---
title: "Risk Stratification of Incidental T-cell Clonality: A Practical Clinical Framework"
id: "pubmed-42314037"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42314037"
content_type: "clinical_feed_article"
specialty: "Oncology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42314037/"
doi: "10.1182/bloodadvances.2026020090"
published_at: "2026-09-22T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Risk Stratification of Incidental T-cell Clonality: A Practical Clinical Framework
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42314037
- **Specialty:** [Oncology](https://medichelpline.com/clinical-feed/oncology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42314037/)
- **DOI:** [10.1182/bloodadvances.2026020090](https://doi.org/10.1182%2Fbloodadvances.2026020090)
- **Published At:** 2026-09-22T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Sensitive assays such as **flow cytometry** (including TRBC/TCR constant-region staining) and molecular T-cell receptor testing increasingly detect **T-cell clonality** incidentally in patients without clinical suspicion for T-cell malignancy. - Incidentally detected clones are variably termed **T-cell clones of uncertain significance (TCUS)** and do not always represent premalignant or malignant disease. - Nonneoplastic causes of detectable clonality include antigen-driven clonal/oligoclonal expansion (infection, autoimmunity) and homeostatic proliferation in lymphopenia; neoplastic clones arise from molecular or cytogenetic abnormalities driving proliferation or survival. - The authors propose a practical risk-stratification framework and an algorithm for peripheral blood T-cell clonality in patients without an established T-cell neoplasm to reduce unnecessary procedures while retaining vigilance for true neoplasia. - The framework categorizes findings into low-risk, abnormal population, and features suggesting clinical T-cell neoplasm (eg, hepatosplenomegaly, lymphadenopathy, diffuse rash, B symptoms, persistent unexplained cytopenias or eosinophilia, autoimmune hemolysis). - For **low-risk** clones the recommendation is against top-line reporting; document the clone in a comment with absolute and relative abundance and recommend surveillance rather than immediate intervention. - Recommended surveillance for low-risk clones includes repeat CBC and clinical follow-up at 3–6 months and typically repeat flow cytometry to assess resolution, stability, or progression. - For an **abnormal population** identified by flow cytometry, recommended next steps include molecular testing on peripheral blood; for clones suspicious for T-cell large granular lymphocytic leukemia (T-LGLL), consider **STAT3** testing for CD8+ clones and **STAT5B** testing for CD4+ clones. - Reporting guidance: do not list TCUS in the top line of diagnostic reports; if multiple small TRBC-monotypic populations are present, report them as compatible with reactive oligoclonal expansion; in lymphopenia, comment that findings can reflect homeostatic proliferation. - Imaging for staging may be considered when indicated. The authors note that distinguishing CD4+ TCUS from CD4+ LGLL is not critical because CD4+ LGLL rarely requires treatment even when pathogenic **STAT5B** mutations are present. - The article includes illustrative figures: pathophysiologic mechanisms for detection of clonality, an algorithm for peripheral blood clonality assessment, and three clinical case examples demonstrating application of the approach.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Department of Pathology, Stanford University School of Medicine, Stanford, CA. * 2 Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA. * 3 Department of Dermatology, Stanford University School of Medicine, Stanford, CA. * PMID: **42314037** * PMCID: [ PMC13583949 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13583949/) * DOI: [ 10.1182/bloodadvances.2026020090 ](https://doi.org/10.1182/bloodadvances.2026020090) Item in Clipboard Review # A practical approach to risk stratification of incidental T-cell clonality Aaron J Wilk et al. Blood Adv. 2026. Show details Display options Display options Format Abstract PubMed PMID Blood Adv Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Blood+Adv%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Blood+Adv%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42314037/) . 