Cutaneous B‐lymphoblastic lymphoma with <i>IL3/IgH</i> translocation presenting with hypereosinophilia and acute endocarditis

Bomken, Simon; Haigh, Shaun; Bown, Nick; Carey, Peter; Wood, Katrina; Windebank, Kevin

doi:10.1002/pbc.25318

Cited by 12 publications

(6 citation statements)

References 20 publications

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“…It has been shown that hypereosinophilia heralds the onset and/or relapse of this particular subtype of ALL even in the absence of discernible clonal proliferation . These observations, including ours, suggest that the eosinophil counts can be a sensitive MRD barometer.…”

supporting

confidence: 68%

“…To the Editor: Acute lymphoblastic leukemia (ALL) with eosinophilia was first reported by Spitzer and Garson in 1973, and it was later classified as a distinct clinicopathological entity of B lymphoblastic leukemia/lymphoma with IL3‐IgH translocation in the revised WHO classification in 2008 . The chronological association between ALL and hypereosinophilia has been reported in the literature, but the exact molecular pathogenesis still remains uncertain.…”

mentioning

confidence: 99%

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Paraneoplastic hypereosinophilic syndrome associated with IL3‐IgH positive acute lymphoblastic leukemia

Kobayashi

Mizuta

Yamane

et al. 2018

Pediatric Blood & Cancer

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classified as a distinct clinicopathological entity of B lymphoblastic leukemia/lymphoma with IL3-IgH translocation in the revised WHO classification in 2008. 2 The chronological association between ALL and hypereosinophilia has been reported in the literature, 3-6 but the exact molecular pathogenesis still remains uncertain.We encountered an 11-year-old male with ALL with hypereosinophilia. He visited our emergency department with complaints of progressive dyskinesia, slurred speech, and general fatigue for the previous 2 weeks. Laboratory examination showed a hemoglobin level of 10.6 g/dl, a platelet count of 122 × 10 9 /l, and a leukocyte count of 126.6 × 10 9 /l. The differential count of white blood cells was eosinophils 88%, segmented neutrophils 7.5%, band forms 1.0%, basophils 2.0%, monocytes 1%, and lymphoblasts 0.5%. Transthoracic echocardiography showed an intramural thrombus with severe mitral regurgitation, and he was diagnosed as having eosinophilic cardiomyopathy, also termed Löeffler endocarditis 7 ( Figures 1A and 1B). We also found cardioembolic cerebral infarction ( Figure 1C). Flow cytometric analysis disclosed that lymphoblasts were positive for the cell surface antigens CD19, CD34, and CD79a. A bone marrow examination disclosed proliferation of both ALL blast cells and dysplastic eosinophils ( Figure 1D).Chromosome analyses combined with spectral karyotyping chromosome analysis showed t (5;14)(q31; q32) ( Figure 1E), and IgH translocation was verified with FISH analysis ( Figure 1F). We confirmed headto-head gene fusion between the immunoglobulin heavy-chain joining enhancer and IL3 promoter region 8 ( Figure 1G).Three-drug therapy with prednisolone, vincristine, and Lasparaginase was successful with an induction of morphological remission (less than 5% lymphoblasts in bone marrow). Pertinent endomyocardial biopsy showed a complete resolution of eosinophilic infiltrates in the myocardium, but he was in need of supportive measures, including an angiotensin-converting enzyme (ACE) inhibitor, diuretics, and beta blockers due to co-occurrence of congestive heart failure. 9 Thus, to circumvent the treatment-induced cardiotoxicity, we excluded anthracycline from the intensification therapy. Furthermore, to allow quick recovery from concurrent cardiac complications, we also placed him on less toxic therapies of oral hydroxyurea and mercaptopurine for consolidation therapy. We confirmed cytogenic remission (less than 0.5% lymphoblasts with flow cytometry) at the completion of consolidation therapy, but prolonged eosinophilia was noted beyond the initial response suggesting the persistence of minimal residual disease (MRD). Following the normalization of serum cardiac troponin T levels, 10,11 we commenced a re-induction therapy including anthracycline under the prophylactic cardioprotective dexrazoxane. 12 The subsequent clinical course was successful with matched-sibling allogeneic bone marrow transplantation, which was coincident with the resolution of hypereosinophilia ( Figure 1H).Hypereosinophil...

