Evidence map›Paper›PMID 25148579›Full record

ArticleThe Journal of investigative dermatology2015

Identification of p38β as a therapeutic target for the treatment of Sézary syndrome.

Meghan Bliss-Moreau, Cristian Coarfa, Preethi H Gunaratne, Joan Guitart, Nancy L Krett, Steven T Rosen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. p38β and Cancer: The Beginning of the Road.International journal of molecular sciences · 2020
    Review
  6. Article
  7. JID VisualDx Quiz: February 2015.The Journal of investigative dermatology · 2015
    Article
  8. 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

6 authors at 3 institutions in 1 country.

Meghan Bliss-MoreauRobert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Cristian CoarfaDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
Preethi H GunaratneDepartment of Biology and Biochemistry, University of Houston, Houston, Texas, USA.
Joan GuitartDepartment of Dermatology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA; Division of Hematology and Oncology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Nancy L KrettRobert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
Steven T RosenRobert H. Lurie Comprehensive Cancer Center, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA; Division of Hematology and Oncology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA; City of Hope Comprehensive Cancer Center, Duarte, California, USA. Electronic address: srosen@coh.org.
Northwestern University · USBaylor College of Medicine · USUniversity of Houston · US

Funding

CARCINOGENESIS TRAINING PROGRAMT32CA009560 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Kathleen Janee Green · 1986 to 2026
$8.4M
NCI NIH HHS T32 CA009560NCI NIH HHS T32CA09560
6 · The paper itself

Abstract

Cutaneous T-cell lymphomas (CTCLs) represent a group of hematopoietic malignancies that home to the skin and have no known molecular basis for disease pathogenesis. Sézary syndrome (SS) is the leukemic variant of CTCL. Currently, CTCL is incurable, highlighting the need for new therapeutic modalities. We have previously observed that combined small-molecule inhibition of protein kinase C-β (PKCβ) and glycogen synthase kinase 3 (GSK3) causes synergistic apoptosis in CTCL cell lines and patient cells. Through microarray analysis of a SS cell line, we surveyed global gene expression following combined PKCβ-GSK3 treatment to elucidate therapeutic targets responsible for cell death. Clinically relevant targets were defined as genes differentially expressed in SS patients that were modulated by combination-drug treatment of SS cells. Gene set enrichment analysis uncovered candidate genes enriched for an immune-cell signature, specifically the T-cell receptor and mitogen-activated protein kinase signaling pathways. Further analysis identified p38 as a potential therapeutic target that is overexpressed in SS patients and decreased by synergistic-inhibitor treatment. This target was verified through small-molecule inhibition of p38, leading to cell death in both SS cell lines and patient cells. These data establish p38 as a SS biomarker and a potential therapeutic target for the treatment of CTCL.

Indexed as

ApoptosisCell Line, TumorGlycogen Synthase Kinase 3HumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 11Protein Kinase C betaSezary SyndromeSkin NeoplasmsGlycogen Synthase Kinase 3Mitogen-Activated Protein Kinase 11Protein Kinase C beta

Identifiers

PMID25148579
PMCPMC4289446
OpenAlexW2049632801

What OpenQuestion holds

Textmetadata
LicenceTDM
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.