Evidence map›Paper›PMID 26928911›Full record

ArticleCancer science2016

Xenotransplantation elicits salient tumorigenicity of adult T-cell leukemia-derived cells via aberrant AKT activation.

Kazunori Yamaguchi, Tomoka Takanashi, Kentaro Nasu, Keiichi Tamai, Mai Mochizuki, Ikuro Satoh, Shoji Ine, Osamu Sasaki, Kennichi Satoh, Nobuyuki Tanaka and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Article
  3. 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 at 2 institutions in 1 country.

Kazunori YamaguchiDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Tomoka TakanashiDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Kentaro NasuDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Keiichi TamaiDepartment of Cancer Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
Mai MochizukiDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Ikuro SatohDepartment of Cancer Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
Shoji IneDivision of Hematology, Miyagi Cancer Center, Natori, Japan.
Osamu SasakiDivision of Hematology, Miyagi Cancer Center, Natori, Japan.
Kennichi SatohDepartment of Cancer Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
Nobuyuki TanakaDepartment of Cancer Science, Tohoku University Graduate School of Medicine, Sendai, Japan.
Hideo HarigaeDepartment of Hematology and Rheumatology, Tohoku University Graduate School of Medicine, Sendai, Japan.
Kazuo SugamuraDivision of Molecular and Cellular Oncology, Miyagi Cancer Center Research Institute, Natori, Japan.
Miyagi Prefectural Hospital Organization · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transplantation of human cancer cells into immunodeficient NOD/SCID/IL-2Rγc(null) (NOG) mice often causes highly malignant cell populations like cancer stem cells to emerge. Here, by serial transplantation in NOG mice, we established two highly tumorigenic adult T-cell leukemia-derived cell lines, ST1-N6 and TL-Om1-N8. When transplanted s.c., these cells formed tumors significantly earlier and from fewer initial cells than their parental lines ST1 and TL-Om1. We found that protein kinase B (AKT) signaling was upregulated in ST1-N6 and TL-Om1-N8 cells, and that this upregulation was due to the decreased expression of a negative regulator, INPP5D. Furthermore, the introduction of a constitutively active AKT mutant expression vector into ST1 cells augmented the tumorigenicity of the cells, whereas treatment with the AKT inhibitor MK-2206 attenuated the progression of tumors induced by ST1-N6 cells. Collectively, our results reveal that the AKT signaling pathway plays a critical role in the malignancy of adult T-cell leukemia-derived cells.

Indexed as

Neoplasm TransplantationTransplantation, HeterologousAnimalsCell Line, TumorCell Transformation, NeoplasticDown-RegulationEnzyme ActivationHumansLeukemia-Lymphoma, Adult T-CellMicePhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesProto-Oncogene MasProto-Oncogene Proteins c-aktSignal TransductionUp-RegulationINPP5D protein, humanMAS1 protein, humanPhosphatidylinositol-3,4,5-Trisphosphate 5-PhosphatasesPhosphatidylinositol 3-KinasesProto-Oncogene MasProto-Oncogene Proteins c-aktAdult T-cell leukemiaproto-oncogene protein Aktsevere combined immunodeficient micetumor-initiating cellsxenotransplantation

Identifiers

PMID26928911
PMCPMC4970830
OpenAlexW2292230709

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.