Pneumatosis intestinalis (PI) is an imaging phenomenon that represents air in the bowel wall. The cause of PI is variable, although specific etiologic factors remain unknown. It is an infrequent complication in leukemia patients and is associated with several medical and surgical conditions. PI often represents a benign condition, but it can also require surgery. Therefore, the assessment of PI with or without complications can be difficult. Herein, we report on an unusual case of a 63 year-old woman with refractory acute precursor B-cell lymphoblastic leukemia-lymphoma who presented with PI resulting from the leukemic process, and finally expired due to sepsis.
Female ; Humans ; Leukemia ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; Sepsis

Therapy-related myeloid neoplasms have been well characterized. However, precursor B-cell acute lymphoblastic leukemia in patients with prior malignancies is uncommon, and the effect of prior cytotoxic therapy on development of precursor B-cell acute lymphoblastic leukemia is controversial. Therapy-related precursor B-cell acute lymphoblastic leukemia has been reported occasionally. However, cytotoxic therapy-related precursor B-cell acute lymphoblastic leukemia has been reported in Korea only rarely. We herein describe two cases of therapy-related precursor B-cell acute lymphoblastic leukemia.
Humans ; Korea ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid

We present a case of Korean pediatric patient with pre-B cell type acute lymphoblastic leukemia (ALL) with trisomy 5 as a sole cytogenetic anomaly. Here, we compare and describe the present case with previous pediatric case reports and provide a review of the literature. This case report may help elucidate the poor prognostic impact of trisomy 5 as a sole cytogenetic anomaly in pediatric patients with ALL. Additional studies are needed to confirm this hypothesis.
Cytogenetics ; Humans ; Pediatrics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; Prognosis ; Trisomy

B-Lymphocytes ; Child ; Humans ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; immunology ; Precursor Cells, B-Lymphoid ; pathology

Hemophagocytic lymphohistiocytosis (HLH), although uncommon, is illustrated as a dramatic clinical presentation of multi-systemic inflammation due to the impaired activity of cytotoxic T-cell and NK cell. Etoposide, an important component of the HLH treatment, is thought to have a leukemogenic potential. Furthermore, it has been suggested that the underlying immunologic dysfunction in HLH might be involved in the occurrence of secondary leukemia. Only a few cases of secondary ALLs after HLH have been reported. We report herein a case of secondary precursor B-cell ALL which occurred after the treatment of HLH.
Etoposide ; Inflammation ; Killer Cells, Natural ; Leukemia ; Lymphohistiocytosis, Hemophagocytic ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; T-Lymphocytes

Precursor B-cell acute lymphoblastic leukemia (ALL), which is the most common subtype of pediatric acute leukemia, generally has a good prognosis. However, the prognosis also depends on the genetic abnormalities of the leukemic blast. Concurrent MYC and IGH/BCL2 translocations have recently been reported as a “double hit” in adult patients, but non-immunoglobulin (non-IG)/MYC translocation has rarely been reported. In this paper, we report a case of pediatric precursor B-cell ALL associated with translocations (14;18)(q32;q21) and (8;9)(q24;p13). The patient was a previously healthy 13-year-old boy. Complete remission was not achieved after first-line four-drug induction chemotherapy; thus, intensive salvage regimen, including high-dose cytarabine and L-asparaginase, were administered, which resulted in morphologic remission. However, his disease relapsed during the second cycle of salvage regimen, and he died of sepsis-induced multiorgan failure.
Adolescent ; Adult ; Cytarabine ; Humans ; Induction Chemotherapy ; Leukemia ; Male ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; Prognosis

