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Cancers
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T-Cell Lymphoma: From Diagnosis to Treatment
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T-Cell Lymphoma: From Diagnosis to Treatment

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: 31 May 2026 | Viewed by 1720

Special Issue Editors

Dr. Lubomir Sokol

E-Mail Website
Guest Editor
Department of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA
Interests: cutaneous lymphoma (CTCL); Hodgkin lymphoma; leukemia; non-Hodgkin lymphoma
Dr. Yumeng Zhang

E-Mail Website
Guest Editor
Department of Malignant Hematology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA
Interests: cutaneous lymphoma (CTCL); Hodgkin lymphoma; non-Hodgkin lymphoma

Special Issue Information

Dear Colleagues,

Cutaneous and peripheral T-cell lymphomas (CTCL and PTCL) represent a heterogeneous group of malignancies characterized by variable clinical presentations, diverse molecular landscapes, and often unpredictable responses to therapy. Among these, Sezary syndrome (SS) and mycosis fungoides (MF) exemplify the complex interplay between cellular origin, genetic aberrations, and microenvironmental influences that underpin disease heterogeneity and therapeutic resistance. Despite advances in diagnosis and treatment, achieving durable remission remains a significant clinical challenge, highlighting the urgent need to deepen our understanding of the molecular and immunologic mechanisms driving these diseases.

This Special Issue seeks to elucidate critical, interconnected facets of T-cell lymphomagenesis and therapeutic vulnerability, spanning cellular, genetic, epigenetic, and immunologic dimensions. Together, this series presents a cohesive narrative from cellular origin to cutting-edge therapy, uniting mechanistic insights with clinical relevance. The novel findings highlighted herein ranging from the impact of clonotypic heterogeneity and driver mutations to the therapeutic promise of epigenetic modulation and immunotherapy offer a roadmap for precision medicine in T-cell lymphomas. By integrating these discoveries into clinical practice, hematologists, oncologists, and pathologists are better equipped to predict disease behavior, tailor interventions, and ultimately improve patient outcomes in a landscape that has long been defined by complexity and unmet need.

Dr. Lubomir Sokol
Dr. Yumeng Zhang
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cutaneous T-cell lymphomas (CTCLs)
  • peripheral T-cell lymphomas (PTCLs)
  • Sezary syndrome (SS)
  • mycosis fungoides (MF)
  • genetic
  • epigenetic
  • therapeutic strategies

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Published Papers (2 papers)

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Review

15 pages, 653 KB  
Review
Revisiting the Origins of Cutaneous T-Cell Lymphoma: A Progenitor-Based Model
by Yumeng Zhang and Lubomir Sokol
Cancers 2026, 18(9), 1393; https://doi.org/10.3390/cancers18091393 - 28 Apr 2026
Viewed by 481
Abstract
Cutaneous T-cell lymphoma (CTCL), primarily mycosis fungoides (MF) and Sézary syndrome (SS), has long been characterized as a neoplasm of mature memory T cells, based on monoclonal T-cell receptor (TCR) rearrangements and tissue-resident memory (TRM)/central memory (TCM) T-cell phenotypes. This review synthesizes converging [...] Read more.
Cutaneous T-cell lymphoma (CTCL), primarily mycosis fungoides (MF) and Sézary syndrome (SS), has long been characterized as a neoplasm of mature memory T cells, based on monoclonal T-cell receptor (TCR) rearrangements and tissue-resident memory (TRM)/central memory (TCM) T-cell phenotypes. This review synthesizes converging population-genetic, multi-omic, and single-cell evidence to argue that this characterization is incomplete and that a progenitor-based model better accounts for the full spectrum of disease biology. We present evidence that initiating mutations arise in hematopoietic stem or early lymphoid progenitor survive thymic selection, and diversify after TCR assembly, resulting in branched evolution across both blood and skin. In SS, paired analyses reveal > 200 shared variants between CD34+ progenitors and Sézary cells, as well as signal-joint T-cell receptor excision circle (sjTREC) positivity, providing direct progenitor-level evidence. In MF, convergent signals, multiple malignant clonotypes per lesion, greater blood–skin than skin–skin clonotype overlap, and compartment-specific CNV subclones, implicate hematogenous seeding and reseeding. Population-scale lymphoid clonal hematopoiesis and lymphoid-pattern mosaic chromosomal alterations define a compatible antecedent state. Spatial single-cell atlases and trajectory analyses map site-conditioned programs in skin, including Th2-skewed cytokines, microbial responses, and UV signatures, that select and expand subclones and explain inter- and intra-patient heterogeneity. This framework reconciles mature immunophenotypes with upstream initiation and clarifies why compartment-focused therapies often reshape rather than eradicate disease. It yields testable predictions and actionable implications: trials should pair multicompartment cytoreduction with strategies that attenuate progenitor-derived reservoirs, restore immune balance, and repair skin barrier dysfunction. A progenitor-initiated, niche-adapted model provides a coherent scaffold for more durable control in CTCL. Full article
(This article belongs to the Special Issue T-Cell Lymphoma: From Diagnosis to Treatment)
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12 pages, 237 KB  
Review
JAK Inhibitors in the Treatment of T-Cell Lymphomas: Current Evidence and Future Directions
by Gardenia Taza, Naveed Ahmed and John L. Vaughn
Cancers 2026, 18(5), 799; https://doi.org/10.3390/cancers18050799 - 28 Feb 2026
Viewed by 867
Abstract
T-cell lymphomas are a heterogeneous group of lymphoid neoplasms with a variable prognosis. They can be further divided into cutaneous T-cell lymphomas and peripheral T-cell lymphomas. Treatment options are relatively limited for patients with relapsed or refractory disease. Janus kinase (JAK) inhibitors have [...] Read more.
T-cell lymphomas are a heterogeneous group of lymphoid neoplasms with a variable prognosis. They can be further divided into cutaneous T-cell lymphomas and peripheral T-cell lymphomas. Treatment options are relatively limited for patients with relapsed or refractory disease. Janus kinase (JAK) inhibitors have emerged as promising new drugs for these lymphomas, as increasing evidence supports the JAK and signal transducer and activator of transcription (STAT) pathway as a potential target. The objective of this review is to summarize the current evidence supporting the use of JAK inhibitors in the treatment of T-cell lymphomas and highlight areas for future research. Although many JAK inhibitors have been developed for the treatment of autoimmune conditions, only a subset of these have been tested in T-cell lymphomas and reported in the literature. These include abrocitinib, cerdulatinib, golidocitinib, ruxolitinib, tofacitinib, and upadacitinib. Other drugs are currently being tested in clinicals trials, including pacritinib and ivarmacitinib, but results are not yet available. Most of the published data are for ruxolitinib, which was found to have a clinical benefit rate of up to 53% in patients with PTCL with activating JAK and/or STAT mutations. Response durations are limited, which may be overcome through combination therapies in the future. JAK inhibitors are associated with multiple adverse effects, including cytopenias and infections, and long-term safety data are lacking for newer agents. Future studies will need to clarify long-term safety and efficacy through well-designed clinical trials involving larger groups of patients. Full article
(This article belongs to the Special Issue T-Cell Lymphoma: From Diagnosis to Treatment)
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