2026 Sep 22;10(18):6134-6144. doi: 10.1182/bloodadvances.2026020090. ### Authors [Aaron J Wilk](https://pubmed.ncbi.nlm.nih.gov/?term=Wilk+AJ&cauthor_id=42314037)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42314037/#short-view-affiliation-1 "Department of Pathology, Stanford University School of Medicine, Stanford, CA."), [Michael Khodadoust](https://pubmed.ncbi.nlm.nih.gov/?term=Khodadoust+M&cauthor_id=42314037)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42314037/#short-view-affiliation-2 "Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42314037/#short-view-affiliation-3 "Department of Dermatology, Stanford University School of Medicine, Stanford, CA."), [Jean Oak](https://pubmed.ncbi.nlm.nih.gov/?term=Oak+J&cauthor_id=42314037)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42314037/#short-view-affiliation-1 "Department of Pathology, Stanford University School of Medicine, Stanford, CA.") ### Affiliations * 1 Department of Pathology, Stanford University School of Medicine, Stanford, CA. * 2 Division of Oncology, Department of Medicine, Stanford University School of Medicine, Stanford, CA. * 3 Department of Dermatology, Stanford University School of Medicine, Stanford, CA. * PMID: **42314037** * PMCID: [ PMC13583949 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13583949/) * DOI: [ 10.1182/bloodadvances.2026020090 ](https://doi.org/10.1182/bloodadvances.2026020090) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Because T-cell neoplasms often present with nonspecific findings, T-cell clonality assessment is performed across many clinical scenarios, including the workup of cytopenias, lymphocytosis, eosinophilia, and suspected lymphoma. Sensitive assays, including flow cytometric staining of the T-cell receptor (TCR) constant region and molecular-based TCR clonality testing, have enhanced our ability to detect T-cell neoplasms, but these techniques frequently identify T-cell clones in patients without suspicion of T-cell malignancy. These incidentally detected clones, sometimes called T-cell clones of uncertain significance, do not clearly have universal potential for progression to overt T-cell neoplasia. However, their detection can prompt unnecessary diagnostic procedures, generate unwarranted patient anxiety, and even lead to inappropriate therapeutic interventions. Here, we propose a practical framework for risk stratification of unexpected T-cell clones in peripheral blood that minimizes the risk of unnecessary intervention while maintaining vigilance for true T-cell malignancy. © 2026 American Society of Hematology. Published by Elsevier Inc. Licensed under Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0), permitting only noncommercial, nonderivative use with attribution. All other rights reserved. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Conflict-of-interest disclosure: The authors declare no competing financial interests. ## Figures [ ![Figure 1.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de76/13583949/ebe194ac6bcc/BLOODA_ADV-2026-020090-gr1.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de76/13583949/ab4ecb6cdde2/BLOODA_ADV-2026-020090-gr1.webp) ** Figure 1. ** **Pathophysiologic mechanisms underlying detection of…** ** Figure 1. ** **Pathophysiologic mechanisms underlying detection of T-cell clonality by flow cytometry or molecular methods.** … **Figure 1.** **Pathophysiologic mechanisms underlying detection of T-cell clonality by flow cytometry or molecular methods.** T-cell neoplasia is initiated when a T cell acquires a molecular or cytogenetic abnormality that drives cellular proliferation and/or survival (top). In the period of time before diagnostic criteria for a T-cell neoplasm entity are met, or before the T-cell clone becomes clinically apparent, the clone may still be detectable by sensitive techniques such as flow cytometry or molecular techniques. Nonneoplastic mechanisms may also drive detectable T-cell clonality (bottom). These include robust clonal or oligoclonal expansion in the setting of antigen stimulation, such as in infection or autoimmunity, as well as homeostatic proliferations in the setting of lymphopenia. Clones generated by these mechanisms do not have inherent malignant or premalignant potential. There is emerging but limited evidence that, in the setting of sufficiently robust and persistent antigen stimulation, T-cell clones may acquire pathogenic mutations. However, the frequency of such acquisitions remains unclear. Here, we define a TCUS as any T-cell clone detectable by flow cytometry or molecular techniques that does not meet diagnostic criteria for a T-cell neoplasm, thereby, encompassing both neoplastic and nonneoplastic mechanisms of T-cell clonality. Figure created with biorender.com. Wilk, A. (2026) https://app.biorender.com/illustrations/canvas-beta/6a430b640cb10096131bea9c. [ ![Figure 2.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de76/13583949/269ab409aa9c/BLOODA_ADV-2026-020090-gr2.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de76/13583949/b4523fc2df55/BLOODA_ADV-2026-020090-gr2.webp) ** Figure 2. ** **Algorithm for approaching peripheral blood…** ** Figure 2. ** **Algorithm for approaching peripheral blood T-cell clonality in patients without established diagnosis of…** **Figure 2.** **Algorithm for approaching peripheral blood T-cell clonality in patients without established diagnosis of T-cell neoplasm.