TRPM7, a cation channel protein permeable to various metal ions such as Mg2+, is ubiquitously expressed in variety of cells including lymphocytes. The activity of TRPM7 is tightly regulated by intracellular Mg2+, thus named Mg2+-inhibited cation (MIC) current, and its expression is known to be critical for the viability and proliferation of B lymphocytes. In this study, the level of MIC current was compared between immature (WEHI-231) and mature (Bal-17) B lymphocytes. In both cell types, an intracellular dialysis with Mg2+-free solution (140 mM CsCl) induced an outwardly-rectifying MIC current. The peak amplitude of MIC current and the permeability to divalent cation (Mn2+) were several fold higher in Bal-17 than WEHI-231. Also, the level of mRNAs for TRPM7, a molecular correspondence of the MIC channel, was significantly higher in Bal-17 cells. The amplitude of MIC was further increased, and the relation between current and voltage became linear under divalent cation-free conditions, demonstrating typical properties of the TRPM7. The stimulation of B cell receptors (BCR) by ligation with antibodies did not change the amplitude of MIC current. Also, increase of extracellular [Mg2+]c to enhance the Mg2+ influx did not affect the BCR ligation-induced death of WEHI-231 cells. Although the level of TRPM7 was not directly related with the cell death of immature B cells, the remarkable difference of TRPM7 might indicate a fundamental change in the permeability to divalent cations during the development of B cells.
Antibodies ; B-Lymphocytes* ; Cations, Divalent ; Cell Death ; Dialysis ; Ions ; Ligation ; Lymphocytes ; Permeability ; Precursor Cells, B-Lymphoid ; RNA, Messenger

Regulation of B cell receptor (BCR)-induced Ca2+ signaling by CD40 co-stimulation was compared in long-term BCR-stimulated immature (WEHI-231) and mature (Bal-17) B cells. In response to long-term pre-stimulation of immature WEHI-231 cells to alpha-IgM antibody (0.5~48 hr), the initial transient decrease in BCR-induced [Ca2+]i was followed by spontaneous recovery to control level within 24 hr. The recovery of Ca2+ signaling in WEHI-231 cells was not due to restoration of internalized receptor but instead to an increase in the levels of PLCgamma2 and IP3R-3. CD40 co-stimulation of WEHI-231 cells prevented BCR-induced cell cycle arrest and apoptosis, and it strongly inhibited the recovery of BCR-induced Ca2+ signaling. CD40 co-stimulation also enhanced BCR internalization and reduced expression of PLCgamma2 and IP3R-3. Pre-treatment of WEHI-231 cells with the antioxidant N-acetyl-L-cysteine (NAC) strongly inhibited CD40-mediated prevention of the recovery of Ca2+ signaling. In contrast to immature WEHI-231 cells, identical long-term alpha-IgM pre-stimulation of mature Bal-17 cells abolished the increase in BCR-induced [Ca2+]i, regardless of CD40 co-stimulation. These results suggest that CD40-mediated signaling prevents antigen-induced cell cycle arrest and apoptosis of immature B cells through inhibition of sustained BCR-induced Ca2+ signaling.
Acetylcysteine ; Apoptosis ; B-Lymphocytes ; Cell Cycle Checkpoints ; Phospholipase C gamma ; Precursor Cells, B-Lymphoid ; Reactive Oxygen Species

We herein present a case of a 2-year-old girl with non-Hodgkin's lymphoma(NHL) of the lymphoblastic type involving cutaneous sites at the time of diagnosis. The histological finding was typical of lymphoblastic lymphoma. However, immunophenotypically, this lymphoma was not of the T-cell or B-cell type, although the vast majority of lymphoblastic lymphomas involving the skin are usually of the pre-B cell or T-ce11 type. Until now, there have been few reports of non-T, non-B primary cutaneous lymphoblastic lymphoma expressing surface CD10 and CD56 antigens as in this case.
Antigens, CD56 ; B-Lymphocytes ; Child, Preschool ; Diagnosis ; Female ; Humans ; Lymphoma ; Precursor Cell Lymphoblastic Leukemia-Lymphoma* ; Precursor Cells, B-Lymphoid ; Skin ; T-Lymphocytes

In this report, we present a case of a patient with Philadelphia chromosome-positive (Ph+) B-cell acute lymphoblastic leukemia after renal transplantation. The patient, a 65-year-old man, had received a kidney transplantation 20 years prior to diagnosis with Ph+ precursor B-cell ALL. Because he was refractory to intensive chemotherapy and had refused to receive additional intensive chemotherapy, he was treated with imatinib and dexamethasone. While this patient experienced a complete hematologic and cytogenetic response, he did not show a complete molecular remission. Eighty days after imatinib combination therapy, the patient relapsed and died from intracerebral hemorrhage.
Aged ; B-Lymphocytes ; Benzamides ; Cerebral Hemorrhage ; Cytogenetics ; Dexamethasone ; Humans ; Kidney Transplantation ; Philadelphia ; Philadelphia Chromosome ; Piperazines ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; Precursor Cells, B-Lymphoid ; Pyrimidines ; Imatinib Mesylate