Evidence map›Paper›PMID 40723261›Full record

ArticleCancers2025

Cutaneous T-Cell Lymphoma: Yin-Yang Effects of Transcription Factors HLF and NFIL3 in Regulation of Malignant T-Cell Markers in the Context of HDAC Inhibitor Romidepsin Treatment.

Andrew V Kossenkov, Noor Dawany, Sonali Majumdar, Celia Chang, Calen Nichols, Maria Wysocka, Richard Piekarz, Michael K Showe, Susan E Bates, Alain H Rook and 2 more

Abstract read
In one paragraph

Article in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Andrew V KossenkovThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Noor DawanyThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.ORCID 0000-0003-2983-3893
Sonali MajumdarThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.ORCID 0009-0007-9046-8799
Celia ChangThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Calen NicholsThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Maria WysockaDepartment of Dermatology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Richard PiekarzCancer Therapy Evaluation Program, National Cancer Institute, Rockville, MD 20850, USA.ORCID 0000-0002-3591-7893
Michael K ShoweThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.
Susan E BatesDepartment of Hematology/Oncology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Alain H RookDepartment of Dermatology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Ellen J KimDepartment of Dermatology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Louise C ShoweThe Wistar Institute, 3601 Spruce Street, Philadelphia, PA 19104, USA.ORCID 0000-0002-7818-4220

Funding

Tumor Microenvironment and MetastasisP30CA010815 · NCI · WISTAR INSTITUTE · PI Aaron Robert Goldman · 1985 to 2026
$75.9M
HDAC Inhibitors and CTCLR01CA132098 · NCI · WISTAR INSTITUTE · PI SHOWE, LOUISE C. · 2009 to 2013
$2.0M
Integrative Approach to Comprehensive Analysis of High Throughput Data on a Cancer Center LevelR50CA211199 · NCI · WISTAR INSTITUTE · PI Andrew V Kossenkov · 2016 to 2026
$1.6M
Toll Receptor Ligand Therapy of Cutaneous T-Cell LymphomaR01CA122569 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROOK, ALAIN H · 2008 to 2011
$1.1M
NCI NIH HHS CA132098NCI NIH HHS P30 CA010815NCI NIH HHS R01 CA122569NCI NIH HHS R01 CA132098NCI NIH HHS R50 CA211199
6 · The paper itself

Abstract

BACKGROUND/

objectivesWe examined the in vivo effects of successive treatments with the histone deacetylase (HDAC) inhibitor romidepsin in patients with cutaneous T-cell lymphoma (CTCL), using changes in gene expression in peripheral blood mononuclear cells (PBMCs).

methodsExploiting data from a highly responsive CTCL patient through 12 months of treatment, we identified a malignant cell predictor (MCP), a gene signature associated with the diminishing numbers of circulating malignant cells.

resultsThe MCP was successfully validated in the patient's relapse sample 9 months after treatment was terminated and via an independent set of CTCL patient samples.

conclusionsThe MCP set of genes contained novel CTCL markers, including membrane-associated proteins not normally expressed in lymphocytes. A subclass of those markers was also detectable in residual malignant cells undetected by flow cytometry in remission samples from a patient who relapsed 10 months later. We identified a subset of transcriptional regulators, miRNAs and methylation patterns associated with the effect of progressive treatments revealing potential mechanisms of transcriptional dysregulation and functional effects in the malignant cells. We demonstrate a role for transcriptional activator HLF, over-expressed in malignant cells, and downregulated transcriptional-suppressor and immune-modulator NFIL3, as regulators of CTCL-specific genes.

Indexed as

CTCLHDAC inhibitorPAR bZIPromidepsin

Identifiers

PMID40723261
PMCPMC12293868

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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.