Evidence map›Paper›PMID 19775286›Full record

ArticleCancer science2009

Dual antitumor mechanisms of Notch signaling inhibitor in a T-cell acute lymphoblastic leukemia xenograft model.

Shigeo Masuda, Keiki Kumano, Takahiro Suzuki, Taisuke Tomita, Takeshi Iwatsubo, Hideaki Natsugari, Arinobu Tojo, Makoto Shibutani, Kunitoshi Mitsumori, Yutaka Hanazono and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cancer science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. [Advances in pharmacological research for retinopathy of prematurity].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
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  11. Prolonged inhibition of glioblastoma xenograft initiation and clonogenic growth following in vivo Notch blockade.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013
    Article
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  14. Notch inhibition as a promising new approach to cancer therapy.Advances in experimental medicine and biology · 2012
    Review
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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

13 authors at 6 institutions in 2 countries.

Shigeo MasudaDepartment of Cell Therapy and Transplantation Medicine, University of Tokyo Hospital, Tokyo, Japan.
Keiki Kumano
Takahiro Suzuki
Taisuke Tomita
Takeshi Iwatsubo
Hideaki Natsugari
Arinobu Tojo
Makoto Shibutani
Kunitoshi Mitsumori
Yutaka Hanazono
Seishi Ogawa
Mineo Kurokawa
Shigeru Chiba
The University of Tokyo · JPUniversity of Tokyo Hospital · JPJichi Medical University · JPTokyo University of Agriculture and Technology · JPTokyo Medical University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Constitutive activation of Notch signaling is required for the proliferation of a subgroup of human T-cell acute lymphoblastic leukemias (T-ALL). Previous in vitro studies have demonstrated the therapeutic potential of Notch signaling inhibitors for treating T-ALL. To further examine this possibility, we applied a gamma-secretase inhibitor (GSI) to T-ALL xenograft models. Treatment of established subcutaneous tumors with GSI resulted in partial or complete regression of tumors arising from four T-ALL cell lines that were also sensitive to GSI in vitro. To elucidate the mechanism of action, we transduced DND-41 cells with the active form of Notch1 (aN1), which conferred resistance to in vitro GSI treatment. Nevertheless, in vivo treatment with GSI induced a partial but significant regression of subcutaneous tumors that developed from aN1-transduced DND-41 cells, whereas it induced complete regression of tumors that developed from mock-transduced DND-41 cells. These findings indicate that the remarkable efficacy of GSI might be attributable to dual mechanisms, directly via apoptosis of DND-41 cells through the inhibition of cell-autonomous Notch signaling, and indirectly via disturbance of tumor angiogenesis through the inhibition of non-cell-autonomous Notch signaling.

Indexed as

Amyloid Precursor Protein SecretasesAnimalsAntineoplastic AgentsCell Line, TumorHumansMiceMice, SCIDPrecursor T-Cell Lymphoblastic Leukemia-LymphomaReceptors, NotchSignal TransductionXenograft Model Antitumor AssaysAmyloid Precursor Protein SecretasesAntineoplastic AgentsReceptors, Notch

Identifiers

PMID19775286
PMCPMC11159026
OpenAlexW2014253046

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.