A Unique Case of Concomitant T‐Prolymphocytic Leukemia and B‐Cell Acute Lymphoblastic Leukemia

T-prolymphocytic leukemia (T-PLL) is a rare lymphoid malignancy with a poor prognosis. B-cell acute lymphoblastic leukemia (B-ALL) also confers a poor prognosis, especially in patients with high-risk features without an option for transplant. Here, we present a case of a patient with T-PLL initially treated with multi-agent chemotherapy who then developed B-ALL, the management strategies, and possible pathogenesis of two concurrent rare malignancies. One proposed mechanism for the development of both hematologic malignancies in this patient is the acquisition of a <i>KMT2A</i> rearrangement, raising the possibility of clonal evolution resulting in therapy-related or secondary leukemia. Another explanation is the presence of a common clonal stem cell progenitor harboring a <i>JAK3</i> mutation.

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Publication Details

Journal
eJHaem
Published
2026-02-01
DOI
https://doi.org/10.1002/jha2.70252
Primary Topic
Chronic Lymphocytic Leukemia Research
Type
article
Field-Weighted Citation Impact
0.00
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A Unique Case of Concomitant T‐Prolymphocytic Leukemia and B‐Cell Acute Lymphoblastic Leukemia

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eJHaem
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A Unique Case of Concomitant T‐Prolymphocytic Leukemia and B‐Cell Acute Lymphoblastic Leukemia

Weina Chen, Monica Chintapenta, Jonathan Hyak, Soolmaz Laknezhad, Radhika Kainthla, Prapti A. Patel, Viral Patel
article en

Abstract

T-prolymphocytic leukemia (T-PLL) is a rare lymphoid malignancy with a poor prognosis. B-cell acute lymphoblastic leukemia (B-ALL) also confers a poor prognosis, especially in patients with high-risk features without an option for transplant. Here, we present a case of a patient with T-PLL initially treated with multi-agent chemotherapy who then developed B-ALL, the management strategies, and possible pathogenesis of two concurrent rare malignancies. One proposed mechanism for the development of both hematologic malignancies in this patient is the acquisition of a <i>KMT2A</i> rearrangement, raising the possibility of clonal evolution resulting in therapy-related or secondary leukemia. Another explanation is the presence of a common clonal stem cell progenitor harboring a <i>JAK3</i> mutation.

eJHaemVol. 7(1)
Parkland Health & Hospital System (US), The University of Texas Southwestern Medical Center (US)
No poverty
Openalex Percentile: Top 52%
Chronic Lymphocytic Leukemia Research
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