtein Kinase InhibitorsBRAF protein, humanMAP Kinase Kinase KinasesProtein Kinase InhibitorsProto-Oncogene Proteins B-rafDNA damageDNA repairdrug resistanceimmune checkpoint inhibitorsMAPK inhibitorsmelanomatargeted therapy

Identifiers

PMID33800547
PMCPMC8036881
OpenAlexW3151078502

What OpenQuestion 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 OpenQuestion graph.