OBJECTIVE: To analyze the flow immunophenotype and clinical characteristics of leukemia patients with positive SET-CAN fusion gene. METHODS: A total of 7 newly diagnosed acute leukemia patients with SET-CAN fusion gene admitted to Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology from February 2016 to February 2020 were collected. Multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) was used to detect the expression of SET-CAN fusion gene. The immunophenotype was detected by four-color flow cytometry. The case information of 17 literatures published at home and abroad was extracted for statistical analysis. RESULTS: Among the 7 patients, 2 cases were diagnosed as mixed phenotype acute leukemia (MPAL), 2 cases as acute myeloid leukemia (AML), and 3 cases as T-acute lymphoblastic leukemia (ALL)/lymphoblastic lymphoma (LBL). Leukemia cells in bone marrow specimens of all cases expressed or partially expressed CD34, CD33 and CD7. CD5 and cytoplasmic CD3 were expressed in 5 patients except 2 patients diagnosed with AML. Bone marrow and lymph node specimens were both detected in 2 patients, and the immunophenotypes of the two specimens were not completely consistent, with differences in lineage or maturity related markers. Two patients with MPAL showed differentiated response to treatment. One AML patient gave up treatment, and another AML patient with FLT3-ITD gene mutation had a poor prognosis. All three T-ALL/LBL patients maintained a long duration of remission after induced remission, and one case underwent allogeneic hematopoietic stem cell transplantation. CONCLUSIONS There are common characteristics of immunophenotype in patients with positive SET-CAN fusion gene. Differential expression of immunophenotype in samples from different parts is observed in some cases. The prognosis of these diseases varies.
Humans ; Leukemia, Myeloid, Acute/pathology* ; Bone Marrow/pathology* ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics* ; Antigens, CD34 ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; Immunophenotyping

Humans ; Lymphoma ; Lymphoma, T-Cell ; Myeloproliferative Disorders/genetics* ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology* ; T-Lymphocytes/pathology*

Warthin tumor is a benign salivary gland tumor comprising ductal epithelium and lymphoid stroma. To date, reports about the malignant transformations of intraepithelial and lymphoid components in Warthin tumor are extremely rare; lymphoid malignant transformation into B-cell lymphoma is particularly rare in combination with T-cell lymphoma. The case of Warthin tumor complicated with T-lymphoblastic lymphoma is reported to emphasize the importance of a careful light microscopic evaluation of lymphoid tissue in Warthin tumor for identifying occult lymphoma presence, reducing misdiagnosis and missed diagnosis, and determining a timely treatment.
Humans ; Adenolymphoma/pathology* ; Parotid Neoplasms/pathology* ; Salivary Gland Neoplasms ; Epithelium/pathology* ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications*

Acute lymphoblastic leukemia (ALL) is the most common malignant hematological disease in childhood. Glucocorticoids are frequently used in the chemoradiotherapy regimen for ALL and can induce the apoptosis of ALL cells through several signaling pathways, but about 10% of ALL children have poor response to glucocorticoids. Studies have revealed that glucocorticoids induce the apoptosis of ALL cells by upregulating the expression of BIM gene, and BIM gene is associated with glucocorticoid resistance in childhood ALL. This article reviews the recent studies on glucocorticoid resistance in childhood ALL, especially the role of BIM and its expression products in this process.
Apoptosis ; Bcl-2-Like Protein 11 ; genetics ; Child ; Drug Resistance ; Glucocorticoids ; therapeutic use ; Humans ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; genetics ; pathology

