Poor prognosis of B‐cell acute lymphoblastic leukemia with TCF / PBX1 fusion gene and ovarian involvement at diagnosis: Two case reports and review of the literature

2021 ◽  
Author(s):  
Luciana Vinti ◽  
Giada Del Baldo ◽  
Mariachiara Lodi ◽  
Francesca Stocchi ◽  
Maria Giuseppina Cefalo ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Poor Prognosis ◽  
Fusion Gene ◽  
Case Reports ◽  
Lymphoblastic Leukemia ◽  
Review Of The Literature ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Ovarian Involvement

Mature B-Cell Acute Lymphoblastic Leukemia With Associated Translocations (14;18)(q32;q21) and (8;9)(q24;p13)

2003 ◽  
Vol 127 (5) ◽  
pp. 610-613
Author(s):  
Cherie H. Dunphy ◽  
Hendrik W. van Deventer ◽  
Kathryn J. Carder ◽  
Kathleen W. Rao ◽  
Georgette A. Dent
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
Follicular Lymphoma ◽  
B Cell ◽  
Lymphoblastic Leukemia ◽  
The Other ◽  
Review Of The Literature ◽  
Marker Chromosomes ◽  
Cell Acute Lymphoblastic Leukemia

Abstract The translocation t(14;18)(q32;q21) is most commonly associated with follicular lymphoma but has also been described in acute lymphoblastic leukemia (ALL) of B-cell origin. Although these ALL cases have had a pre-pre-B, pre-B, or mature B-cell immunophenotype and L2 or L3 morphology, all have been associated with an abnormality of 8q24. In fact, 91% (10 of 11) have been associated with t(8;22) or t(8;14), marker chromosomes for Burkitt-type ALL. The other case was associated with del(8)(q24). Thus, Burkitt-type ALL may have various immunophenotypes and morphology when associated with t(14;18). We describe a case of mature B-cell ALL associated with t(14;18) and t(8;9)(q24;p13). The morphology was suggestive but not entirely characteristic of the L3 subtype. However, on the basis of the cytogenetic findings and the review of the literature, perhaps this case represents a variant of Burkitt-type ALL, which would be important to recognize for prognostic and therapeutic purposes. We describe our findings and review the literature to heighten awareness of this group of ALLs associated with t(14;18). Additional cases need to be accrued and documented to determine the significance of an associated abnormality of 8q24 in this setting.

A fluorescence in situ hybridization study of TEL-AML1 fusion gene in B-cell acute lymphoblastic leukemia (1984–2001)

2003 ◽  
Vol 144 (2) ◽  
pp. 143-147 ◽  
Author(s):  
Nathalie Douet-Guilbert ◽  
Frédéric Morel ◽  
Marie-Josée Le Bris ◽  
Angèle Herry ◽  
Geneviève Le Calvez ◽  
...  
Keyword(s):  
In Situ Hybridization ◽  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Fluorescence In Situ Hybridization ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Hybridization Study ◽  
Cell Acute Lymphoblastic Leukemia

B-cell acute lymphoblastic leukemia with mature phenotype and MLL rearrangement: report of five new cases and review of the literature

2016 ◽  
Vol 57 (10) ◽  
pp. 2289-2297 ◽  
Author(s):  
Elisa Olga Sajaroff ◽  
Adrian Mansini ◽  
Patricia Rubio ◽  
Cristina Noemí Alonso ◽  
Marta S. Gallego ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Lymphoblastic Leukemia ◽  
Review Of The Literature ◽  
Cell Acute Lymphoblastic Leukemia

Single-Cell Phospho-Profiling in Pediatric B-Cell Precursor Acute Lymphoblastic Leukemia Reveals Signaling Differences in Cytogenetic and Prognostic Subgroups.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 2653-2653
Author(s):  
Manon Queudeville ◽  
Sarah M. Eckhoff ◽  
Klaus-Michael Debatin ◽  
Lueder H. Meyer
Keyword(s):  
Flow Cytometry ◽  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Single Cell ◽  
Poor Prognosis ◽  
Conflicts Of Interest ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Cell Precursor ◽  
Cytogenetic Aberrations

