Pediatric T-cell prolymphocytic leukemia with an isolated 12(p13) deletion and aberrant CD117 expression

Bellone, Michael; Svensson, Annika; Zaslav, Ann-Leslie; Spitzer, Silvia; Golightly, Marc G.; Celiker, Mahmut; Hu, Youjun; Ma, Yupo; Ahmed, Tahmeena

doi:10.1186/2162-3619-1-7

Cited by 7 publications

(5 citation statements)

References 29 publications

(31 reference statements)

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“…The high T-ALL failure rate is mainly the result of an insufficient understanding of T-ALL biology, which hampers the identification of reliable prognostic factors that enable appropriate therapy adjustment [1]. To improve T-ALL outcome, characterization of the biological features of T-ALL blast cells and the immune status of patients is needed to design specific therapeutic strategies [6-10]. T-ALL is generally considered to be a clonal disorder that arises from the expansion of committed lymphoid precursors, and leukemic clones in different patients vary due to the T cell receptor (TCR) gene rearrangements that occur during T-cell differentiation [1,11].…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, clonally expanded T cells may be derived from donor lymphocytes after allo-HSCT or donor lymphocyte infusion (DLI), which may increase survival following allo-HSCT in patients with advanced-stage acute leukemia [26,29]. These clonally expanded T cells are derived from TCR αβ or γδ T cells [10]. Increasing data have demonstrated that γδ T cells may be used to develop specific immunotherapies for patients with cancers such as bladder cancer and hepatocellular carcinoma [30].…”

Section: Resultsmentioning

confidence: 99%

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The evolution of malignant and reactive γδ + T cell clones in a relapse T-ALL case after allogeneic stem cell transplantation

et al. 2013

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BackgroundTo improve the outcome of patients with T-cell acute lymphoblastic leukemia (T-ALL), characterization of the biological features of T-ALL blast cells and the immune status of patients with T-ALL is needed to identify specific therapeutic strategies.FindingsUsing a novel approach based on the combination of fine-tiling comparative genomic hybridization (FT-CGH) and ligation-mediated PCR (LM-PCR), we molecularly identified a malignant γδ + T cell clone with a Vδ5Dδ2Jδ1 rearrangement that was paired with a T cell receptor (TCR) VγI and comprised a Vγ1Vδ5 T cell clone in a relapse T-ALL patient. This malignant Vδ5 T cell clone disappeared after chemotherapy, but the clone was detected again when disease relapsed post allogeneic hematopoietic stem cell transplantation (allo-HSCT) at 100 weeks. Using PCR and GeneScan analyses, the distribution and clonality of the TCR Vγ and Vδ subfamilies were examined before and after allo-HSCT in the patient. A reactive T cell clone with a Vδ4Dδ3Jδ1 rearrangement was identified in all samples taken at different time points (i.e., 4, 8, 68, 100 and 108 weeks after allo-HSCT). The expression of this Vδ4+ T cell clone was higher in the patient during complete remission (CR) post allo-HSCT and at disease relapse.ConclusionsThis study established a sensitive methodology to detect T cell subclones, which may be used to monitor minimal residual disease and immune reconstitution.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

The evolution of malignant and reactive γδ + T cell clones in a relapse T-ALL case after allogeneic stem cell transplantation

et al. 2013

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“…Although being the most frequent mature T-cell leukemia in Western countries, T-PLL represents only ~3% of all T-cell malignancies (136)(137)(138). Its clinical course is typically aggressive with poor responses to conventional chemotherapies resulting in a median overall survival (OS) of usually <2-3 years (139,140).…”

Section: T-cell Prolymphocytic Leukemia (T-pll)mentioning

confidence: 99%

CCR7 in Blood Cancers – Review of Its Pathophysiological Roles and the Potential as a Therapeutic Target

Cuesta-Mateos

Terrón²,

Herling³

2021

Front. Oncol.

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According to the classical paradigm, CCR7 is a homing chemokine receptor that grants normal lymphocytes access to secondary lymphoid tissues such as lymph nodes or spleen. As such, in most lymphoproliferative disorders, CCR7 expression correlates with nodal or spleen involvement. Nonetheless, recent evidence suggests that CCR7 is more than a facilitator of lymphatic spread of tumor cells. Here, we review published data to catalogue CCR7 expression across blood cancers and appraise which classical and novel roles are attributed to this receptor in the pathogenesis of specific hematologic neoplasms. We outline why novel therapeutic strategies targeting CCR7 might provide clinical benefits to patients with CCR7-positive hematopoietic tumors.

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“…CD117 (KIT), a type III receptor tyrosine kinase that participates in intracellular signal transduction in several cell types, is associated with the myeloid lineage, usually expressed in myeloid blasts, and aberrantly expressed on occasion in T-cell lymphoblastic leukemia (T-LL) [ 13 ], but has been rarely reported in T-PLL [ 2 , 14 ].…”

Section: Introductionmentioning

confidence: 99%

Advances in the understanding and management of T-cell prolymphocytic leukemia

et al. 2017

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T-prolymphocytic leukemia (T-PLL) is a rare T-cell neoplasm with an aggressive clinical course. Leukemic T-cells exhibit a post-thymic T-cell phenotype (Tdt−, CD1a−, CD5+, CD2+ and CD7+) and are generally CD4+/CD8−, but CD4+/CD8+ or CD8+/CD4− T-PLL have also been reported. The hallmark of T-PLL is the rearrangement of chromosome 14 involving genes for the subunits of the T-cell receptor (TCR) complex, leading to overexpression of the proto-oncogene TCL1. In addition, molecular analysis shows that T-PLL exhibits substantial mutational activation of the IL2RG-JAK1-JAK3-, STAT5B axis. T-PLL patients have a poor prognosis, due to a poor response to conventional chemotherapy. Monoclonal antibody therapy with antiCD52-alemtuzumab has considerably improved outcomes, but the responses to treatment are transient; hence, patients who achieve a response to therapy are considered for stem cell transplantation (SCT). This combined approach has extended the median survival to four years or more. Nevertheless, new approaches using well-tolerated therapies that target growth and survival signals are needed for most patients unable to receive intensive chemotherapy.

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Pediatric T-cell prolymphocytic leukemia with an isolated 12(p13) deletion and aberrant CD117 expression

Cited by 7 publications

References 29 publications

The evolution of malignant and reactive γδ + T cell clones in a relapse T-ALL case after allogeneic stem cell transplantation

The evolution of malignant and reactive γδ + T cell clones in a relapse T-ALL case after allogeneic stem cell transplantation

CCR7 in Blood Cancers – Review of Its Pathophysiological Roles and the Potential as a Therapeutic Target

Advances in the understanding and management of T-cell prolymphocytic leukemia

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