Evidence map›Paper›PMID 27872090›Full record

ArticleCancer research2017

Mutational Landscape of Pediatric Acute Lymphoblastic Leukemia.

Ling-Wen Ding, Qiao-Yang Sun, Kar-Tong Tan, Wenwen Chien, Anand Mayakonda, Allen Eng Juh Yeoh, Norihiko Kawamata, Yasunobu Nagata, Jin-Fen Xiao, Xin-Yi Loh and 19 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
10.9field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 91 citations in OpenAlex.

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  13. SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors at 3 institutions in 2 countries.

Ling-Wen Ding *Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Qiao-Yang Sun *Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Kar-Tong Tan *Cancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Wenwen ChienCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Anand MayakondaCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Allen Eng Juh YeohCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Norihiko KawamataDepartment of Molecular and Cellular Biology, Beckman Research Institute of City of Hope, Duarte, CA, USA.
Yasunobu NagataDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Jin-Fen XiaoCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Xin-Yi LohCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
De-Chen LinCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Manoj GargCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Yan-Yi JiangCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Liang XuCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Su-Lin LimCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Li-Zhen LiuCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Vikas MadanCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Masashi SanadaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Lucia Torres FernándezCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
S S Hema PreethiCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
Michael LillDivision of Hematology/Oncology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, USA.
Hagop M KantarjianDepartment of Leukemia, University of Texas, MD Anderson Cancer Center, Houston, USA.
Steven M KornblauDepartment of Leukemia, University of Texas, MD Anderson Cancer Center, Houston, USA.
Satoru MiyanoLaboratory of DNA Information Analysis, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan.
Der-Cherng LiangDepartment of Pediatrics, Mackay Memorial Hospital, Taipei, Taiwan.
Seishi OgawaDepartment of Pathology and Tumor Biology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Lee-Yung ShihDivision of Hematology-Oncology, Chang Gung Memorial Hospital, Linkou, Chang Gung University, Taipei, Taiwan.
Henry YangCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
H Phillip KoefflerCancer Science Institute of Singapore, National University of Singapore, Singapore, Singapore.
National University Cancer Institute, Singapore · SGNational University of Singapore · SGKyoto University · JP

Funding

REGULATION OF HEMATOPOIETIC CYTOKINESR01CA026038 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI KOEFFLER, HAROLD PHILLIP · 1985 to 2013
$4.7M
NCI NIH HHS R01 CA026038
6 · The paper itself

Abstract

Current standard of care for patients with pediatric acute lymphoblastic leukemia (ALL) is mainly effective, with high remission rates after treatment. However, the genetic perturbations that give rise to this disease remain largely undefined, limiting the ability to address resistant tumors or develop less toxic targeted therapies. Here, we report the use of next-generation sequencing to interrogate the genetic and pathogenic mechanisms of 240 pediatric ALL cases with their matched remission samples. Commonly mutated genes fell into several categories, including RAS/receptor tyrosine kinases, epigenetic regulators, transcription factors involved in lineage commitment, and the p53/cell-cycle pathway. Unique recurrent mutational hotspots were observed in epigenetic regulators CREBBP (R1446C/H), WHSC1 (E1099K), and the tyrosine kinase FLT3 (K663R, N676K). The mutant WHSC1 was established as a gain-of-function oncogene, while the epigenetic regulator ARID1A and transcription factor CTCF were functionally identified as potential tumor suppressors. Analysis of 28 diagnosis/relapse trio patients plus 10 relapse cases revealed four evolutionary paths and uncovered the ordering of acquisition of mutations in these patients. This study provides a detailed mutational portrait of pediatric ALL and gives insights into the molecular pathogenesis of this disease. Cancer Res; 77(2); 390-400. ©2016 AACR.

Indexed as

AdolescentAnimalsBlotting, WesternChildChild, PreschoolDNA Mutational AnalysisFemaleHigh-Throughput Nucleotide SequencingHumansInfantMaleMiceMutationPrecursor Cell Lymphoblastic Leukemia-Lymphoma

Identifiers

PMID27872090
PMCPMC5243866
OpenAlexW2555713721

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.