CD33


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CD33

a type I transmembrane protein present on myeloid cells and myeloid precursors; expressed in many acute nonlymphoblastic leukemias and some B-cell chronic lymphocytic leukemias.
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The winners in the student category were as follows: joint first - Sulaiman al-Shakhs with the poster Inhibition of the CD33 Pathway as a Novel Strategy to Alleviate Alzheimer's Disease Neuropathological, and Hisham Abdelwahab with AAV-mediated anti-Notch1 Antibody Expression to treat Glioblastoma Multiforme; second was Nada Darwish with Regulation of integrin linked kinase by calreticulin as a mechanism for cancer development and metastasis; and third Abdulla al-Mulla with the poster Dysregulation in crp, tnf-alpha and il-6 markers associated with obese bipolar patients.
When Mylotarg binds to the CD33 antigen on the cell surface it is absorbed into the cell and calicheamicin is released causing cell death.
The monoclonal antibodies (MoAb) used for diagnosis of AL were: for B-lineage: CD19, CD22, CD20, CD10, for T-lineage: CD2, CD3, CD5, CD7, CD4, CD8, for myelo-monocytic lineage: CD13, CD33, CD11c, CD64, CD14, other cells surface markers: CD34, CD117, HLA-DR and intracellular MoAb: CD79a, CD3 and MPO.
Flow cytometry confirmed the presence of myeloid blasts, which were positive for CD13, CD33, CD34, CD117, HLA-DR, CD56, and CD64; and negative for CD3 and CD19.
However, it is common for acute leukemias to aberrantly express protein markers more typically associated with other lineages, for example, expression of the myeloid markers CD13 and CD33 in B-ALL or T-ALL and expression of the T/NK-cell markers CD7 and CD56 in AML.
The therapy works by targeting CD33, a cancer antigen that is highly expressed in AML.
It is also the only AML therapy that targets CD33, an antigen expressed on AML cells in up to 90% of patients.
Flow cytometric studies performed on the bone marrow aspirate revealed a prominent population of leukemic promyelocytes with expression of CD13, CD15, CD33, CD56, and CD117.
The Phase III Children's Oncology Group Trial AAML0531 demonstrated that pediatric AML patients with a higher CD33 expression had a significantly reduced RR and improved EFS with the addition of GO to conventional chemotherapy.
In 2008, my colleagues and I discovered a gene called CD33 that controls AD-related inflammation in the brain.
The myeloid series showed 94% CD13, 82% CD33, 88% CD117, 73% CD34, and 41% HLA-DR positive.
15) These cells showed a positive reaction to MSC markers, such as CD10, CD13, CD29, CD44, and CD90 and a negative reaction to CD14, CD33, CD56, CD31, CD34, CD45, and HLA-DR.