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Keywords
transformation of acute lympho...
transformation of acute lymphoid leukemia to acute myeloid leukemia
#1
JOURNAL ARTICLE
Margot F van Spronsen, Sofie Van Gassen, Carolien Duetz, Theresia M Westers, Yvan Saeys, Arjan A van de Loosdrecht
Myelodysplastic neoplasms (MDS) encompass haematological malignancies, which are characterised by dysplasia, ineffective haematopoiesis and the risk of progression towards acute myeloid leukaemia (AML). Myelodysplastic neoplasms are notorious for their heterogeneity: clinical outcomes range from a near-normal life expectancy to leukaemic transformation or premature death due to cytopenia. The Molecular International Prognostic Scoring System made progress in the dissection of MDS by clinical outcomes. To contribute to the risk stratification of MDS by immunophenotypic profiles, this study performed computational clustering of flow cytometry data of CD34+ cells in 67 MDS, 67 AML patients and 49 controls...
March 8, 2024: Leukemia
#2
JOURNAL ARTICLE
Naranie Shanmuganathan, Timothy P Hughes
Despite the dramatic improvements in outcomes for the majority of chronic myeloid leukemia (CML) patients over the past 2 decades, a similar improvement has not been observed in the more advanced stages of the disease. Blast phase CML (BP-CML), although infrequent, remains poorly understood and inadequately treated. Consequently, the key initial goal of therapy in a newly diagnosed patient with chronic phase CML continues to be prevention of disease progression. Advances in genomic investigation in CML, specifically related to BP-CML, clearly demonstrate we have only scratched the surface in our understanding of the disease biology, a prerequisite to devising more targeted and effective therapeutic approaches to prevention and treatment...
December 8, 2023: Hematology—the Education Program of the American Society of Hematology
#3
JOURNAL ARTICLE
Ritul Sharma, Chunfen Zhang, Aru Narendran
The E26-transformation-specific (ETS) transcription factors regulate multiple aspects of the normal hematopoietic system. There is an increasing body of evidence suggesting aberrant ETS activity and its contribution to leukemia initiation and progression. In this study, we evaluated the small-molecule ETS inhibitor TK216 and demonstrated its anti-tumor activity in pediatric leukemia. We found TK216 induced growth inhibition, cell cycle arrest and apoptosis and inhibited the migratory capability of leukemic cells, without significantly inhibiting the cell viability of normal blood mononuclear cells...
October 8, 2023: Genes
#4
JOURNAL ARTICLE
Sean J McKeague, Kacey O'Rourke, Stephen Fanning, Christopher Joy, Duncan Throp, Rebecca Adams, Yasmin Harvey, Tee Beng Keng
OBJECTIVES: Myeloid/lymphoid neoplasms with FGFR1 rearrangement are a rare group of neoplasms that share features of eosinophilia and lineage promiscuity. First, we described a challenging case of acute leukemia with lineage switch and cytogenetically cryptic FGFR1. Second, we aimed to systemically review this phenomenon in published literature. METHODS: A 68-year-old man with a history of chemotherapy exposure presented with acute leukemia of myeloid lineage without eosinophilia or 8p11 abnormalities on karyotyping...
October 19, 2023: American Journal of Clinical Pathology
#5
JOURNAL ARTICLE
Jonathan Tarquino, Sara Arabyarmohammadi, Rafael Enrique Tejada, Anant Madabhushi, Eduardo Romero
Acute leukemia is usually diagnosed when a test of peripheral blood shows at least 20% of abnormal immature cells (blasts), a figure even lower in case of recurrent cytogenetic abnormalities. Blast identification is crucial for White Blood Cell (WBC) Counting, which depends on both identifying the cell type and characterizing the cellular morphology, processes susceptible of inter- and intraobserver variability. The present work introduces an image combined-descriptor to detect blasts and determine their probable lineage...
August 11, 2023: Cytometry. Part A: the Journal of the International Society for Analytical Cytology
#6
Dong Chen, Guang Liu, Michael R Lewis, Xia Li, Matthew Ulrickson, Rajneesh Nath, Weina Chen
We report a case of myeloid/lymphoid neoplasm with ZMYM2::FGFR1 rearrangement (MLN ZMYM2::FGFR1 ) exhibiting a complex disease evolution. This neoplasm initially presented as T-lymphoblastic lymphoma (T-LBL) in lymph node and myeloproliferative neoplasm (MPN) with eosinophilia in bone marrow, then transitioned to systemic mastocytosis (SM) likely accompanied by additional JAK3 and other mutations and finally transformed to acute myeloid leukemia (AML) accompanied by additional/secondary genetic abnormality (gain of chromosome 21, der(13)t(8;13), and RUNX1 mutation)...
