ArticleThe Journal of clinical investigation2007
Gene expression analysis of peripheral T cell lymphoma, unspecified, reveals distinct profiles and new potential therapeutic targets.
Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02431403 (Open-labeled, Multicenter, Phase I/II Study of Imatinib Combined With ESHAP as Salvage Therapy in Relapsed/Refractory Non-Hodgkin's Lymphoma), which is not on this map. Cited by 143 papers, 1 of them a synthesis that pooled 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.
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.
Open-labeled, Multicenter, Phase I/II Study of Imatinib Combined With ESHAP as Salvage Therapy in Relapsed/Refractory Non-Hodgkin's Lymphoma
Who cites it
143 citing papers in PubMed, 1 synthesis or guideline pooled it, 304 citations in OpenAlex.
- An integrated genome-wide approach to discover tumor-specific antigens as potential immunologic and clinical targets in cancer.Cancer research · 2012Pooled it
- Phase I/II study of dasatinib and exploratory genomic analysis in relapsed or refractory non-Hodgkin lymphoma.British journal of haematology · 2019Trial
- Pathogenetic and diagnostic significance of microRNA deregulation in peripheral T-cell lymphoma not otherwise specified.Blood cancer journal · 2014Trial
- stabel: An R package for variable selection and prediction in high-dimensional cross-sectional data.Software impacts · 2026Article
- From Cell Lines to Avatars: Charting the Future of Preclinical Modeling in T-Cell Malignancies.Cells · 2026Review
- GANT61 suppresses proliferation and induces apoptosis in ALK-Positive anaplastic large cell lymphoma via modulating the Hh-PIK3IP1-Akt signaling axis.Annals of hematology · 2026Article
- Identification and Validation of BATF3 as a Promising Biomarker Gene for Peripheral T-cell Lymphoma.Current medicinal chemistry · 2026Article
- The Roles of SHCBP1 in Cancer Hallmarks: Molecular Mechanisms and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Review
- Review
- The gene expression profile and cell of origin of canine peripheral T-cell lymphoma.BMC cancer · 2024Article
- KMT2D regulates activation, localization, and integrin expression by T-cells.Frontiers in immunology · 2024Article
- TP63 fusions drive multicomplex enhancer rewiring, lymphomagenesis, and EZH2 dependence.Science translational medicine · 2023Article
- Aberrant expression of GOLM1 protects ALK+ anaplastic large cell lymphoma from apoptosis by enhancing BCL-XL stability.Blood advances · 2023Article
- Emerging Insights into Liver X Receptor α in the Tumorigenesis and Therapeutics of Human Cancers.Biomolecules · 2023Review
- Histopathological Evaluation of Angiogenic Markers in Non-Hodgkin's Lymphoma.Journal of laboratory physicians · 2023Article
- PTCL, NOS: An update on classification, risk-stratification, and treatment.Frontiers in oncology · 2023Review
- Tyrosine kinases in nodal peripheral T-cell lymphomas.Frontiers in oncology · 2023Review
- Article
- Article
83 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peripheral T cell lymphoma, unspecified (PTCL/U), the most common form of PTCL, displays heterogeneous morphology and phenotype, poor response to treatment, and poor prognosis. We demonstrate that PTCL/U shows a gene expression profile clearly distinct from that of normal T cells. Comparison with the profiles of purified T cell subpopulations (CD4+, CD8+, resting [HLA-DR-], and activated [HLA-DR+]) reveals that PTCLs/U are most closely related to activated peripheral T lymphocytes, either CD4+ or CD8+. Interestingly, the global gene expression profile cannot be surrogated by routine CD4/CD8 immunohistochemistry. When compared with normal T cells, PTCLs/U display deregulation of functional programs often involved in tumorigenesis (e.g., apoptosis, proliferation, cell adhesion, and matrix remodeling). Products of deregulated genes can be detected in PTCLs/U by immunohistochemistry with an ectopic, paraphysiologic, or stromal location. PTCLs/U aberrantly express, among others, PDGFRalpha, a tyrosine-kinase receptor, whose deregulation is often related to a malignant phenotype. Notably, both phosphorylation of PDGFRalpha and sensitivity of cultured PTCL cells to imatinib (as well as to an inhibitor of histone deacetylase) were found. These results, which might be extended to other more rare PTCL categories, provide insight into tumor pathogenesis and clinical management of PTCL/U.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.