Abstract Abstract 2653 Poster Board II-629 Oncogenesis and tumor progression are supported by alterations in cellular signaling. We used phospho-specific antibodies in combination with surface staining in flow cytometry to analyze specific signaling profiles of leukemia cells at a single cell level. We anayzed 22 xenograft samples derived from NOD/SCID-mice transplanted with primary pediatric B- cell precursor acute lymphoblastic leukemia (BCP- ALL) cells. The cells were isolated from the spleens of leukemia bearing mice and stimulated ex vivo in vitro with different stimulants and cytokines. Activation of various phosphoepitopes was analyzed by flow cytometry and compared to the basal state of unstimulated samples. TEL/AML1 fusion and MLL-rearrangements are the most common cytogenetic aberrations in childhood BCP- ALL and are associated with a good or very poor prognosis, respectively. Although there were no differences detectable in basal phosphorylation between the different cytogenetic subgroups, TEL/AML1- positive samples (n= 5) displayed a significantly lower phosphorylation of extracellular regulated kinase (ERK1/2) after stimulation with PMA (Phorbol-12-myristat-13-acetate, activator of protein kinase C) or interleukin 7 (IL-7), while they showed a significantly higher activation of p38 after stimulation with PMA, compared to samples without translocation (n= 13). Additionally, the fusion gene negative samples showed a downregulation of STAT1-phosphorylation after stimulation with interleukin 10 (IL-10) whereas the TEL/AML1-positive samples showed no change. Interestingly, the MLL- positive samples (n= 3) also did not show a difference in STAT1-phosphorylation after IL-10, but showed significantly stronger STAT1 activation in response to interferon alpha (IFN-a) compared to samples without fusion genes. Moreover, the MLL- positive samples also displayed a weaker reaction in ERK-phosphorylation after IL-7 compared to the leukemia samples without cytogenetic aberrations. Differences in other prognostic subgroups analysed include a weaker phosphorylation of p38 and JNK after anisomycin in samples where the patient initially presented with hyperleucocytosis (> 100.000 WBC/μl) (n= 3), an indicator of poor prognosis. A decrease in STAT3- activation after IL-10 was observed in samples where the patients displayed bone marrow remission on day 15 of therapy (n= 8), compared to no change in the samples of patients with > 5% residual blasts (n= 8), indicative of therapy resistance, at this timepoint. Similar to the results for the cytogenetic subgroups, there were no differences detectable at basal phosphorylation levels between the prognostic subgroups. Taken together, these data show that basal phosphorylation states of specific signaling molecules do not discriminate between the different prognostic subgroups of BCP- ALL analyzed. Cytogenetic and other prognostic subgroups however display specific profiles of signaling networks after stimulation. This strategy will prove helpful to identify mechanisms by which different subgroups with distinct clinical outcomes interpret environmental signals and hereby define pathways important for continued survival, proliferation and resistance eventually leading to novel biomarkers and targeted therapies. Disclosures: No relevant conflicts of interest to declare.

Episomal amplification of NUP214-ABL1 fusion gene in B-cell acute lymphoblastic leukemia

Blood ◽  
2012 ◽  
Vol 120 (22) ◽  
pp. 4441-4443 ◽  
Author(s):  
Toby Eyre ◽  
Claire J. Schwab ◽  
Ross Kinstrie ◽  
Ann Keen McGuire ◽  
Jen Strefford ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Fusion Gene ◽  
Lymphoblastic Leukemia ◽  
Cell Acute Lymphoblastic Leukemia

High expression of Musashi-2 indicates poor prognosis in adult B-cell acute lymphoblastic leukemia

2013 ◽  
Vol 37 (8) ◽  
pp. 922-927 ◽  
Author(s):  
Qitian Mu ◽  
Yungui Wang ◽  
Bing Chen ◽  
Wenbin Qian ◽  
Haitao Meng ◽  
...  
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Poor Prognosis ◽  
Lymphoblastic Leukemia ◽  
High Expression ◽  
Cell Acute Lymphoblastic Leukemia

scholarly journals Myelodysplastic Syndrome with Myelofibrosis Transformed to a Precursor B-Cell Acute Lymphoblastic Leukemia: A Case Report with Review of the Literature

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Ayed A. Algarni ◽  
Mojtaba Akhtari ◽  
Kai Fu
Keyword(s):  
Acute Lymphoblastic Leukemia ◽  
B Cell ◽  
Myeloid Leukemia ◽  
Lymphoblastic Leukemia ◽  
Review Of The Literature ◽  
Acute Leukemias ◽  
Allogenic Stem Cell Transplantation ◽  
Increased Risk ◽  
Cell Acute Lymphoblastic Leukemia ◽  
Acute Myeloid

Myelodysplastic syndromes (MDS) comprise a group of heterogeneous clonal hematopoietic cell disorders characterized by cytopenias, bone marrow hypercellularity, and increased risk of transformation to acute leukemias. MDS usually transformed to acute myeloid leukemia, and transformation to acute lymphoblastic leukemia (ALL) is rare. Herein, we report a unique patient who presented with MDS with myelofibrosis. Two months after the initial diagnosis, she progressed to a precursor B-cell acute lymphoblastic leukemia. She was treated with induction therapy followed by allogenic stem cell transplantation. She was alive and doing well upon last followup. We have also reviewed the literature and discussed the clinicopathologic features of 36 MDS patients who progressed to ALL reported in the literature.

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