2023: Leukemia Research Reports
#7
JOURNAL ARTICLE
Giuseppe Visani, Maryam Etebari, Fabio Fuligni, Antonio Di Guardo, Alessandro Isidori, Federica Loscocco, Stefania Paolini, Mohsen Navari, Pier Paolo Piccaluga
Primary myelofibrosis (PMF) is a chronic myeloproliferative neoplasm (MPN) characterized by progressive bone marrow sclerosis, extra-medullary hematopoiesis, and possible transformation to acute leukemia. In the last decade, the molecular pathogenesis of the disease has been largely uncovered. Particularly, genetic and genomic studies have provided evidence of deregulated oncogenes in PMF as well as in other MPNs. However, the mechanisms through which transformation to either the myeloid or lymphoid blastic phase remain obscure...
March 15, 2023: Cancers
#8
JOURNAL ARTICLE
Maha Hameed, Mohammed Alnoamani, Mohammed Marei, Imran Tailor, Hassan Alshehri, Soha A Tashkandi, Azizah Alswayyed, Abdullah M Alrajhi, Syed Z A Zaidi, Ibraheem Motabi, Nawal AlShehry, Mansour Alfayez
OBJECTIVE: We herein describe two cases of de novo lymphoid blastic transformation in patients with no history of chronic-phase chronic myeloid leukemia (CP-CML), both of whom were labeled initially as Philadelphia positive B-Acute Lymphoblastic Leukemia (B-ALL). METHODS: The first patient was an 18-year-old male who presented with subjective fever, intentional weight loss, generalized fatigue, and headache. Investigations showed leukocytosis (312 × 10^3/ul), thrombocytopenia and anemia...
December 2022: Hematology (Amsterdam, Netherlands)
#9
REVIEW
Carsten Riether
Adult bone marrow (BM) hematopoietic stem cells (HSCs) are maintained in a quiescent state and sustain the continuous production of all types of blood cells. HSCs reside in a specialized microenvironment the so-called HSC niche, which equally promotes HSC self-renewal and differentiation to ensure the integrity of the HSC pool throughout life and to replenish hematopoietic cells after acute injury, infection or anemia. The processes of HSC self-renewal and differentiation are tightly controlled and are in great part regulated through cellular interactions with classical (e...
2022: Frontiers in Immunology
#10
JOURNAL ARTICLE
Baohuan Cai, Yun Liu, Yating Chong, Hualei Zhang, Stephanie Mori, Atsuko Matsunaga, Xuexiu Fang, John Cowell, Tianxiang Hu
CONTEXT: Myeloid and lymphoid malignancies associated with chimeric FGFR1 kinases are the hallmark of stem cell leukemia and lymphoma syndrome (SCLL). In all cases, FGFR1 kinase is constitutively phosphoactivated in the cytoplasm as a result of chromosome translocations. Recently, we demonstrated that these chimeric kinases could be cleaved by granzyme B to generate a truncated derivative, tnFGFR1, which localized exclusively into the nucleus and was not phosphorylated. OBJECTIVE: In this study, we used the mouse bone marrow transduction and transplantation model to demonstrate the leukemic transformation ability of this tnFGFR1 and identified its critical downstream targets, FLT3 and KIT, in mouse and acute myeloid leukemia (AML) patient samples...
October 2022: Clinical Lymphoma, Myeloma & Leukemia
#11
REVIEW
Jason H Kurzer, Olga K Weinberg
Acute leukemia is a heterogeneous disorder of hematologic malignancies composed primarily of hematopoietic precursors that have acquired unregulated self-renewal and proliferation. Hematology classification systems typically divide these neoplasms into lymphoid (B- or T-) and myeloid-lineage subtypes, with therapy dependent upon this distinction. Infrequently, certain acute leukemias may undergo a complete lineage switch at relapse, subsequently complicating the diagnosis and treatment of these recurrent diseases...
September 2022: International Journal of Laboratory Hematology
#12
JOURNAL ARTICLE
Maria Siddiqui, Marina Konopleva
INTRODUCTION: Venetoclax has transformed the treatment landscape in hematologic malignancies, especially in elderly population. With high rates of remission, deep and durable responses, and safe toxicity profile, venetoclax in combination therapy has been extremely effective, garnering accelerated approval and becoming standard of care in lymphoid and myeloid malignancies. AREAS COVERED: Preclinical and clinical experience of venetoclax monotherapy and combination therapy in relapsed/refractory and frontline CLL, AML, ALL, high-risk MDS and BPDCN with an emphasis on key clinical trials and efficacy of combination regimens in distinct mutational landscapes...
