Evidence map›Paper›PMID 20194733›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents.

Monique Dail, Qing Li, Andrew McDaniel, Jason Wong, Keiko Akagi, Ben Huang, Hio Chung Kang, Scott C Kogan, Kevan Shokat, Linda Wolff and 2 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Notch Partners in the Long Journey of T-ALL Pathogenesis.International journal of molecular sciences · 2023
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Leukemia-specific delivery of mutant NOTCH1 targeted therapy.The Journal of experimental medicine · 2018
    Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

12 authors.

Monique DailDepartments of Pediatrics, Medicine, Laboratory Medicine, and Pharmaceutical Chemistry, University of California, San Francisco, CA 94143, USA.
Qing Li
Andrew McDaniel
Jason Wong
Keiko Akagi
Ben Huang
Hio Chung Kang
Scott C Kogan
Kevan Shokat
Linda Wolff
Benjamin S Braun
Kevin Shannon

Funding

MOUSE MODELS OF MYELOID LEUKEMIAU01CA084221 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHANNON, KEVIN M. · 1999 to 2009
$8.7M
Research Training in Childhood CancerT32CA128583 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Eric Alejandro Sweet-Cordero · 2007 to 2026
$6.0M
Translational Investigation of KRas & NF1 in Myeloid LeukemiaR37CA072614 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SHANNON, KEVIN M. · 2007 to 2016
$3.4M
Modeling Multi-step Leukemogenesis Nf1 and Kras Mutant MiceK08CA119105 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LAUCHLE, JENNIFER O · 2006 to 2009
$384k
Intramural NIH HHSNCI NIH HHS K08 CA119105NCI NIH HHS R37 CA072614NCI NIH HHS R37 CA72614NCI NIH HHS T32 CA128583NCI NIH HHS U01 CA084221NCI NIH HHS U01 CA84221
6 · The paper itself

Abstract

Mice that accurately model the genetic diversity found in human cancer are valuable tools for interrogating disease mechanisms and investigating novel therapeutic strategies. We performed insertional mutagenesis with the MOL4070LTR retrovirus in Mx1-Cre, Kras(G12D) mice and generated a large cohort of T lineage acute lymphoblastic leukemias (T-ALLs). Molecular analysis infers that retroviral integration within Ikzf1 is an early event in leukemogenesis that precedes Kras(G12D) expression and later acquisition of somatic Notch1 mutations. Importantly, biochemical analysis uncovered unexpected heterogeneity, which suggests that Ras signaling networks are remodeled during multistep tumorigenesis. We tested tumor-derived cell lines to identify biomarkers of therapeutic response to targeted inhibitors. Whereas all T-ALLs tested were sensitive to a dual-specificity phosphoinosityl 3-kinase/mammalian target of rapamycin inhibitor, biochemical evidence of Notch1 activation correlated with sensitivity to gamma-secretase inhibition. In addition, Kras(G12D) T-ALLs were more responsive to a MAP/ERK kinase inhibitor in vitro and in vivo. Together, these studies identify a genetic pathway involving Ikzf1, Kras(G12D), and Notch1 in T lineage leukemogenesis, reveal unexpected diversity in Ras-regulated signaling networks, and define biomarkers of drug responses that may inform treatment strategies.

Indexed as

Cell LineageAmino Acid SubstitutionAmyloid Precursor Protein SecretasesAnimalsAntineoplastic AgentsBenzamidesCell Line, TumorClone CellsDiphenylamineEnzyme InhibitorsGenetic LociHumansIkaros Transcription FactorIntegrasesMiceModels, ImmunologicalAmyloid Precursor Protein SecretasesAntineoplastic AgentsBenzamidesCre recombinaseDiphenylamineEnzyme InhibitorsHras protein, mouseIkaros Transcription FactorIntegrasesmirdametinibMutant ProteinsNotch1 protein, mouseProto-Oncogene Proteins p21(ras)Receptor, Notch1Zfpn1a1 protein, mouse

Identifiers

PMID20194733
PMCPMC2841878

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.