Imat 400 mg tablet is an inhibitor of tyrosine kinase. Further, it treats chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST). It effectively blocks the activity of the BCR-ABL protein which is responsible for the uncontrolled growth and division of leukemia cells. In addition to its therapeutic benefits, Imatinib also has cytogenetic properties that are crucial for the diagnosis and monitoring of CML.
Activity of the BCR-ABL protein | Imat
The BCR-ABL protein is a hybrid protein, by joining BCR and ABL genes. This protein causes chronic myeloid leukemia (CML), an aggressive form of blood cancer. The activity of the BCR-ABL protein drives the uncontrolled proliferation of white blood cells and their accumulation in the bone marrow and bloodstream. This leads to various symptoms such as weakness, fatigue, fever, enlarged spleen, and rapid weight loss. BCR-ABL inhibitors are a class of drugs that specifically target this protein’s activity to eliminate cancerous cells from the body. By blocking the signaling pathways that drive cell division and growth, these drugs prevent CML progression significantly. Understanding the activity of BCR-ABL is critical for developing better therapies for CML patients who can benefit from personalized medicine approaches in treating their disease.
Description about cytogenetics Imat
Cytogenetics is the study of chromosomes and their abnormalities. This field of genetics is particularly for 95% of CML patients having Philadelphia chromosomes. This chromosomal abnormality results from a translocation between chromosomes 9 and 22, which creates a fusion gene called BCR-ABL. This fusion gene produces the BCR-ABL protein, which has tyrosine kinase activity and promotes the survival and proliferation of leukemia cells.
Factors affecting Imatinib response
targets the BCR-ABL protein and inhibits its tyrosine kinase activity, thus reducing the growth and division of leukemia cells. In CML patients this Imatinib property is reflected as a cytogenetic response. This response is classified into three categories: complete cytogenetic response (CCR), partial cytogenetic response (PCR), and no cytogenetic response (NCR).
CCR is the desired outcome of Imatinib therapy. CCR involves the absence of metaphase and Philadelphia chromosomes in bone marrow alongside the presence of 20 metaphase cells.
PCR and Imatinib
PCR is a partial reduction between 1% and 35% of metaphase cells & 5% interphase cells with the Philadelphia chromosome and BCR-ABL fusion gene respectively. Fluorescence in situ hybridization (FISH). PCR indicates a good response to Imatinib, but it is not as desirable as CCR.
NCR and Imatinib
NCR is the absence of any reduction in the number of cells with the Philadelphia chromosome. It indicates a poor response to Imatinib or a lack of compliance with treatment. This is the gradual reason for the change in therapy.
Achievement of CCR with Imat Imatinib therapy
In conclusion, the cytogenetic properties oftablets are essential for the diagnosis, monitoring, and management of CML. Imatinib ability to inhibit the tyrosine kinase activity of the BCR-ABL protein causes a reduction in the number of cells with the Philadelphia chromosome. The achievement of CCR is the primary goal of Imatinib therapy, and it is a reliable predictor of long-term survival in patients with high risk.