December 2021: Expert Review of Clinical Pharmacology
#13
JOURNAL ARTICLE
Briana A Fitch, Mi Zhou, Jamilla Situ, Sangeetha Surianarayanan, Melissa Q Reeves, Michelle L Hermiston, Joseph L Wiemels, Scott C Kogan
Exposures to a wide repertoire of common childhood infections and strong inflammatory responses to those infections are associated with the risk of pediatric B-cell acute lymphoblastic leukemia (B-ALL) in opposing directions. Neonatal inflammatory markers are also related to risk by unknown mechanism(s). Here, we demonstrate that interleukin-10 (IL-10) deficiency, which is associated with childhood B-ALL, indirectly impairs B lymphopoiesis and increases B-cell DNA damage in association with a module of 6 proinflammatory/myeloid-associated cytokines (IL-1α, IL-6, IL-12p40, IL-13, macrophage inflammatory protein-1β/CCL4, and granulocyte colony-stimulating factor)...
January 8, 2022: Blood Advances
#14
JOURNAL ARTICLE
Hila Fishman, Shreyas Madiwale, Ifat Geron, Vase Bari, Wouter Van Loocke, Yael Kirschenbaum, Itamar Ganmore, Eitan Kugler, Avigail Rein-Gil, Gilgi Friedlander, Ginette Schiby, Yehudit Birger, Sabine Strehl, Jean Soulier, Birgit Knoechel, Adolfo Ferrando, Sharon Noy-Lotan, Arnon Nagler, James C Mulloy, Pieter Van Vlierberghe, Shai Izraeli
Mixed-phenotype acute leukemia is a rare subtype of leukemia in which both myeloid and lymphoid markers are co-expressed on the same malignant cells. The pathogenesis is largely unknown, and the treatment is challenging. We previously reported the specific association of the recurrent t(8;12)(q13;p13) chromosomal translocation that creates the ETV6-NCOA2 fusion with T/myeloid leukemias. Here we report that ETV6-NCOA2 initiates T/myeloid leukemia in preclinical models; ectopic expression of ETV6-NCOA2 in mouse bone marrow hematopoietic progenitors induced T/myeloid lymphoma accompanied by spontaneous Notch1-activating mutations...
January 20, 2022: Blood
#15
REVIEW
Romane Joudinaud, Thomas Boyer
Myelodysplastic syndromes (MDSs) are associated with a significant risk of transformation to acute myeloid leukemia (AML), supported by alterations affecting malignant stem cells. This review focuses on the metabolic, phenotypic and genetic characteristics underlying this dynamic evolution, from myelodysplastic stem cells (MDS-SCs) to leukemic stem cells (LSCs). MDS-SCs are more likely to be derived from healthy hematopoietic stem cells (HSCs), whereas LSCs may originate from healthy progenitors, mostly LMPP (lymphoid-primed multipotential progenitors)...
2021: Frontiers in Oncology
#16
Hamdi Al-Janazreh, Yousef S Abuzneid, Iman Khamayseh, Fortunato Morabito, Bilal Alqam, Rosaline M F Abusabbah, Fatima K Mustafa, Shifa Sarahneh
BACKGROUND: Chronic myelogenous leukemia (CML) is a chronic myeloproliferative disease characterized by a massive overproduction of myeloid cells. It is associated with the Philadelphia chromosome [Ph1, t (9; 22) (q34; q11)] or BCR-ABL fusion gene. CML usually undergoes a triphasic clinical course ending in a blast crisis, an accelerated phase of blasts and promyelocyte production. Ten percent of CML patients reach the blast crisis phase, with 20-30% of leukemias belonging to B-cell lymphoid lineage...
