Evidence map›Paper›PMID 25482130›Full record

ArticleLeukemia2015

L-type amino-acid transporter 1 (LAT1): a therapeutic target supporting growth and survival of T-cell lymphoblastic lymphoma/T-cell acute lymphoblastic leukemia.

C Rosilio, M Nebout, V Imbert, E Griessinger, Z Neffati, J Benadiba, T Hagenbeek, H Spits, J Reverso, D Ambrosetti and 5 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
5.2field-weighted citation impact, top 5% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Pooled it
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  15. Small molecule inhibitors for cancer metabolism: promising prospects to be explored.Journal of cancer research and clinical oncology · 2023
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24 more citing papers are in PubMed but not listed here.

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

15 authors at 7 institutions in 4 countries.

C Rosilio1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France.
M Nebout1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France.
V Imbert1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France.
E Griessinger1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France.
Z Neffati1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France.
J Benadiba1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France [3] Centre Hospitalier Universitaire de Nice, Service d'Oncologie Pédiatrique, Hôpital de l'Archet, Nice, France.
T HagenbeekDepartment of Molecular Biology, Genentech, Inc., South San Francisco, CA, USA.
H SpitsTytgat Institute of Intestinal and Liver Research, Academic Medical Center, Amsterdam, The Netherlands.
J ReversoCentre Hospitalier Universitaire de Nice, Laboratoire Central d'Anatomie et Cytologie Pathologiques, Hôpital de l'Archet, Nice, France.
D AmbrosettiCentre Hospitalier Universitaire de Nice, Laboratoire Central d'Anatomie et Cytologie Pathologiques, Hôpital de l'Archet, Nice, France.
J-F MichielsCentre Hospitalier Universitaire de Nice, Laboratoire Central d'Anatomie et Cytologie Pathologiques, Hôpital de l'Archet, Nice, France.
B Bailly-MaitreINSERM, U1065, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Complications hépatiques de l'obésité, Nice, France.
H Endou1] Department of Pharmacology and Toxicology, Kyorin University, Tokyo, Japan [2] J-Pharma, Co., Ltd, Yokohama, Japan.
M F WempeMedicinal Chemistry Core Facility, School of Pharmacy, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
J-F Peyron1] UMR INSERM U1065/UNS, Centre Méditerranéen de Médecine Moléculaire (C3M), Equipe Inflammation, Cancer, Cellules Souches Cancéreuses, Nice, France [2] Université de Nice-Sophia Antipolis, UFR Médecine, Faculté de Médecine, Nice, France [3] Centre Hospitalier Universitaire de Nice, Service d'Oncologie Pédiatrique, Hôpital de l'Archet, Nice, France.
Centre Méditerranéen de Médecine Moléculaire · FRCentre Hospitalier Universitaire de Nice · FRInserm · FRAcademic Medical Center · NLHôpital l'Archet · FRKyorin University · JPUniversity of Colorado Anschutz Medical Campus · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The altered metabolism of cancer cells is a treasure trove to discover new antitumoral strategies. The gene (SLC7A5) encoding system L amino-acid transporter 1 (LAT1) is overexpressed in murine lymphoma cells generated via T-cell deletion of the pten tumor suppressor, and also in human T-cell acute lymphoblastic leukemia (T-ALL)/lymphoma (T-LL) cells. We show here that a potent and LAT1 selective inhibitor (JPH203) decreased leukemic cell viability and proliferation, and induced transient autophagy followed by apoptosis. JPH203 could also alter the in vivo growth of luciferase-expressing-tPTEN-/- cells xenografted into nude mice. In contrast, JPH203 was nontoxic to normal murine thymocytes and human peripheral blood lymphocytes. JPH203 interfered with constitutive activation of mTORC1 and Akt, decreased expression of c-myc and triggered an unfolded protein response mediated by the C/EBP homologous protein (CHOP) transcription factor associated with cell death. A JPH203-resistant tPTEN-/-clone appeared CHOP induction deficient. We also demonstrate that targeting LAT1 may be an efficient broad spectrum adjuvant approach to treat deadly T-cell malignancies as the molecule synergized with rapamycin, dexamethasone, doxorubicin, velcade and l-asparaginase to alter leukemic cell viability.

Indexed as

Large Neutral Amino Acid-Transporter 1Precursor T-Cell Lymphoblastic Leukemia-LymphomaAnimalsApoptosisCell Line, TumorCell ProliferationCell SurvivalFlow CytometryHumansMiceXenograft Model Antitumor AssaysLarge Neutral Amino Acid-Transporter 1SLC7A5 protein, humanSlc7a5 protein, mouse

Identifiers

PMID25482130
OpenAlexW2047118904

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.