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supporting

confidence: 68%

mentioning

confidence: 99%

Paraneoplastic hypereosinophilic syndrome associated with IL3‐IgH positive acute lymphoblastic leukemia

Kobayashi

Mizuta

Yamane

et al. 2018

Pediatric Blood & Cancer

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“…Cases of HE secondary to ALL are very rare. In addition to this child, only 61 patients <25 years (mean age 11 years) with HE and ALL have been described since 1973 to December 2017 ( Table 1 ) [ 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 ].…”

Section: Discussionmentioning

confidence: 99%

Acute Lymphoblastic Leukemia with Hypereosinophilia in a Child: Case Report and Literature Review

Ferruzzi

Santi

Gurdo

et al. 2018

IJERPH

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Background: Hypereosinophilia in children can be primary or secondary. Numerous malignant diseases can cause hypereosinophilia, but it is seldom caused by acute lymphoblastic leukemia (ALL). In the event of protracted hypereosinophilia, it is extremely important to make a correct differential diagnosis. Case presentation: We present the case of an 11-year-old boy of Moroccan origin with ALL with hypereosinophilic onset (eosinophils in peripheral blood, 10,000/µL) in the absence of other signs of neoplastic disease, and compare this case with 61 similar cases in the literature. Following hospital admission, the patient initially presented with headache-caused nocturnal awakenings, evening fever, and cough, and he also lost approximately 7 kg in weight in a month not associated with sweating or itching. We first performed bone marrow aspiration, which showed an increase in eosinophils without cellular morphological abnormalities, and bone marrow immunophenotyping showed that 4.5% of cells had a phenotype compatible with lymphoid blasts. A lumbar puncture was negative. Given the poor marrow involvement, it was necessary to repeat a new bone marrow aspiration two days later, which showed an increase in blasts to 14%. A concomitant bone marrow biopsy showed an infiltration of blasts typical of B-cell ALL equal to 20–30% with associated hypereosinophilia. Cytogenetic analysis showed an hyperdiploid karyotype: 53–55, XY, +X, add(1)(q21q25), +4, +9, +10, +14, +2, +1, +21/46, XY. Conclusions: ALL is one of the possible causes of persistent hypereosinophilia. In patients with ALL and hypereosinophilia, peripheral hypereosinophilia can precede the appearance of blasts. Due to the negative prognosis and the increased risk of complications in these patients, bone marrow aspiration and biopsy are recommended if common causes of secondary hypereosinophilia are excluded.

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“…It has been suggested to combine IL-3 and G-CSF injection in peripheral blood for peripheral blood stem cell propagation and allogenic stem cell transplantation [ 45 , 46 ]. Recently, IL-3 hypersecretion has been reported to be associated with cutaneous B-lymphoblastic lymphoma [ 47 ]. Our study reveals another aspect of IL-3 functions, namely stimulating the stemness of prostate cancer cells.…”

Section: Discussionmentioning

confidence: 99%

ILs-3, 6 and 11 increase, but ILs-10 and 24 decrease stemness of human prostate cancer cells in vitro

et al. 2015

Oncotarget

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Cancer stem cells (CSCs) are associated with cancer recurrence and metastasis. Prostate cancer cells often metastasize to the bone with a complex microenvironment of cytokines favoring cell survival. In this study, the cell stemness influence of a group of interleukins including IL-3, 6, 10, 11 and 24 on human prostate cancer cell lines LNCaP and PC-3 was explored in vitro. Sulforhodamine B(SRB) and 5-ethynyl-2′-deoxyuridine (EdU) assays were applied to examine the effect on cell proliferation, and wound healing and transwell assays were used for migration and invasion studies, in addition to colony formation, Western blotting and flowcytometry for the expression of stemness factors and chemotherapy sensitivity. We observed that ILs-3, 6 and 11 stimulated while ILs-10 and 24 inhibited the growth, invasion and migration of both cell lines. Interestingly, ILs-3, 6 and 11 significantly promoted colony formation and increased the expression of SOX2, CD44 and ABCG2 in both prostate cancer cell lines. However, ILs-10 and 24 showed the opposite effect on the expression of these factors. In line with the above findings, treatment with either IL-3 or IL-6 or IL-11 decreased the chemosensitivity to docetaxel while treatment with either IL-10 or IL-24 increased the sensitivity of docetaxel chemotherapy. In conclusion, our results suggest that ILs-3, 6 and 11 function as tumor promoters while ILs-10 and 24 function as tumor suppressors in the prostate cancer cell lines PC-3 and LNCaP in vitro, and such differences may attribute to their different effect on the stemness of PCa cells.

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Cutaneous B‐lymphoblastic lymphoma with IL3/IgH translocation presenting with hypereosinophilia and acute endocarditis

Cited by 12 publications

References 20 publications

Paraneoplastic hypereosinophilic syndrome associated with IL3‐IgH positive acute lymphoblastic leukemia

Paraneoplastic hypereosinophilic syndrome associated with IL3‐IgH positive acute lymphoblastic leukemia

Acute Lymphoblastic Leukemia with Hypereosinophilia in a Child: Case Report and Literature Review

ILs-3, 6 and 11 increase, but ILs-10 and 24 decrease stemness of human prostate cancer cells in vitro

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