August 2021: Annals of Medicine and Surgery
#17
JOURNAL ARTICLE
Lindsey E Montefiori, Sonja Bendig, Zhaohui Gu, Xiaolong Chen, Petri Pölönen, Xiaotu Ma, Alex Murison, Andy Zeng, Laura Garcia-Prat, Kirsten Dickerson, Ilaria Iacobucci, Sherif Abdelhamed, Ryan Hiltenbrand, Paul E Mead, Cyrus M Mehr, Beisi Xu, Zhongshan Cheng, Ti-Cheng Chang, Tamara Westover, Jing Ma, Anna Stengel, Shunsuke Kimura, Chunxu Qu, Marcus B Valentine, Marissa Rashkovan, Selina Luger, Mark R Litzow, Jacob M Rowe, Monique L den Boer, Victoria Wang, Jun Yin, Steven M Kornblau, Stephen P Hunger, Mignon L Loh, Ching-Hon Pui, Wenjian Yang, Kristine R Crews, Kathryn G Roberts, Jun J Yang, Mary V Relling, William E Evans, Wendy Stock, Elisabeth M Paietta, Adolfo A Ferrando, Jinghui Zhang, Wolfgang Kern, Torsten Haferlach, Gang Wu, John E Dick, Jeffery M Klco, Claudia Haferlach, Charles G Mullighan
Lineage-ambiguous leukemias are high-risk malignancies of poorly understood genetic basis. Here, we describe a distinct subgroup of acute leukemia with expression of myeloid, T lymphoid, and stem cell markers driven by aberrant allele-specific deregulation of BCL11B , a master transcription factor responsible for thymic T-lineage commitment and specification. Mechanistically, this deregulation was driven by chromosomal rearrangements that juxtapose BCL11B to superenhancers active in hematopoietic progenitors, or focal amplifications that generate a superenhancer from a noncoding element distal to BCL11B ...
November 2021: Cancer Discovery
#18
JOURNAL ARTICLE
Yujie Chen, Rafee Talukder, Brian Y Merritt, Katherine Y King, Marek Kimmel, Gustavo Rivero, Romina Sosa
BACKGROUND: We report a patient with Essential Thrombocythemia (ET), subsequently diagnosed with concurrent myeloid and lymphoid leukemia. Generally, the molecular mechanisms underlying leukemic transformation of Philadelphia-negative myeloproliferative neoplasms (Ph-MPN) are poorly understood. Risk of transformation to acute myelogenous leukemia (AML) is low; transformation to both AML and acute lymphoblastic leukemia (ALL) is extremely low. Genetic defects, including allele burden, order of mutation acquisition, clonal heterogeneity and epigenetic mechanisms are important contributors to disease acceleration...
May 22, 2021: BMC Medical Genomics
#19
JOURNAL ARTICLE
Rachel Thijssen, Sarah T Diepstraten, Donia Moujalled, Edward Chew, Christoffer Flensburg, Melissa X Shi, Michael A Dengler, Veronique Litalien, Sarah MacRaild, Maoshan Chen, Natasha S Anstee, Boris Reljić, Sarah S Gabriel, Tirta M Djajawi, Chris D Riffkin, Brandon J Aubrey, Catherine Chang, Lin Tai, Zhen Xu, Thomas Morley, Giovanna Pomilio, Claudia Bruedigam, Axel Kallies, David A Stroud, Ashish Bajel, Ruth M Kluck, Steven W Lane, Marie Schoumacher, Sébastien Banquet, Ian J Majewski, Andreas Strasser, Andrew W Roberts, David C S Huang, Fiona C Brown, Gemma L Kelly, Andrew H Wei
Selective targeting of BCL-2 with the BH3-mimetic venetoclax has been a transformative treatment for patients with various leukemias. TP-53 controls apoptosis upstream of where BCL-2 and its prosurvival relatives, such as MCL-1, act. Therefore, targeting these prosurvival proteins could trigger apoptosis across diverse blood cancers, irrespective of TP53 mutation status. Indeed, targeting BCL-2 has produced clinically relevant responses in blood cancers with aberrant TP-53. However, in our study, TP53-mutated or -deficient myeloid and lymphoid leukemias outcompeted isogenic controls with intact TP-53, unless sufficient concentrations of BH3-mimetics targeting BCL-2 or MCL-1 were applied...
May 20, 2021: Blood
#20
REVIEW
Afaf E G Osman, Michael W Deininger
Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm caused by a reciprocal translocation [t(9;22)(q34;q11.2)] that leads to the fusion of ABL1 gene sequences (9q34) downstream of BCR gene sequences (22q11) and is cytogenetically visible as Philadelphia chromosome (Ph). The resulting BCR/ABL1 chimeric protein is a constitutively active tyrosine kinase that activates multiple signaling pathways, which collectively lead to malignant transformation. During the early (chronic) phase of CML (CP-CML), the myeloid cell compartment is expanded, but differentiation is maintained...
September 2021: Blood Reviews
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