scholarly journals Secondary basophilic leukemia in Ph-negative myeloid neoplasms: A distinct subset with poor prognosis

Neoplasia ◽  
2021 ◽  
Vol 23 (12) ◽  
pp. 1183-1191
Author(s):  
Daniela Berger ◽  
Karin Bauer ◽  
Christoph Kornauth ◽  
Susanne Gamperl ◽  
Gabriele Stefanzl ◽  
...  
Keyword(s):  
Poor Prognosis ◽  
Distinct Subset ◽  
Myeloid Neoplasms ◽  
Basophilic Leukemia

scholarly journals Clinical characteristics and outcomes of therapy-related chronic myelomonocytic leukemia

Blood ◽  
2013 ◽  
Vol 122 (16) ◽  
pp. 2807-2811 ◽  
Author(s):  
Koichi Takahashi ◽  
Naveen Pemmaraju ◽  
Paolo Strati ◽  
Graciela Nogueras-Gonzalez ◽  
Jing Ning ◽  
...  
Keyword(s):  
Poor Prognosis ◽  
Clinical Characteristics ◽  
Chronic Myelomonocytic Leukemia ◽  
Myeloid Neoplasms ◽  
Key Points ◽  
Myelomonocytic Leukemia

Key Points t-CMML is associated with higher-risk cytogenetics and manifests poor prognosis. t-CMML should be recognized as one of the therapy-related myeloid neoplasms.

scholarly journals Mutations in EZH2 are associated with poor prognosis for patients with myeloid neoplasms

2019 ◽  
Vol 6 (3) ◽  
pp. 276-281 ◽  
Author(s):  
Qi Zhang ◽  
Qi Han ◽  
Jie Zi ◽  
Jinlong Ma ◽  
Huihui Song ◽  
...  
Keyword(s):  
Poor Prognosis ◽  
Myeloid Neoplasms

A Challenging Diagnosis of Acute Myeloid Leukemia with Myelodysplasia Related Changes in the Setting of Ayurvedic Supplements and B12 Deficiency

2020 ◽  
Vol 154 (Supplement_1) ◽  
pp. S108-S109
Author(s):  
R Goff ◽  
R Levyq
Keyword(s):  
Acute Myeloid Leukemia ◽  
Vitamin B12 ◽  
Myeloid Leukemia ◽  
Poor Prognosis ◽  
Vitamin B12 Deficiency ◽  
Final Diagnosis ◽  
Metal Analysis ◽  
Myeloid Neoplasms ◽  
B12 Deficiency ◽  
Acute Myeloid

Abstract Introduction/Objective Bone marrow findings of myelodysplastic changes can be associated with vitamin or mineral deficiencies (B12, folic acid or copper), infections, inflammatory disorders, exposure to toxins, heavy metals, zinc excess, recent radio- or chemotherapy, or myeloid neoplasms including myelodysplasia (MDS) and acute myeloid leukemia (AML). We present a case of a 32 year old Indian woman who presented with fatigue and weakness. She has a history of vitamin B12 deficiency and has been taking Ayurvedic supplements. This clinical history is very important because studies have shown that vitamin B12 deficiency has led to incorrect diagnoses of AML and/or MDS. Additionally, Ayurvedic supplements can contain a variety of heavy metals which can contribute to myelodysplastic changes. Results A complete blood count and peripheral smear analysis showed pancytopenia with rare blasts. A bone marrow core biopsy with ancillary testing was performed to evaluate for a hematologic malignancy. Vitamin B12 testing and heavy metal analysis was necessary to reach a final diagnosis. Flow cytometric analysis of the marrow identified 19.5% CD34 positive myeloblasts. The aspirate and core are hypercellular with increased blasts (17% on aspirate and 20-25% on core biopsy) with trilineage dyspoiesis. AML panel by fluorescence in situ hybridization showed no abnormalities. Heavy metal analysis shows no increase in lead, cadmium, mercury and arsenic levels. Recent vitamin B12 tests show results within normal range secondary to successful replacement. Ultimately, chromosome analysis identifies t(3;12)(q26,p13) involving ETV6/MECOM characteristic of a very poor prognosis in MDS or AML. Molecular AML panel identified BCOR and PTPN11 gene mutations which are associated with more aggressive disease and a poor prognosis in myeloid neoplasms. Conclusion This case had multiple possible causes of myelodysplastic changes and it was necessary to exclude these factors before yielding the final diagnosis of Acute Myeloid Leukemia with myelodysplastic related changes which demonstrated a rare translocation t(3;12) ETV6/MECOM which has a poor prognosis.

scholarly journals Therapy-related myeloid neoplasms: does knowing the origin help to guide treatment?

