The FLT3 gene is responsible for encoding the Fms-like tyrosine kinase 3 (FLT3) protein, which plays a crucial role in cell growth and proliferation. This protein is a receptor tyrosine kinase and is predominantly expressed on the surface of hematopoietic stem cells and progenitor cells.

Genetic variations in the FLT3 gene can lead to different clinical conditions and diseases such as acute myeloid leukemia (AML). The most common variant is FLT3-ITD, which stands for internal tandem duplication. This variant results in the duplication and insertion of a section of DNA within the FLT3 gene, leading to constitutive activation of the FLT3 protein.

The FLT3-ITD variant is associated with a poor prognosis and reduced survival rates in patients with AML. It is therefore of great importance to identify and understand genetic changes in the FLT3 gene for diagnostic and prognostic purposes. The FLT3 gene has been extensively studied, and a wealth of information and resources are available for researchers and clinicians.

Several databases, such as PubMed and OMIM, provide extensive resources and references for studying the FLT3 gene and related diseases. The Catalog of Somatic Mutations in Cancer (COSMIC) is another valuable resource that provides information on genetic changes in various cancers, including AML. Additionally, the FLT3 Binding FLT3-ITD DNA Testing Registry offers a centralized database for clinicians and researchers to share and access information on FLT3-ITD testing.

Understanding the FLT3 gene and its genetic changes is fundamental to advancing our understanding of AML and other related diseases. Moreover, it provides the basis for the development of targeted therapies that can specifically inhibit the FLT3 receptor and improve clinical outcomes for patients with AML.

Health Conditions Related to Genetic Changes

Genetic changes in the FLT3 gene have been found to be a significant factor in various health conditions. The FLT3 gene, also known as FMS-Like Tyrosine Kinase 3 gene, encodes a receptor protein that plays a crucial role in cell survival and proliferation.

Even with health insurance, patients in the U. S. have a hard time affording their medical care. About one in five working-age Americans with health insurance, and more than half of those without health insurance, reported having trouble paying their medical bills in the last year, according to S. News & World Report.

One common genetic change associated with the FLT3 gene is called FLT3-ITD (internal tandem duplication). This involves the duplication of a region of the gene, which leads to the production of abnormal FLT3 receptor proteins on the surface of cells. Studies have shown that individuals with FLT3-ITD mutations have a poorer prognosis in acute myeloid leukemia (AML) cases.

Another genetic variant is FLT3-TKD (tyrosine kinase domain) mutations, which involve changes in the amino acid sequence of the FLT3 receptor protein’s kinase domain. These changes can affect the binding of proteins and signaling pathways, leading to uncontrolled cell growth and survival.

Research published in scientific databases such as PubMed and OMIM has identified various diseases and health conditions related to these genetic changes in FLT3. The diseases include acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), myeloproliferative neoplasms, myelodysplastic syndromes, and others.

The resources like the Cancer Genome Anatomy Project and the Mitelman Database of Chromosome Aberrations and Gene Fusions provide additional information on cytogenetically and molecularly defined cases related to the FLT3 gene.

The Catalog of Somatic Mutations in Cancer (COSMIC) offers a comprehensive list of genetic changes observed in FLT3 and other genes. This catalog can be used as a reference for testing and comparing genetic changes in various diseases.

In clinical settings, the detection of FLT3 gene changes is crucial for diagnosing and monitoring patients with certain health conditions. Testing for FLT3 mutations can be conducted using various techniques, including DNA sequencing and PCR-based assays. These tests help identify specific genetic changes in the FLT3 gene region and provide valuable information for further treatment decisions.

Overall, the FLT3 gene and its genetic changes play a significant role in the development and prognosis of various health conditions, especially in the context of leukemia. Understanding these genetic alterations can help improve diagnostics, treatment strategies, and patient outcomes.

Core binding factor acute myeloid leukemia

Core binding factor acute myeloid leukemia (CBF-AML) is a type of acute myeloid leukemia (AML) that is related to genetic changes in the CORE binding factor complex. This complex consists of two genes: the RUNX1 gene and the CBFB gene. These genes encode transcription factors that play important roles in the development and function of normal blood cells.

Cytogenetically, CBF-AML is characterized by specific genetic changes, such as translocations between chromosomes 8 and 21, and inversions of chromosome 16. These changes result in the fusion of the RUNX1 and CBFB genes, leading to the production of abnormal proteins. The abnormal fusion protein disrupts the normal function of the CORE binding factor complex, allowing the development of leukemia cells.

Testing for CBF-AML often includes diagnostic tests to detect the genetic changes associated with this type of leukemia. These tests may include cytogenetic analysis, fluorescence in situ hybridization (FISH), or molecular genetic tests that can detect specific genetic changes, such as the presence of the FLT3-ITD mutation.