** ∗ _Clinical features of T-cell neoplasm_ : hepatosplenomegaly, lymphadenopathy, diffuse rash, B-symptoms, unexplained persistent cytopenias, unexplained eosinophilia, and autoimmune hemolysis. † _Large granular lymphocyte phenotype_ : CD57+, CD5 dim, CD7 dim to negative, CD2 normal to bright, and CD16 and CD56 negative or dim variable. § _T-cell clone reporting recommendations for pathologists_. TCUS: do not report a TCUS in the top line of a diagnostic report, because this will frequently prompt unnecessary diagnostic workup. A population meeting criteria for TCUS as defined in this algorithm should be documented in a comment or other interpretation section for surveillance purposes. If multiple TCUS are identified in a specimen, we recommend reporting that "multiple small TRBC-monotypic T-cell populations are identified, compatible with reactive oligoclonal expansion." If this is observed in the setting of lymphopenia, we recommend commenting that this finding is consistent with homeostatic proliferation. Low risk: for populations meeting criteria for "low risk" in this algorithm, we recommend against reporting this in the top line of a diagnostic report. Instead, we recommend reporting the clone in a comment, documenting its absolute and relative abundance, and recommending clinical and laboratory surveillance. Abnormal population: report in the top line of diagnostic report, document immunophenotype as well as absolute and relative abundance. ‡ _Workup recommendations for clinicians._ Low risk: for clones meeting the "low-risk" criteria defined in this algorithm, we recommend surveillance with repeat CBC and clinical follow-up at an interval of 3 to 6 months. We also typically perform repeat flow cytometry at this time to access for resolution, stability, or progression of the clone. Abnormal population: upon flow cytometric characterization of an abnormal circulating T-cell population by this algorithm, we recommend beginning workup with molecular testing on peripheral blood. For clones suspicious for T-LGLL, consider _STAT3_ and _STAT5B_ molecular testing for CD8+ and CD4+ clones, respectively. Imaging studies for staging may also be considered when indicated. ∗∗ _Note:_ Distinguishing between CD4+ TCUS and CD4+ LGLL is not critical, because CD4+ LGLL rarely requires treatment, even when pathogenic _STAT5B_ mutations are present. [ ![Figure 3.](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de76/13583949/b3a21a9306c0/BLOODA_ADV-2026-020090-gr3.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de76/13583949/f466887348d4/BLOODA_ADV-2026-020090-gr3.webp) ** Figure 3. ** **Three cases of incidental T-cell…** ** Figure 3. ** **Three cases of incidental T-cell clones.** (A-B) Case 1: clinical history and pertinent… **Figure 3.** **Three cases of incidental T-cell clones.** (A-B) Case 1: clinical history and pertinent laboratory results (A) and flow cytometry immunophenotyping (B). (C-D) Case 2: clinical history and pertinent laboratory results (C) and flow cytometry results showing restricted T cells (orange) and NK cells (blue) (D). (E-H) Case 3: clinical history and pertinent laboratory results (E) and flow cytometry immunophenotyping (F). (G) Longitudinal analysis of clonal TCR sequences present at diagnosis and present in the current specimen. (H) Immunophenotypic aberrancies at diagnosis compared to immunophenotype of atypical T-cell population in current specimen. ALC, absolute lymphocyte count; ANC, absolute neutrophil count; FITC, fluorescein isothiocyanate; Hgb, hemoglobin; PD-1, Programmed cell death protein 1; PE, phycoerythrin; WBC, white blood cells. [See this image and copyright information in PMC](https://pubmed.ncbi.nlm.nih.gov/42314037/) ## Similar articles * [ Flow cytometric immunophenotypic assessment of T-cell clonality by Vβ repertoire analysis: detection of T-cell clonality at diagnosis and monitoring of minimal residual disease following therapy. ](https://pubmed.ncbi.nlm.nih.gov/21571962/) Tembhare P, Yuan CM, Xi L, Morris JC, Liewehr D, Venzon D, Janik JE, Raffeld M, Stetler-Stevenson M.Tembhare P, et al.Am J Clin Pathol. 2011 Jun;135(6):890-900. doi: 10.1309/AJCPV2D1DDSGJDBW.Am J Clin Pathol. 2011.PMID: 21571962Free PMC article. * [ T-cell clonality is detected in a high frequency among patients with incidental lymphocytosis by PCR assays for TCR gene rearrangements. ](https://pubmed.ncbi.nlm.nih.gov/23703853/) Cao F, Wang S, Zhao H, Zhou J, Yang G, Wang C.Cao F, et al.J Clin Pathol. 2013 Sep;66(9):749-52. doi: 10.1136/jclinpath-2012-201417. Epub 2013 May 23.J Clin Pathol. 2013.PMID: 23703853 * [ Emerging Role of T-cell Receptor Constant β Chain-1 (TRBC1) Expression in the Flow Cytometric Diagnosis of T-cell Malignancies. ](https://pubmed.ncbi.nlm.nih.gov/33673033/) Horna P, Shi M, Olteanu H, Johansson U.Horna P, et al.Int J Mol Sci. 2021 Feb 12;22(4):1817. doi: 10.3390/ijms22041817.Int J Mol Sci. 2021.PMID: 33673033Free PMC article.Review. * [ A parallel comparison of T-cell clonality assessment between an in-house PCR assay and the BIOMED-2 assay leading to an efficient and cost-effective strategy. ](https://pubmed.ncbi.nlm.nih.gov/21490377/) Kuo SY, Liu H, Liao YL, Chang ST, Hsieh YC, Bandoh BA, Du MQ, Chuang SS.Kuo SY, et al.J Clin Pathol. 2011 Jun;64(6):536-42. doi: 10.1136/jcp.2010.086637. Epub 2011 Apr 13.J Clin Pathol. 2011.PMID: 21490377 * [ T-cell clones of uncertain significance. W
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