Engineering Leukemia Cell Kasumi-1 for Self-destruction

Equipped with a team of seasoned scientists specifically to meet very challenging requirements in the research of tumor lymphangiogenesis, Creative Biolabs offers fast and reliable support for any phase of leukemia cell Kasumi-1 engineering for self-destruction purposes.

Introduction of Acute Myeloid Leukemia (AML)

AML is the most common leukemia among the adult population and accounts for about 80% of all cases. It is a relatively rare cancer with a median age of presentation in the late 60s. In younger patients, the incidence is two to three per 100,000, which rises to 13 to 15 per 100,000 in the seventh and eighth decades. This disease is a highly heterogeneous disease characterized by uncontrolled proliferation of clonal neoplastic hematopoietic precursor cells and impaired production of normal hematopoiesis leading to neutropenia, anemia, and thrombocytopenia. Morphology remains the initial diagnostic tool for any patient with acute leukemia, more and more new method has been developed, including cell-surface antigen expression analysis by flow cytometry, as well as cytogenetic and molecular markers.

Treatment Approaches for AML

The choice of treatment approach and outcome in AML depends on the age of the patient. Although improvement in outcomes has occurred in younger adults with AML during the past 4 decades, progress in older adults has been much less conspicuous. If untreated, patients die of infection or bleeding usually in a few weeks. Some older adults may have a slower progressive clinical course. Approximately 50% to 75% of adults with AML achieve complete remission (CR) with cytarabine and tetracycline. However, only approximately 20% to 30% of the patients enjoy long-term disease survival. Various strategies have been explored to eliminate minimal residual disease. During the past few years, a wide variety of cytotoxic antileukemic agents has been developed. Most recently, insights into the molecular pathogenesis of AML have led to the development of a more specific targeted therapy. Although several of the current new agents being investigated are likely to have a role in the future therapy for AML, diverse drug resistance is a big problem. Although combinations of several approaches may hold greater promise. Novel strategies for new therapy for AML are seriously needed.

Major types of leukemia.Fig.1 Major types of leukemia. (Udensi & Tchounwou, 2014)

Leukemia Cell Kasumi-1 Engineering Services at Creative Biolabs

Since its establishment in 1991, Kasumi1 is a key tool to study the peculiar molecular, morphologic, immunophenotypic findings, and the consequences of the AML1-ETO fusion oncogene on myeloid differentiation. This cell line is a powerful cell model that recapitulates the natural history and the hematopoietic developmental abnormalities of AML with t(8;21), which is a representative example of leukemia cell lines. Kasumi-1 has played an important role in an experimental model and also constitutes a major prerequisite for bench-to-bedside translation of AML therapy.

New evidence has shown that tumor lymphangiogenesis can enhance cancer immunotherapy and boost T cell immunity. With an experienced team of in-house experts in the field of immunology, Creative Biolabs has accumulated rich experience in inspiring the lymphangiogenic potentiation of immunotherapy to Turning Cancer Cells Against Themselves.

Kasumi1 is a useful model in the research of new therapies for AML. We have developed several different Strategies for engineering BV173 for cancer cell self-destruction. Different Genetic Methods for engineering cancer cells for self-destruction are available, including but not limited to:

What's more, it is important to assess the effect of self-destruction cancer cells. We are proud to launch our custom Ex Vivo Immune Reactivity Assessment services and Toxicity Assessment services.

For more detailed information, please feel free to contact us or directly send us an inquiry.

References

  1. Udensi, U.K.; Tchounwou, P.B. Dual effect of oxidative stress on leukemia cancer induction and treatment. Journal of Experimental & Clinical Cancer Research. 2014, 33(1): 1-5.
  2. Burnett, A.; et al. Therapeutic advances in acute myeloid leukemia. J Clin Oncol. 2011, 29(5): 487-94.

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