Evidence map›Paper›PMID 39389815›Full record

ArticleTrends in pharmacological sciences2024

DOT1L: orchestrating methylation-dependent radiotheRAPy responses via BRCA1.

Justin W Leung, Kyle M Miller

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Trends in pharmacological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Justin W LeungDepartment of Radiation Oncology, University of Texas Health and Science Center, San Antonio, TX 78229, USA. Electronic address: leungj@uthscsa.edu.
Kyle M MillerDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA. Electronic address: kyle.miller@austin.utexas.edu.

Funding

Shaping DNA Damage Response Networks Via Histone H2A VariantsR01CA198279 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI Kyle M Miller · 2016 to 2026
$3.3M
Mechanisms of Endogenous DNA Damage PromotionR01CA250905 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MILLER, KYLE M, ROSENBERG, SUSAN M · 2020 to 2024
$3.3M
Deciphering the chromatin-based DNA damage response pathwayR35GM137798 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI Justin Wai Chung Leung · 2020 to 2026
$2.4M
Mechanistic characterization of the cell cycle-dependent DNA repair pathway- ResubmissionR01CA244261 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI Justin Wai Chung Leung · 2021 to 2026
$1.5M
NCI NIH HHS R01 CA198279NCI NIH HHS R01 CA244261NCI NIH HHS R01 CA250905NIGMS NIH HHS R35 GM137798
6 · The paper itself

Abstract

Breast Cancer Type 1 Susceptibility Protein (BRCA)-1 existing in several functionally distinct complexes, promotes DNA repair of DNA double-strand breaks (DSBs). A recent study by Tang and colleagues identifies the lysine methyltransferase Disruptor of Telomeric Silencing 1-Like (DOT1L) involved in modifying Receptor-Associated Protein 80 (RAP80) to promote BRCA1-A complex localization and repair functions at DNA breaks. This study illuminates a potential therapeutic target for cancer radiotherapy.

Indexed as

BRCA1 ProteinHistone-Lysine N-MethyltransferaseAnimalsBreast NeoplasmsDNA Breaks, Double-StrandedDNA MethylationDNA RepairFemaleHumansMethylationMethyltransferasesBRCA1 ProteinBRCA1 protein, humanDOT1L protein, humanHistone-Lysine N-MethyltransferaseMethyltransferasesBRCA1DOT1Lhomologous recombinationradiotherapyRAP80

Identifiers

PMID39389815
PMCPMC11580024

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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.