Evidence map›Paper›PMID 32747750›Full record

ArticleOncogene2020

Autocrine HGF/c-Met signaling pathway confers aggressiveness in lymph node adult T-cell leukemia/lymphoma.

Haruhito Totani, Keiko Shinjo, Miho Suzuki, Keisuke Katsushima, Shoko Mase, Ayako Masaki, Asahi Ito, Masaki Ri, Shigeru Kusumoto, Hirokazu Komatsu and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
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

14 authors at 2 institutions in 1 country.

Haruhito TotaniDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keiko ShinjoDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Miho SuzukiDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Keisuke KatsushimaDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.ORCID http://orcid.org/0000-0001-7770-432X
Shoko MaseDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Ayako MasakiDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Asahi ItoDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Masaki RiDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.ORCID http://orcid.org/0000-0002-9617-486X
Shigeru KusumotoDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Hirokazu KomatsuDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Takashi IshidaDepartment of Immunology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
Hiroshi InagakiDepartment of Pathology and Molecular Diagnostics, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Shinsuke IidaDepartment of Hematology and Oncology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
Yutaka KondoDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya, Japan. ykondo@med.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0003-3746-3191
Nagoya City University · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adult T-cell leukemia/lymphoma (ATL) is an aggressive T-cell neoplasm. While ATL cells in peripheral blood (PB-ATL) are sensitive to anti-CC chemokine receptor 4 treatment, non-PB-ATLs, including lymph node ATLs (LN-ATLs), are more aggressive and resistant. We examined characteristic cytokines and growth factors that allow non-PB-ATLs to proliferate and invade compared with PB-ATLs. Protein array analysis revealed hepatocyte growth factor (HGF) and C-C motif chemokine 2 (CCL2) were significantly upregulated in non-PB-ATLs compared with PB-ATLs. The HGF membrane receptor, c-Met, was expressed in PB-ATL and non-PB-ATL cell lines, but CCR2, a CCL2 receptor, was not. Immunohistochemical analysis in clinical ATLs revealed high HGF expression in LNs, pharynx, bone marrow, and tonsils. The HGF/c-Met signaling pathway was active downstream in non-PB-ATLs. Downregulation of HGF/c-Met by siRNA or chemical inhibitors decreased in vitro and in vivo proliferation and invasion by non-PB-ATLs. Treatment with bromodomain and extra-terminal motif inhibitor suppressed HGF expression and decreased levels of histone H3 lysine 27 acetylation (H3K27Ac) and bromodomain-containing protein 4 (BRD4) binding promoter and enhancer regions, suppressing non-PB-ATL cellular growth. Our data indicate H3K27Ac/BRD4 epigenetics regulates the HGF/c-MET pathway in ATLs; targeting this pathway may improve treatment of aggressive non-PB-ATLs.

Indexed as

AnimalsCell Line, TumorHepatocyte Growth FactorHumansLeukemia-Lymphoma, Adult T-CellLymph NodesMiceSignal TransductionHepatocyte Growth FactorHGF protein, human

Identifiers

PMID32747750
OpenAlexW3047133528

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.