Hematology ◽  
2016 ◽  
Vol 2016 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Michael Heuser
Keyword(s):  
Poor Prognosis ◽  
Hematopoietic Cell Transplantation ◽  
Cell Clone ◽  
Alkylating Agents ◽  
Short Interval ◽  
Rapid Progression ◽  
Prognostic Impact ◽  
Hematopoietic Stem ◽  
Myeloid Neoplasms ◽  
Selection Of

Therapy-related myeloid neoplasms (t-MN) combine t-MDS and therapy related acute myeloid leukemia (t-AML) patients in one entity because of their similar pathogenesis, rapid progression from t-MDS to t-AML, and their equally poor prognosis. Treatment with epipodophyllotoxins like etoposide has been associated with a short interval between treatment and development of t-AML, with fusion oncogenes like KMT2A/MLL-MLLT3 and a better prognosis. In contrast, treatment with alkylating agents has been associated with a longer latency, an initial MDS phase, adverse cytogenetics, and a poor prognosis. The pathogenesis of t-MN can be explained by direct induction of an oncogene through chromosomal translocations, induction of genetic instability, or selection of a preexisting treatment-resistant hematopoietic stem cell clone. Recent evidence has highlighted the importance of the last mechanism and explains the high frequency of TP53 mutations in patients with t-MN. After previous cytotoxic therapy, patients present with specific vulnerabilities, especially evident from the high nonrelapse mortality in patients with t-MN after allogeneic hematopoietic cell transplantation. Here, the prognostic impact of currently known risk factors and the therapeutic options in different patient subgroups will be discussed.

scholarly journals Therapy-related myeloid neoplasms: does knowing the origin help to guide treatment?

Hematology ◽  
2016 ◽  
Vol 2016 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Michael Heuser
Keyword(s):  
Poor Prognosis ◽  
Hematopoietic Cell Transplantation ◽  
Cell Clone ◽  
Alkylating Agents ◽  
Short Interval ◽  
Rapid Progression ◽  
Prognostic Impact ◽  
Hematopoietic Stem ◽  
Myeloid Neoplasms ◽  
Selection Of

Abstract Therapy-related myeloid neoplasms (t-MN) combine t-MDS and therapy related acute myeloid leukemia (t-AML) patients in one entity because of their similar pathogenesis, rapid progression from t-MDS to t-AML, and their equally poor prognosis. Treatment with epipodophyllotoxins like etoposide has been associated with a short interval between treatment and development of t-AML, with fusion oncogenes like KMT2A/MLL-MLLT3 and a better prognosis. In contrast, treatment with alkylating agents has been associated with a longer latency, an initial MDS phase, adverse cytogenetics, and a poor prognosis. The pathogenesis of t-MN can be explained by direct induction of an oncogene through chromosomal translocations, induction of genetic instability, or selection of a preexisting treatment-resistant hematopoietic stem cell clone. Recent evidence has highlighted the importance of the last mechanism and explains the high frequency of TP53 mutations in patients with t-MN. After previous cytotoxic therapy, patients present with specific vulnerabilities, especially evident from the high nonrelapse mortality in patients with t-MN after allogeneic hematopoietic cell transplantation. Here, the prognostic impact of currently known risk factors and the therapeutic options in different patient subgroups will be discussed.

scholarly journals Myeloid neoplasms with isolated isochromosome 17q: a yet to be defined entity

2017 ◽  
Vol 9 (1) ◽  
pp. e2017066 ◽  
Author(s):  
Eleftheria Lamprianidou ◽  
Chryssoula Kordella ◽  
Menelaos Papoutselis ◽  
Zoi Bezyrgiannidou ◽  
Evangelia Nakou ◽  
...  
Keyword(s):  
Disease Progression ◽  
Poor Prognosis ◽  
Refractory Anemia ◽  
Molecular Heterogeneity ◽  
Distinct Entity ◽  
Leukemic Transformation ◽  
Ringed Sideroblasts ◽  
Aggressive Form ◽  
Myeloid Neoplasms ◽  
Molecular Complexity

It has been suggested that myeloid neoplasms with isolated isochromosome 17q[MN i(17q)] comprise a distinct entity with poor prognosis. However, literature reports show a considerable clinical and molecular heterogeneity. We describe a 58-year-old male patient who was diagnosed as refractory anemia with multilineage dysplasia and ringed sideroblasts with isolated i(17q). Though he initially responded well to erythropoietin, he gradually progressed to an aggressive form of MDS/MPN refractory to azacytidine and died 29 months after first diagnosis. Notably, in contrast to disease advancement, his karyotype reverted to normal, whereas his mutational profile remained unchanged. To our knowledge this is the first report of karyotype normalization during disease progression in patients with MN i(17q), suggesting that the i(17q) anomaly is dispensable for the leukemic transformation and highlighting the underlying clinical and molecular complexity which both have to be resolved before the establishment of MN with isolated i(17q) as a distinct entity.

The distribution of antigen on the surface of RBL-2H3 rat basophilic leukemia cells observed by back-scattered electron imaging

1986 ◽  
Vol 44 ◽  
pp. 274-275
Author(s):  
R.F. Stump ◽  
J.R. Pfeiffer ◽  
JC. Seagrave ◽  
D. Huskisson ◽  
J.M. Oliver
Keyword(s):  
Cell Surface ◽  
Dynamic Properties ◽  
Leukemia Cells ◽  
Antigen Binding ◽  
Scattered Electron ◽  
Ige Receptor ◽  
Receptor Complexes ◽  
Rat Basophilic Leukemia Cells ◽  
Electron Imaging ◽  
Basophilic Leukemia

In RBL-2H3 rat basophilic leukemia cells, antigen binding to cell surface IgE-receptor complexes stimulates the release of inflammatory mediators and initiates a series of membrane and cytoskeletal events including a transformation of the cell surface from a microvillous to a lamellar topography. It is likely that dynamic properties of the IgE receptor contribute to the activation of these responses. Fewtrell and Metzger have established that limited crosslinking of IgE-receptor complexes is essential to trigger secretion. In addition, Baird and colleagues have reported that antigen binding causes a rapid immobilization of IgE-receptor complexes, and we have demonstrated an apparent increase with time in the affinity of IgE-receptor complexes for antigen.

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