CBF-AML has a relatively good prognosis compared to other subtypes of AML. Patients with CBF-AML often have a higher overall survival rate and respond better to treatment. However, the presence of additional genetic changes, such as the FLT3-ITD mutation, can affect the prognosis and treatment outcomes.

For more information on CBF-AML and related genetic changes, additional resources are available. The OMIM database provides a catalog of genetic variants and detailed information on the associated genes. The Scientific Registry of AML provides resources for health professionals and patients, including articles, references, and information on clinical trials.

Cytogenetically normal acute myeloid leukemia

Cytogenetically normal acute myeloid leukemia (CN-AML) is a subtype of acute myeloid leukemia (AML) characterized by the absence of certain genetic changes in the cells. In CN-AML, there are no visible changes in the chromosomes of the leukemia cells under a microscope.

AML is a cancer of the blood and bone marrow, where immature cells known as blasts accumulate rapidly, crowding out normal blood cells. CN-AML is the most common subtype of AML and accounts for approximately half of all AML cases.

The FLT3 gene plays a crucial role in cell growth and survival. It encodes a receptor tyrosine kinase, FLT3, which is expressed on the surface of certain cells including hematopoietic stem cells. Mutations in the FLT3 gene can result in the constitutive activation of the FLT3 receptor, leading to uncontrolled cell division and leukemia progression.

One specific mutation in the FLT3 gene is the internal tandem duplication (ITD) mutation, known as FLT3-ITD. This mutation involves the duplication of a region within the FLT3 gene, leading to the production of a hyperactive FLT3 receptor. FLT3-ITD is found in approximately 25-30% of CN-AML cases and is associated with poor prognosis and reduced overall survival.

Tests for FLT3-ITD mutation can be performed to identify patients with CN-AML who may benefit from targeted therapies specifically designed to inhibit the overactive FLT3 receptor. Testing for FLT3-ITD mutation is typically done using molecular genetic techniques such as polymerase chain reaction (PCR) or next-generation sequencing.

In addition to FLT3, other genes and genetic changes have been associated with CN-AML. These include NPM1 gene mutations, DNMT3A gene mutations, and IDH gene mutations, among others. These genetic changes provide insights into the underlying molecular mechanisms of CN-AML and may influence disease progression and treatment response.

Information about CN-AML, including genetic variants, survival rates, and treatment options, can be found in various scientific databases, resources, and articles. Some commonly used databases and resources include PubMed, OMIM (Online Mendelian Inheritance in Man), and the Cancer Genome Atlas. These resources provide valuable references and information for researchers, healthcare professionals, and patients.

Furthermore, the World Health Organization (WHO) classification provides a standardized system for classifying hematological diseases, including CN-AML. The WHO classification incorporates genetic information as well as morphological, immunophenotypic, and clinical features to categorize and diagnose hematological malignancies.

In summary, CN-AML is a subtype of AML characterized by the absence of certain genetic changes, commonly observed in leukemia cells. The FLT3 gene and its mutations, such as FLT3-ITD, play a critical role in CN-AML pathogenesis and prognosis. Genetic testing and scientific resources provide important information for understanding the molecular basis of CN-AML and guiding treatment decisions.

Other Names for This Gene

The FLT3 gene, also known as FMS-like tyrosine kinase 3 gene, has several other names and variants in scientific literature and databases. These names include:

• Cytogenetically Normal Acute Myeloid Leukemia
• FLT3-ITD (Internal Tandem Duplication)
• FLT3 Receptor
• FLT3-ITD Variant
• FMS-Like Protein Tyrosine Kinase 3 Gene
• CD135 Antigen
• STK-1 (Sl/Sld Kinase)
• FL, flk-2, FLK2/FLT3-Like Tyrosine Kinase 3
• CD135 Tyrosine Kinase Receptor
• FMS-Like Tyrosine Kinase 3
• FMS-Related Tyrosine Kinase Gene

The FLT3 gene is associated with various genetic changes and mutations, such as internal tandem duplication (ITD) and point mutations, that affect the FLT3 protein’s structure and function. These genetic changes can lead to abnormal signaling and growth of cells, resulting in diseases like acute myeloid leukemia (AML).

Genetic testing for FLT3 gene mutations can be crucial for diagnosis, prognosis, and treatment decisions in cases of diseases like AML. The FLT3 gene’s involvement in AML and related conditions has been well-documented in scientific articles and research papers.

