Evidence map›Paper›PMID 26314984›Full record

ArticleBlood cancer journal2015

Prognostic signature and clonality pattern of recurrently mutated genes in inactive chronic lymphocytic leukemia.

A M Hurtado, T-H Chen-Liang, B Przychodzen, C Hamedi, J Muñoz-Ballester, B Dienes, M D García-Malo, A I Antón, F de Arriba, R Teruel-Montoya and 4 more

Open access · goldAbstract read
In one paragraph

Article in Blood cancer journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 20% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Oncotarget · 2017
    Article
  8. Review
  9. Prognostic Factors for Chronic Lymphocytic Leukemia.Current hematologic malignancy reports · 2016
    Review
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

14 authors at 3 institutions in 2 countries.

A M HurtadoHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
T-H Chen-LiangHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
B PrzychodzenTraslational Hematology and Oncology Research, Cleveland Clinic, Cleveland, OH, USA.
C HamediHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
J Muñoz-BallesterHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
B DienesTraslational Hematology and Oncology Research, Cleveland Clinic, Cleveland, OH, USA.
M D García-MaloHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
A I AntónHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
F de ArribaHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
R Teruel-MontoyaHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
F J OrtuñoHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
V VicenteHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
J P MaciejewskiTraslational Hematology and Oncology Research, Cleveland Clinic, Cleveland, OH, USA.
A JerezHematology and Medical Oncology Department, Hospital Morales Meseguer, IMIB, Murcia, Spain.
Hospital General Universitario Morales Meseguer · ESCleveland Clinic · USCase Comprehensive Cancer Center

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing numbers of patients are being diagnosed with asymptomatic early-stage chronic lymphocytic leukemia (CLL), with no treatment indication at baseline. We applied a high-throughput deep-targeted analysis, especially designed for covering widely TP53 and ATM genes, in 180 patients with inactive disease at diagnosis, to test the independent prognostic value of CLL somatic recurrent mutations. We found that 40/180 patients harbored at least one acquired variant with ATM (n=17, 9.4%), NOTCH1 (n=14, 7.7%), TP53 (n=14, 7.7%) and SF3B1 (n=10, 5.5%) as most prevalent mutated genes. Harboring one 'sub-Sanger' TP53 mutation granted an independent 3.5-fold increase of probability of needing treatment. Those patients with a double-hit ATM lesion (mutation+11q deletion) had the shorter median time to first treatment (17 months). We found that a genomic variable: TP53 mutations, most of them under the sensitivity of conventional techniques; a cell phenotypic factor: CD38-positive expression; and a classical marker as β2-microglobulin, remained as the unique independent predictors of outcome. The high-throughput determination of TP53 status, particularly in this set of patients frequently lacking high-risk chromosomal aberrations, emerges as a key step, not only for prediction modeling, but also for exploring mutation-specific therapeutic approaches and minimal residual disease monitoring.

Indexed as

MutationAgedDNA Mutational AnalysisFemaleGene FrequencyGenes, NeoplasmGenetic Association StudiesGenetic Predisposition to DiseaseHigh-Throughput Nucleotide SequencingHumansKaplan-Meier EstimateLeukemia, Lymphocytic, Chronic, B-CellMalePrognosisProportional Hazards Models

Identifiers

PMID26314984
PMCPMC4558590
OpenAlexW1246965181

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.