Chimeric antigen receptor (CAR) is a recombinant immunoreceptor combining an antibody-derived targeting fragment with signaling domains capable of activating cells, which endows T cells with the ability to recognize tumor-associated surface antigens independent of the expression of major histocompatibility complex (MHC) molecules. Recent early-phase clinical trials of CAR-modified T (CAR-T) cells for relapsed or refractory B cell malignancies have demonstrated promising results (that is, anti-CD19 CAR-T in B cell acute lymphoblastic leukemia (B-ALL)). Given this success, broadening the clinical experience of CAR-T cell therapy beyond hematological malignancies has been actively investigated. Here we discuss the basic design of CAR and review the clinical results from the studies of CAR-T cells in B cell leukemia and lymphoma, and several solid tumors. We additionally discuss the major challenges in the further development and strategies for increasing anti-tumor activity and safety, as well as for successful commercial translation.
Animals ; Humans ; Immunity, Cellular ; Immunotherapy ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ; immunology ; pathology ; therapy ; Receptors, Antigen, T-Cell ; immunology ; Recombinant Fusion Proteins ; immunology ; T-Lymphocytes ; immunology ; transplantation

OBJECTIVETo investigate the role of Tal1 gene, which is aberrantly expressed in 40%-60% of patients with T lymphocytic leukemia (T-ALL), in the proliferation of T-ALL cells.

METHODSWe established stable Jurkat-siTal1 and Jurkat-T1 cell lines by trasnfecting T-ALL Jurkat cells with lentiviral vectors to knock-down or overexpress Tal1. Jurkat cells transfected with negative control siRNAs for Tal1 knock-down (Jurkat-mock1) and over-expression(Jurkat-mock2) served as the control cells. The proliferation of the cells lines was assessed using CCK-8 assay, and the cell cycle distribution was determined by flow cytometry. The mRNA and protein expressions of cyclin-dependent kinase inhibitor 2 (CDKN2A) and cyclin-dependent kinase inhibitor 1 (CDKN2B) were measured by real-time RT-PCR and Western blotting, respectively.

RESULTSJurkat-T1 cells showed more active proliferation in vitro than Jurkat-mock2 cells, while Jurkat-siTal1 cells showed slower growth than Jurkat-mock1 cells. In Jurkat-T1 cells, G0/G1 phase cells were decreased and S phase cells increased compared with Jurkat-mock2 cells, and Jurkat-siTal1 cells showed increased G0/G1 phase cells and decreased S phase cells compared with Jurkat-mock1 cells. Real-time RT-PCR and Western blotting showed that Tal1 inhibited the cellular expression of CDKN2A and CDKN2B at both mRNA and protein levels.

CONCLUSIONTal1 promotes the growth and the transition from G0/G1 phase to S phase in T-ALL cells Jurkat by inhibiting the expressions of G0/G1 and S phase negative regulatory proteins CDKN2A and CDKN2B.

Apoptosis ; Basic Helix-Loop-Helix Transcription Factors ; metabolism ; Cell Cycle ; Cell Proliferation ; Cyclin-Dependent Kinase Inhibitor p15 ; metabolism ; Cyclin-Dependent Kinase Inhibitor p16 ; metabolism ; Humans ; Jurkat Cells ; Lentivirus ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; metabolism ; pathology ; Proto-Oncogene Proteins ; metabolism ; RNA, Small Interfering ; T-Cell Acute Lymphocytic Leukemia Protein 1

OBJECTIVETo study the prognostic value of hematogones (HGs) for childhood B-lineage acute lymphoblastic leukemia (B-ALL) during consolidation chemotherapy.

METHODSA retrospective analysis was conducted for 196 children with newly-diagnosed B-ALL. They were divided into high-risk group (n=55), intermediate-risk group (n=69), and low-risk group (n=72) by risk stratification, and into complete remission group (n=165) and relapse group (n=31) by clinical outcome. The European BIOMED-1 standard flow cytometry for minimal residual disease (MRD) was used to determine the number of HGs during consolidation chemotherapy. The Kaplan-Meier survival curve was used to assess event-free survival (EFS).

RESULTSThe high-risk group had a significantly lower number of HGs than the intermediate-risk and low-risk groups (P<0.05). The number of HGs in the complete remission group was significantly higher than in the relapse group (P<0.05). The children with HGs ≤1.0% had a significantly lower EFS than those with HGs <1.0% (P<0.05).