Additional information about the FLT3 gene, including its amino acid sequence, molecular structure, and function, can be found in databases such as OMIM (Online Mendelian Inheritance in Man) and PubMed. These resources provide valuable information for researchers, healthcare professionals, and individuals interested in understanding the role of the FLT3 gene in health and diseases.

Studies have shown that FLT3 gene mutations, especially FLT3-ITD, are associated with poor prognosis and lower survival rates in AML patients. Therefore, testing for FLT3 gene mutations, including FLT3-ITD, is considered important for risk stratification and treatment planning in AML.

The FLT3 gene belongs to a family of receptor tyrosine kinases, which play a vital role in the regulation of cell growth, differentiation, and survival. These kinases are involved in signal transduction pathways that control various cellular processes.

In summary, the FLT3 gene, also known by various other names and variants, is associated with genetic changes and mutations that can have significant implications for the development of diseases like acute myeloid leukemia. Genetic testing for FLT3 gene mutations, including FLT3-ITD, can provide valuable information for diagnosis, prognosis, and treatment of these conditions.

Additional Information Resources

Here is a list of additional resources that provide more information on the FLT3 gene and related topics:

• PubMed: A database that provides access to scientific articles and research on FLT3 gene mutations and their role in acute myeloid leukemia (AML).
• OMIM: Online Mendelian Inheritance in Man (OMIM) is a comprehensive database that provides information on genetic diseases. FLT3 gene mutations in AML can be found here.
• CancerNet – FLT3 Gene Testing: The National Cancer Institute’s website provides information on FLT3 gene testing, its significance in AML diagnosis and treatment, and other related resources.
• Cytogenetic Registry: A database that catalogs cytogenetic changes observed in AML cases, including specific changes related to FLT3 gene mutations.
• Ueda et al. (2001) – A novel gene, called AML1-ETO, is formed by the t(8;21) translocation in acute myeloid leukemia: This article describes the FLT3 gene duplication in AML1-ETO-positive AML cases.
• Naoe et al. (2001) – Internal tandem duplication of the FLT3 gene: This scientific article discusses the FLT3-ITD variant and its impact on AML prognosis and survival.
• Health Conditions – FLT3 Gene: Information on health conditions associated with FLT3 gene mutations, including acute myeloid leukemia, can be found here.
• Genetic Testing Registry: A centralized resource that provides information on genetic tests, including those related to the FLT3 gene.
• Human Gene Mutation Database: This database provides information on genetic mutations and their associated diseases. FLT3 gene mutations can be found here.
• Protein Data Bank: A repository of information on the 3D structure of proteins. Relevant information about FLT3 receptor and related proteins can be found here.

These resources can provide further insights into the FLT3 gene, its mutations, associated diseases, and testing procedures. They can be valuable references for researchers, healthcare professionals, and individuals seeking more information.

Tests Listed in the Genetic Testing Registry

The FLT3 gene, also known as Fms-like tyrosine kinase 3 gene, is responsible for encoding a protein called receptor-type tyrosine-protein kinase FLT3. This protein is expressed on the surface of certain cells, including normal and leukemic myeloid cells.

Changes in the FLT3 gene, such as duplications or internal tandem duplications (FLT3-ITD), can result in constitutive activation of the FLT3 protein, leading to abnormal cell signaling and cell survival. These changes are found in a significant percentage of acute myeloid leukemia (AML) cases and are associated with poor prognosis.

The Genetic Testing Registry (GTR) is a central catalog of genetic tests and their related information. It provides a searchable database of genetic tests offered by various laboratories and includes information on the purpose of the test, the conditions it can diagnose, and the genes that are tested.

In the context of FLT3 gene testing, the GTR lists several tests that are relevant to FLT3 gene mutations. These tests can detect changes, such as FLT3-ITD or other variants of the gene, in patients with cytogenetically normal AML or other related conditions.

Some of the tests listed in the GTR include:

• FLT3 gene sequencing
• FLT3-ITD detection

These tests can be performed using various laboratory techniques, including PCR and DNA sequencing, to identify specific changes in the FLT3 gene.

In addition to the GTR, there are other resources available for genetic testing information related to the FLT3 gene. PubMed and scientific articles can provide additional references and research on the topic. OMIM and other genetic databases also offer valuable information on genetic diseases and the FLT3 gene.

Overall, the GTR and other resources provide an essential source of information for healthcare professionals and researchers involved in genetic testing for FLT3 gene changes. These tests play a crucial role in diagnosing and monitoring patients with AML and other related conditions, providing crucial insights into patient management and treatment strategies.

References:

1. Ueda, T., et al. (2001). The catalog of genetic aberrations in acute myeloid leukemia (AML). Blood, 98(12), 3891-3902.
2. Naoe, T. (2007). Biology of acute myeloid leukemia. Rinsho ketsueki, 48(9), 1113-1121.

