Last update 01 Nov 2024

CD33 x CD64

Last update 01 Nov 2024

Basic Info

Related Targets

CD33CD64

Drugs associated with CD33 x CD64

Anti-CD33/anti-FcgammaRI bispecific antibody(University of California San Diego)

Target

CD33 x CD64

Mechanism

CD33 inhibitors [+1]

Active Org.

University of California San Diego

Originator Org.

University of California San Diego

Active Indication

Acute Myeloid Leukemia

Inactive Indication-

Drug Highest PhasePhase 1

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CD33 x CD64

100 Translational Medicine associated with CD33 x CD64

0 Patents (Medical) associated with CD33 x CD64

156

Literatures (Medical) associated with CD33 x CD64

01 Jan 2024·Clinical Laboratory

Clinical Characteristics and Diagnosis of Ph-Positive Mixed Phenotype Acute Leukemia

Article

Author: Zhang, Xiao ; Chen, Jiao ; Li, Haixin ; Li, Xiaoli ; Li, Ruimin ; Li, Jiajia ; Zhang, Xiaofang

BACKGROUNDThe goal was to improve the clinical cognition of Ph-positive mixed phenotype acute leukemia and avoid misdiagnosis or delayed diagnosis.METHODSThe clinical manifestations and laboratory results (bone marrow cell morphology, multiparameter flow cytometry, and cytogenetics) of a case of Ph-positive mixed phenotype acute leukemia were analyzed, and related literature was reviewed.RESULTSBlood routine: WBC 386.35 x 109/L, HGB 117.00 g/L, PLT 31 x 109/L; 80% of the original cells can be seen by artificial classification. Morphological examination of bone marrow cells showed that the proliferation of nucleated cells was obviously active, and the original cells accounted for 76%. The size of the original cells was somewhat uniform, most of the cells had less mass, were stained light grayish blue, the cytoplasm particles were not obvious, the nuclei were mostly round or quasi-round, some of them showed distortion and nuclear notch, and the chromatin was coarse. Some of the cells were rich in mass, small azurin granules were seen, the nuclei were regular, most of them were round, the chromatin was fine, the myeloperoxidase and esterase staining were negative, the eosinophils accounted for 2.5%, and the basophils accounted for 0.5%. Flow cytometry immunotyping: Two groups of abnormal cells were seen in the bone marrow. 1. A group included 12.32% of nuclear cells and showed abnormal myeloid primitive cell phenotype. Main expression: CD117, CD34, CD38, HLA-DR, CD33, CD64, CD123, weak expression: CD13, CD19. 2. The other group included 45.61% of the nuclear cells and had a B-lymphoblastic phenotype. Main expression: CD34, CD38, HLA-DR, CD123, CD19, CD10, CD9, cCD79a, TDT, weak expression of CD13, CD22. Mixed phenotype acute leukemia (M/B) immunophenotype was considered. Chromosome: 46,XY,t(9; 22)(q34;q11.2) [20]. BCR-ABL (P210) fusion gene was positive.CONCLUSIONSMixed phenotype acute leukemia (MPAL) is a rare type of malignant hematologic disease. Its diagnosis is based on the comprehensive evaluation of bone marrow cell morphology, immunophenotype, molecular and cytogenetic features.

01 Nov 2023·British Journal of Haematology

Phenotypic subtypes of leukaemic transformation in chronic myelomonocytic leukaemia

Article

Author: Short, Nicholas ; Jabbour, Elias ; Bueso‐Ramos, Carlos ; Chien, Kelly ; Li, Ziyi ; Hammond, Danielle ; Pierce, Sherry ; Kadia, Tapan ; Daver, Naval ; Kanagal‐Shamanna, Rashmi ; Rodriguez‐Sevilla, Juan Jose ; Montalban‐Bravo, Guillermo ; Borthakur, Gautam ; Loghavi, Sanam ; Garcia‐Manero, Guillermo ; Kantarjian, Hagop ; Ravandi, Farhad ; Pemmaraju, Naveen ; Takahashi, Koichi ; DiNardo, Courtney ; Sasaki, Koji ; Issa, Ghayas C.

SummaryChronic myelomonocytic leukaemia (CMML) is a haematological disorder with high risk of transformation to acute myeloid leukaemia (AML). To characterize the phenotypic and genomic patterns of CMML progression, we evaluated a cohort of 189 patients with AML evolving from CMML. We found that transformation occurs through distinct trajectories characterized by genomic profiles and clonal evolution: monocytic (Mo‐AML, 53%), immature myeloid (My‐AML, 43%) or erythroid (Ery‐AML, 2%). Mo‐AML, characterized by expansion of monoblasts and promonocytes (low CD34, CD117 expression; high CD14, CD33, CD56 and CD64 expression), were defined by SRSF2, TET2 and RAS pathway mutation co‐dominance and were more likely to evolve from SRSF2‐TET2 co‐mutant CMML through emergence/expansion of RAS pathway mutant clones. Conversely, My‐AML, characterized by expansion of immature myeloid blasts (high frequency of CD34, CD38, CD117; low frequency of CD14, CD64 and CD56 expression) were less likely to exhibit SRSF2‐TET2 co‐mutations or RAS pathway mutations and had higher frequency of CEBPA mutations. Ery‐AML was defined by complex karyotypes and TP53 mutations. A trend towards improved OS and EFS with hypomethylating agent‐venetoclax combination was observed in My‐AML, but not Mo‐AML. These findings define distinct progression of CMML and set the basis for future studies evaluating the role of phenotype‐specific therapeutics.

30 Sep 2023·Cellular and molecular biology (Noisy-le-Grand, France)

Investigating the interplay of hematological parameters, CD markers, genetic polymorphisms, and database mutations in the IL15 gene in acute myeloid leukemia patients.

Article

Author: Azeez, Darya M ; Salihi, Abbas ; Mohammed, Sarbaz I ; M Hassan, Kawa

Acute myeloid leukemia (AML) is a heterogeneous malignancy characterized by the clonal expansion of myeloid precursor cells in the bone marrow. In this study, we investigated the interplay of hematological parameters, CD markers, genetic polymorphisms, and database mutations in the interleukin 15 (IL15) gene in AML patients. We enrolled 59 newly diagnosed AML patients and analyzed their bone marrow specimens using flow cytometry and molecular techniques. The hematological parameters of the AML patients revealed a significant increase in platelet count and RBC, Hb, and HCT levels compared to healthy individuals. CD marker expression analysis revealed upregulation of CD33, CD45, CD13, CD117, CD38, HLA-DR, CD15, CD64, MPO, CD34, and CD11c in AML patients. Molecular analysis showed 15 mutations in different positions of exon 8 of the IL15 gene, with the most frequent mutation being a homozygous mutation resulting from a nucleotide substitution. Additionally, 10 novel heterozygous mutations were identified in different locations of chromosome 4, with a low variant rate. Finally, database analysis of gnomAD and Mutagene revealed a high number of potential driver mutations in the IL15 gene in leukemia patients. These results provide valuable insights into the genetic and immunophenotypic characteristics of AML patients and highlight the potential role of IL15 in AML pathogenesis.

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