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Pediatric T-Cell Prolymphocytic Leukemia with an Isolated 12(P13

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Pediatric T-Cell Prolymphocytic Leukemia with an Isolated 12(P13 Bellone et al. Experimental Hematology & Oncology 2012, 1:7 http://www.ehoonline.org/content/1/1/7 Experimental Hematology & Oncology CASEREPORT Open Access Pediatric T-cell prolymphocytic leukemia with an isolated 12(p13) deletion and aberrant CD117 expression Michael Bellone1, Annika M Svensson1, Ann-Leslie Zaslav2, Silvia Spitzer3, Marc Golightly4, Mahmut Celiker5, Youjun Hu1, Yupo Ma1,6* and Tahmeena Ahmed1,6* Abstract T-cell Prolymphocytic leukemia (T-PLL) is a rare post-thymic T-cell malignancy that follows an aggressive clinical course. The classical presentation includes an elevated white blood cell (WBC) count with anemia and thrombocytopenia, hepatosplenomegaly, and lymphadenopathy. T-PLL is a disease of the elderly and to our knowledge it has never been described in the pediatric age group. We report a case of T-PLL in a 9 year old male who was initially diagnosed with T-cell acute lymphoblastic lymphoma (ALL), the diagnosis was later refined to T-PLL following additional analysis of bone marrow morphology and immunophenotype. Two unusual findings in our patient included CD117 expression and an isolated chromosomal 12(p13) deletion. The patient failed to respond to standard ALL induction chemotherapy, but achieved complete remission following treatment with a fludarabine and alemtuzumab-based regimen. Keywords: T-cell Prolymphocytic Leukemia, Pediatric T-cell Lymphomas, Alemtuzumab, TCR rearrangement, CD117, 12p13 Introduction the long arm of q11 and q32 and abnormalities of chro- T-cell prolymphocytic leukemia (T-PLL) is an aggressive mosome 8 [1]. lymphoproliferative disorder that represents approxi- T-PLL arises sporadically in adults and is mainly a dis- mately 2% of all mature lymphocytic leukemias in adults. ease of the elderly with a median age at onset of 65 years Most patients present with hepatosplenomegaly, lympha- [2]. A mature T-cell malignancy with phenotypic and denopathy, and marked lymphocytosis. Less commonly genotypic features indistinguishable from T-PLL has skin lesions and serous effusions develop. T-PLL is char- been described in patients with ataxia-telangiectasia [3]. acterized by proliferation of small to medium-sized pro- In contrast to sporadic cases T-PLL, this entity is seen in lymphocytes with nongranular basophilic cytoplasm; younger adults with a median age of onset of 31 years. round, oval, or markedly irregular nuclei; and a promi- We present a case of a 9-year-old male diagnosed with nent nucleolus. In approximately 20% of cases a “small T-PLL based on morphology, immunophenotype, cytoge- cell variant” is seen. The immunophenotype of T-PLL netic and molecular T-cell receptor studies of bone mar- cells resembles that of a mature post-thymic T-cell with row. A thorough literature search through Medline, expression of CD2, CD3, and CD7. The T-cell receptor Pubmed, and Google scholar did not reveal any previous (TCR) beta/gamma genes are clonally rearranged. The description of T-PLL presenting in the pediatric age most frequent chromosomal abnormalities in T-PLL group. Because this patient showed no clinical or cytoge- include inversion of chromosome 14 with breakpoints in netic features of ataxia-telangiectasia, this is likely a case of sporadic T-PLL, making it even more intriguing. * Correspondence: [email protected]; [email protected] Case presentation 1Department of Pathology, Stony Brook University Medical Center, Stony The patient is a 9-year-old African-American male with Brook, NY 11794, USA no significant personal or family medical history who was Full list of author information is available at the end of the article © 2012 Bellone et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Bellone et al. Experimental Hematology & Oncology 2012, 1:7 Page 2 of 8 http://www.ehoonline.org/content/1/1/7 well until about 2 months ago when he started having valacyclovir for prophylaxis against CMV reactivation intermittent fevers, nonbloody nonbilious vomiting, fati- and pentamidine for PCP prophylaxis. gue and abdominal pain. He completed 2 courses of anti- Upon hematopoietic recovery, bone marrow aspiration biotics during that time. Three days prior to admission, and biopsy showed trilineage maturation with no evidence he went back to his pediatrician who started him on of leukemia by morphology or flow cytometry confirming another course of antibiotics. A CBC was done at that remission status. The child had no biological siblings as time which revealed severe anemia. So he was sent to the potential stem cell donor. While the search for a suitable