CONCLUSIONSHGs can be used to assess the treatment outcome and prognosis in children with B-ALL, and proliferation of HGs reflects the good effect of chemotherapy in such children.

Adolescent ; Bone Marrow ; pathology ; Child ; Child, Preschool ; Female ; Flow Cytometry ; Humans ; Infant ; Male ; Neoplasm, Residual ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma ; mortality ; pathology ; Prognosis ; Retrospective Studies

OBJECTIVETo investigate the changes in brain injury after the induction chemotherapy in children with acute lymphoblastic leukemia (ALL) by cranial MRI.

METHODSThe clinical data and cranial MRI results of 62 children with ALL who were hospitalized from March 2014 to June 2015 were analyzed retrospectively.

RESULTSBefore chemotherapy, MRI showed bone marrow infiltration of the skull in 33 patients (53%); the children with WBC<20×10(9)/Lhad a significantly lower incidence rate of bone marrow infiltration of the skull than those with WBC≥20×10(9)/L (16 patients/42% vs 17 patients/71%; P<0.05), and the high-risk group had a significantly higher incidence rate of bone marrow infiltration of the skull than the non-high-risk group (71% vs 44%; P<0.05). Before chemotherapy, there were 4 cases (7%) of brain atrophy, and 2 cases (3%) of abnormal signals in the sensory conduction bundle. MRI reexamination in 28 patients after 3 months of chemotherapy showed 3 new cases (11%) of brain atrophy and 1 aggravated case of brain atrophy.

CONCLUSIONSThe children with ALL have bone marrow infiltration of the skull, brain atrophy, and abnormal signals in the sensory conduction bundle before chemotherapy, especially bone marrow infiltration of the skull, and some changes in brain injury disappear after treatment.

Adolescent ; Bone Marrow ; pathology ; Brain ; drug effects ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Induction Chemotherapy ; adverse effects ; Infant ; Magnetic Resonance Imaging ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; drug therapy ; pathology ; Retrospective Studies ; Skull ; pathology

OBJECTIVETo investigate the influence of spleen on disease status of mouse T-ALL.

METHODSThe leukemia cells were transplanted into the mice, then the development levels of leukemia cells in different organs of transplanted mice were monitored at different time points after transplantation; the transplanted leukemia cell level in different organs was detected by flow cytometry at different time points after transplantation; the survival of transplanted mice was analyzed by means of splenectomy.

RESULTSThe spleen change displayed most severely in process of T-ALL, the number of T-ALL cells in the spleen obviously increased at initial period. The detection of organs showed that along with the progression of leukemia, spleen weight change was the most significant, following by the lever change. The splenectomy test showed that the spleen played a promotive role in progession of T-ALL, and the spleneetomy could difinitely postpone the progression of T-ALL in mice, there was significant difference between splenectomy and non-splenectomy.

CONCLUSIONSIn early stage after transplantation of T-ALL cells, the spleen has the promotive effect on function of T-ALL cells, which suggests that the spleen may be a important microenvironment for T-ALL cell migrating into body.

Animals ; Cellular Microenvironment ; Disease Models, Animal ; Disease Progression ; Flow Cytometry ; Mice ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma ; pathology ; Spleen ; pathology ; Splenectomy

No abstract available.
Chromosomes, Human, Pair 13 ; Chromosomes, Human, Pair 17 ; Chromosomes, Human, Pair 22 ; Chromosomes, Human, Pair 9 ; Female ; Fusion Proteins, bcr-abl/genetics ; Humans ; In Situ Hybridization, Fluorescence ; Karyotype ; Middle Aged ; Precursor B-Cell Lymphoblastic Leukemia-Lymphoma/*genetics/pathology ; Retinoblastoma Binding Proteins/genetics ; *Translocation, Genetic ; Ubiquitin-Protein Ligases/genetics