Imatinib

Definition

Imatinib is a targeted therapy drug used primarily for the treatment of certain types of cancer, particularly chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GISTs). This drug works by specifically inhibiting the BCR-ABL tyrosine kinase, a protein that is active in CML and promotes cancer cell growth. Its effectiveness highlights the importance of understanding molecular mechanisms and post-translational modifications in cancer treatment.

5 Must Know Facts For Your Next Test

1. Imatinib was first approved by the FDA in 2001 and has significantly improved the prognosis for patients with CML.
2. The drug's mechanism involves blocking the ATP-binding site of the BCR-ABL protein, preventing it from phosphorylating other proteins and signaling for cell proliferation.
3. Imatinib is also effective against gastrointestinal stromal tumors (GISTs) that express mutations in the KIT receptor tyrosine kinase.
4. Resistance to imatinib can occur due to mutations in the BCR-ABL gene, leading to altered drug binding and reduced effectiveness.
5. Post-translational modifications of proteins can influence drug response and resistance, making understanding these modifications vital in optimizing cancer therapies.

Review Questions

• How does imatinib specifically target cancer cells, and what role does the BCR-ABL protein play in this mechanism?
  • Imatinib specifically targets cancer cells by inhibiting the BCR-ABL tyrosine kinase, which is produced by a fusion gene commonly found in chronic myeloid leukemia. The BCR-ABL protein promotes uncontrolled cell growth and division through its kinase activity. By blocking this enzyme's function, imatinib effectively halts the proliferation of these cancerous cells, leading to improved outcomes for patients.
• Discuss the implications of post-translational modifications on the effectiveness of imatinib in treating CML.
  • Post-translational modifications can significantly affect how well imatinib works against CML. Changes such as phosphorylation or glycosylation may alter the structure of the BCR-ABL protein, potentially leading to drug resistance. Understanding these modifications can help researchers develop strategies to overcome resistance and enhance imatinib's effectiveness or lead to new therapies targeting resistant forms of the protein.
• Evaluate the impact of imatinib on treatment paradigms for CML and how it has influenced research on targeted therapies.
  • Imatinib has revolutionized treatment paradigms for CML by introducing targeted therapy based on specific molecular abnormalities. Its success has spurred extensive research into other targeted therapies across various cancers, emphasizing the importance of personalized medicine. The knowledge gained from imatinib's use has encouraged exploration into combination therapies and alternative TKIs for cases where resistance develops, ultimately shaping future cancer treatments.

Related terms

BCR-ABL: A fusion gene that encodes for a tyrosine kinase protein responsible for promoting cell division in chronic myeloid leukemia.

Tyrosine Kinase Inhibitors (TKIs): A class of medications that block the action of tyrosine kinases, which are enzymes involved in the signaling pathways that regulate cell functions such as growth and division.

Chronic Myeloid Leukemia (CML): A type of cancer that affects the blood and bone marrow, characterized by the overproduction of myeloid cells due to the presence of the BCR-ABL fusion gene.