Evidence map›Paper›PMID 28461505›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Suppressors and activators of JAK-STAT signaling at diagnosis and relapse of acute lymphoblastic leukemia in Down syndrome.

Omer Schwartzman, Angela Maria Savino, Michael Gombert, Chiara Palmi, Gunnar Cario, Martin Schrappe, Cornelia Eckert, Arend von Stackelberg, Jin-Yan Huang, Michal Hameiri-Grossman and 18 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
9.2field-weighted citation impact, top 2% 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

44 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Leukemogenesis in infants and young children with trisomy 21.Hematology. American Society of Hematology. Education Program · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Frontiers in cell and developmental biology · 2022
    Review
  20. Article
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

28 authors at 14 institutions in 5 countries.

Omer SchwartzmanThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel.
Angela Maria SavinoThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel.
Michael GombertDepartment of Pediatric Hemato-Oncology and Immunology, Medical Faculty, Heinrich-Heine-University, Dusseldorf 40225, Germany.
Chiara PalmiCentro Ricerca M. Tettamanti, Clinica Pediatrica, Università di Milano Bicocca, Fondazione MBBM/Ospedale San Gerardo, 20900 Monza, Italy.
Gunnar CarioDepartment of Pediatrics, Medical University of Schleswig Holstein, 24105 Kiel, Germany.
Martin SchrappeDepartment of Pediatrics, Medical University of Schleswig Holstein, 24105 Kiel, Germany.
Cornelia EckertPediatric Oncology/Hematology, Charité-Universitätsmedizin, 13353 Berlin, Germany.
Arend von StackelbergPediatric Oncology/Hematology, Charité-Universitätsmedizin, 13353 Berlin, Germany.
Jin-Yan HuangState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, Jiao Tong University School of Medicine, Shanghai 200025, China.
Michal Hameiri-GrossmanDepartment of Human Molecular Genetics and Biochemistry, Sackler Medical School, Tel Aviv University, Tel Aviv 69978, Israel.
Smadar AvigadDepartment of Human Molecular Genetics and Biochemistry, Sackler Medical School, Tel Aviv University, Tel Aviv 69978, Israel.
Geertruy Te KronnieDepartment of Women's and Children's Health, University of Padova, 35131 Padova, Italy.
Ifat GeronThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel.
Yehudit BirgerThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel.
Avigail ReinThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel.
Giulia ZarfatiThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel.
Ute FischerDepartment of Pediatric Hemato-Oncology and Immunology, Medical Faculty, Heinrich-Heine-University, Dusseldorf 40225, Germany.
Zohar MukamelDepartment of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel.
Martin StanullaPediatric Hematology and Oncology, Hannover Medical School, 30625 Hannover, Germany.
Andrea BiondiCentro Ricerca M. Tettamanti, Clinica Pediatrica, Università di Milano Bicocca, Fondazione MBBM/Ospedale San Gerardo, 20900 Monza, Italy.
Giovanni CazzanigaCentro Ricerca M. Tettamanti, Clinica Pediatrica, Università di Milano Bicocca, Fondazione MBBM/Ospedale San Gerardo, 20900 Monza, Italy.
Amedeo VetereCenter for the Science of Therapeutics, Proteomics Platform, Medical and Population Genetics Program, Broad Institute, Cambridge, MA 02142.
Bridget K WagnerCenter for the Science of Therapeutics, Proteomics Platform, Medical and Population Genetics Program, Broad Institute, Cambridge, MA 02142.
Zhu ChenState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, Jiao Tong University School of Medicine, Shanghai 200025, China; zchen@stn.sh.cn Arndt.Borkhardt@med.uni-duesseldorf.de sizraeli@sheba.health.gov.il.
Sai-Juan ChenState Key Laboratory of Medical Genomics, Shanghai Institute of Hematology, Rui Jin Hospital, Jiao Tong University School of Medicine, Shanghai 200025, China.
Amos TanayDepartment of Computer Science and Applied Mathematics, Weizmann Institute of Science, Rehovot 76100, Israel.
Arndt BorkhardtDepartment of Pediatric Hemato-Oncology and Immunology, Medical Faculty, Heinrich-Heine-University, Dusseldorf 40225, Germany; zchen@stn.sh.cn Arndt.Borkhardt@med.uni-duesseldorf.de sizraeli@sheba.health.gov.il.
Shai IzraeliThe Gene Development and Environment Pediatric Research Institute, Pediatric Hemato-Oncology, Edmond and Lily Safra Children's Hospital, Sheba Medical Center, Tel Hashomer, Ramat Gan 52621, Israel; zchen@stn.sh.cn Arndt.Borkhardt@med.uni-duesseldorf.de sizraeli@sheba.health.gov.il.
Edmond and Lily Safra Children's Hospital · ILHeinrich Heine University Düsseldorf · DEShanghai Institute of Hematology · CNUniversity of Milano-Bicocca · ITCharité - Universitätsmedizin Berlin · DEHoward Hughes Medical Institute · USSheba Medical Center · ILTel Aviv University · ILWeizmann Institute of Science · ILMedizinische Hochschule Hannover · DESchneider Children's Medical Center · ILUniversity Hospital Schleswig-Holstein · DEUniversity of Lübeck · DEUniversity of Padua · IT

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Children with Down syndrome (DS) are prone to development of high-risk B-cell precursor ALL (DS-ALL), which differs genetically from most sporadic pediatric ALLs. Increased expression of cytokine receptor-like factor 2 (CRLF2), the receptor to thymic stromal lymphopoietin (TSLP), characterizes about half of DS-ALLs and also a subgroup of sporadic "Philadelphia-like" ALLs. To understand the pathogenesis of relapsed DS-ALL, we performed integrative genomic analysis of 25 matched diagnosis-remission and -relapse DS-ALLs. We found that the CRLF2 rearrangements are early events during DS-ALL evolution and generally stable between diagnoses and relapse. Secondary activating signaling events in the JAK-STAT/RAS pathway were ubiquitous but highly redundant between diagnosis and relapse, suggesting that signaling is essential but that no specific mutations are "relapse driving." We further found that activated JAK2 may be naturally suppressed in 25% of CRLF2

Indexed as

AdolescentCell Line, TumorChildChild, PreschoolDown SyndromeFemaleHumansJanus KinasesMaleMutationPrecursor Cell Lymphoblastic Leukemia-LymphomaReceptors, CytokineRecurrenceSignal TransductionSTAT Transcription FactorsUbiquitin ThiolesteraseCRLF2 protein, humanJanus KinasesReceptors, CytokineSTAT Transcription FactorsUbiquitin ThiolesteraseUSP9X protein, humanacute lymphoblastic leukemiaCRLF2Down syndromeJAK-STAT signalingUSP9X

Identifiers

PMID28461505
PMCPMC5441776
OpenAlexW2611874825

What OpenQuestion holds

Textmetadata
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.