FLT3 Mutation and its Role in Acute Myeloid Leukemia
Cells in nearly any part of the body can become cancer if they begin to grow unreasonably.
The growing interest of the pharmaceutical industry in the therapeutic potential for treating blood cancer with fms-like tyrosine kinase 3 (FLT3) positive mutations has been a catalyst for the progress in the global FLT3 inhibitors market.
FLT3 is a gene mutation in leukemia (blood cancer) that is the most common genetic change in acute myeloid leukemia (AML).
What is FLT3 mutation?
Before gaining an understanding of FLT3 mutation, one should understand AML.
Acute myeloid leukemia (AML) begins in the bone marrow but often moves to the blood as well. It may also spread to other parts of the body, including the lymph nodes, liver, spleen, central nervous system (brain and spinal cord), and testicles.
The landscape of treatment of blood cancer with FLT3 positive mutations using novel inhibitory therapeutics is massively growing, with many emerging and legacy companies venturing into the healthcare industry with their respective therapeutic portfolio exclusively developed and designed for the treatment of FLT3 mutated AML.
The FLT3 gene contains instructions for a protein called FLT3, which helps white blood cells grow. Mutations in this gene encourage the growth of many abnormal white blood cells.
There are the following two types of FLT3 mutation:
FLT3-Internal Tandem Duplication (ITD): FLT3-ITD involves multiple copies of the gene in a row.
FLT3-Tyrosine Kinase Domain (TKD): FLT3-TKD involves a single change or gene deletions.
Previously, AML treatments were not very effective against cancers with the FLT3 mutation. People with the FLT3 mutation had a very aggressive form of leukemia that was more likely to return after it was treated. However, new drugs are improving the outlook for people with this AML subtype as they specifically target FLT3 mutation.
Multiple small molecule inhibitors of FLT3 signaling are currently being approved in the U.S., and many more are in clinical trials. Moreover, novel therapeutic strategies to overcome resistance, including combining FLT3 inhibitors with other antileukemic agents, developing new FLT3 inhibitors, and FLT3-directed immunotherapy, are in active clinical development.
With this progress, the growth of the global FLT3 inhibitors market is expected to be driven by the introduction of novel products, the increasing incidence of acute myeloid leukemia, and the rising research and development investments, among others.
According to a report by BIS Research, the global FLT3 inhibitors market is expected to reach $2.06 billion by 2032 from $400.9 million in 2021, growing at a CAGR of 14.88% during the forecast period 2022–2032.
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How does the FLT3 mutation affect AML?
AML with FLT3 mutation is more aggressive and needs an uncommon treatment based on the cancer cells and gene changes in AML. The FLT3 gene helps in regulating the survival and reproduction of cells. The gene mutation causes immature blood cells to multiply uncontrollably.
Patients with FLT3 mutation have a less promising outlook of the treatment as compared to patients with other types of AML. Also, these diseases are more likely to return after the treatment as they have lower survival rates.
FLT3 mutations are likely to occur more often in people who are above 60 years old.
Some of the other risk factors for AML include old age, family history with the same condition, smoking, over-exposure to chemicals such as benzene, blood disorder such as essential thrombocythemia, and receiving chemotherapy in the past.
FLT3 Inhibitors
Previously, FLT3 mutation was treated using chemotherapy which was not that effective in improving survival rates. However, over time, a new drug called FLT3 inhibitor was introduced to improve the outlook for people with the mutation.
Through imaging, genetic, and biomarker studies, researchers are gaining a deeper understanding of the biology of AML, which will likely resolve many current problems in FLT3 mutated AML diagnosis and classification.
With the increasing frequency of FLT3 mutations occurring in patients with AML, several treatment techniques are under development that might disrupt the oncogenic signaling initiated by FLT3.
In patients having FLT3-ITD mutation at diagnosis, the FLT3-ITD mutation is retained with a higher allelic burden at relapse than at diagnosis. However, other clonal possibilities may also occur as the disease progresses from diagnosis to relapse.
More specifically, FLT3-ITD mutations are detected at relapse more often than FLT3-TKD mutations.
Overall, the use of FLT3 inhibitors, as compared to historical treatments, has demonstrated a substantial clinical benefit in the relapsed/refractory AML and offers promising treatment strategies for patients with few treatment options.
Conclusion
Patients with FLT3 mutation along with AML are often concerned about a less positive treatment outcome. However, medications such as FLT3 inhibitors help to improve the outlook. The invention of new and more effective drugs is expected to extend the survival rate of patients with FLT3 mutation in the coming years.
Moreover, the rising interest of the pharmaceutical industry in developing and marketing novel drugs for treating blood cancer using FLT3 positive mutations is accelerating the growth of the global FLT3 inhibitors market.
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