local community hospital emergency department. Physi- stem cell source was underway, the child received a sec- cal examination revealed fever (temperature of 38.9°C), ond course of the FLACC therapy to sustain remission sta- periorbital edema, bilateral pitting pedal edema, hepato- tus. During neutropenic phase of this second cycle the megaly (5 cm), splenomegaly (3 cm), and cervical and child developed respiratory distress with fevers. At the axillary lymphadenopathy. A complete blood count time of neutrophil recovery, respiratory distress worsened showed a hemoglobin of 4.4 g/dl, a white blood cell necessitating mechanical ventilation. This was followed by count of 10.6 × 103/μl with 98% lymphocytes and 2% failure of renal and hepatic systems. All blood cultures blasts, and a platelet count of 119 × 103/μl. Blood bio- remained negative for bacterial or fungal etiology. Bronch- chemical analysis revealed elevated LDH of 739 units/L oalveolar lavage confirmed evidence of PCP as well as (reference range 94-250). Additional studies revealed CMV by PCR with no evidence of fungal elements. His hypoalbuminemia (2.5 g/dl, reference range 3.5-4.8) and blood CMV viral titers were over 3.9 × 106 copies/ml. The increased hyperferritinemia (1,510 ng/mL, reference child succumbed to these complications in spite of aggres- range 22.0-322.0). Serology for HTLV-1 was negative sive therapy including ganciclovir, trimethoprim sulfisoxa- while CMV IgG was positive suggesting prior exposure. zole, pentamidine, broad spectrum antibacterial as well as Bone marrow aspiration was interpreted as T-ALL based antifungal therapies. The family opted against postmortem on morphology and cell surface marker expression as examination. detailed below. Four-drug induction chemotherapy following COG Pathologic findings protocol AALL0434, consisting of intrathecal cytarabine Morphologic analysis and systemic vincristine, prednisone, daunorubicin, and The hemogram revealed anemia normal leukocyte count PEG-asparaginase was started. Day 8 bone marrow aspi- (10.8 × 103/μl; reference range, 4.8-10.8 × 103/mL) with rate showed decrease in leukemic cells. Induction che- neutropenia (ANC 648/μl reference range 1,500-7,600) motherapy was continued as planned. Bone marrow and lymphocytosis (94%; reference range, 20%-40%). The aspiration done on day 15 of induction showed progres- Wright-stained peripheral blood smear revealed leukemic sive disease. The lack of response to standard T-ALL cells having high N/C ratio, relatively dense chromatin induction chemotherapy prompted a revision of the diag- and occasional prominent nucleoli (Figure 1A). The nosis. Evaluation of the bone marrow specimens revealed Wright-stained bone marrow aspirate smears showed a prolymphocytic appearing cells that lacked expression of population of small to medium sized lymphoid cells com- markers of immaturity such as CD34, TdT, and CD1a prising all nucleated cells. These cells were similar in even though there was expression of CD117. This unu- morphology to those seen in the peripheral blood. The sual immunophenotype, morphology and lack of clinical hematoxylin-eosin-stained bone marrow biopsy was response, resulted in a revision of the diagnosis to T-cell highly cellular (90-95%) and displayed sheets of immature prolymphocytic leukemia. lymphoid cells (Figure 1B and 1C) Following change in diagnosis and progressive disease under standard induction chemotherapy, induction che- Immunophenotypic analysis motherapy was abandoned and the patient was started Immunohistochemistry was performed on paraffin- on nelarabine as a single agent with intention to add embedded sections of the bone marrow core biopsy. Anti- cyclophosphamide and cytarabine. Lack of evidence of bodies directed against CD3 and CD117 strongly reacted tumor lysis at the end of nelarabine therapy prompted a to tumor cells (Figure 1D), and an antibody directed CD20 repeat of bone marrow aspiration which showed persis- showed no reaction. The CD3 and CD20 antibodies were ® tent disease. The child then was treated with another purchased from Ventana Medical Systems (Oro Valley, regimen termed FLACC, which consisted of fludarabine, AZ) and the CD117 antibody was purchased from Cell cytarabine, cyclophosphamide, and alemtuzumab with fil- Marque Corporation© (Rocklin, CA). Flow cytometric ana- gastrim (G-CSF) support and was described in detail by lysis was performed on bone marrow aspirate using a Williams et al. [4], who used this regimen to successfully FACSCalibur™ 2000 flow cytometer and monoclonal treat a child with refractory T-cell post-transplant lym- antibodies purchased from Becton Dickinson (San Jose, phoproliferative disorder (PTLD). The patient received CA). Flow cytometry
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