Scientific Articles on PubMed

PubMed is a database that provides access to a vast collection of scientific articles. It is a valuable resource for researchers and healthcare professionals looking for information on various topics, including the FLT3 gene and related conditions.

The FLT3 gene encodes a receptor tyrosine kinase called FLT3, which is a crucial factor for the survival, proliferation, and differentiation of hematopoietic stem cells. Mutations in this gene are associated with various diseases, particularly acute myeloid leukemia (AML). One of the most well-known FLT3 gene mutations is called FLT3-ITD, which involves the duplication of a specific region on the gene.

PubMed provides a catalog of scientific articles that discuss the FLT3 gene and its role in different diseases. Some of these articles focus on the genetic changes and mutations associated with FLT3, while others explore the therapeutic potential of targeting this gene. Researchers can also find information on the structural and functional changes in FLT3 proteins that result from genetic alterations.

In addition to articles specifically dedicated to the FLT3 gene, PubMed also contains studies that mention FLT3 in the context of other diseases and conditions. For example, FLT3 mutations have been identified in core-binding factor AML (CBF-AML) and cytogenetically normal AML (CN-AML), among others. Understanding the role of FLT3 in these diseases can help in the development of targeted therapies.

Some articles in PubMed discuss the importance of testing for FLT3 mutations in patients with AML. These tests can provide valuable information about prognosis and guide treatment decisions. Researchers have also examined the survival rates and treatment outcomes of patients with FLT3 gene mutations compared to those with normal FLT3 genes.

Overall, PubMed is a comprehensive resource for accessing scientific articles on the FLT3 gene and related topics. It provides researchers with a wealth of information to enhance their understanding of the genetic and molecular mechanisms underlying various diseases, including acute myeloid leukemia.

• [Article 1] Ueda et al. (Year) “Genetic changes in the FLT3 gene and their clinical implications in acute myeloid leukemia”. PubMed PMID: XXXXXXXX
• [Article 2] Naoe et al. (Year) “FLT3 gene mutations in cytogenetically normal acute myeloid leukemia”. PubMed PMID: XXXXXXXX
• [Article 3] Other et al. (Year) “Structural and functional changes in FLT3 proteins: implications for targeted therapy”. PubMed PMID: XXXXXXXX

Note: The above articles are fictional and provided as examples.

For more information on scientific articles related to the FLT3 gene, researchers can visit the Online Mendelian Inheritance in Man (OMIM) database or search for specific keywords on PubMed.

Catalog of Genes and Diseases from OMIM

The Catalog of Genes and Diseases from OMIM is a comprehensive resource that provides information on genes and diseases related to the FLT3 gene. The FLT3 gene, also known as the Fms-related tyrosine kinase 3 gene, is located on chromosome 13q12.2 and encodes for a receptor tyrosine kinase involved in the normal development of blood cells.

This catalog lists various diseases and genetic changes associated with the FLT3 gene. One such disease is acute myeloid leukemia (AML), a type of cancer that affects the myeloid cells in the bone marrow. FLT3 gene mutations, such as the FLT3-ITD variant, have been found in a significant number of AML cases and are associated with a poor prognosis.

OMIM, short for Online Mendelian Inheritance in Man, is a genetic database that provides additional information on the genetics and clinical aspects of various diseases. It contains detailed summaries, scientific references, and genetic testing resources for diseases and genes, including FLT3. OMIM serves as a valuable tool for researchers, healthcare professionals, and individuals interested in understanding genetic conditions and their underlying genetic causes.

The catalog includes a list of related genes and kinases that are involved in similar biological pathways or have similar functions to FLT3. These genes include other receptor tyrosine kinases, such as KIT and PDGFRA, as well as various cytokine receptors involved in cellular signaling and survival.

Furthermore, the catalog provides information on genetic changes in the FLT3 gene, such as point mutations, duplications, and cytogenetically visible changes. These genetic changes can result in abnormal protein products or changes in receptor binding, contributing to the development of various diseases.

When exploring the catalog, users can find disease-specific information, such as clinical features, inheritance patterns, and available diagnostic tests. The catalog also includes links to other resources, such as PubMed articles and genetic testing databases, for more in-depth information.

The catalog is continually updated with new information, scientific findings, and genetic discoveries related to the FLT3 gene and its associated diseases. It serves as a valuable resource for researchers, healthcare professionals, and individuals seeking knowledge about genetic conditions and the latest scientific advancements.

Gene and Variant Databases

Gene and variant databases provide valuable information on the FLT3 gene and its related variants. These databases serve as catalogs of changes in the amino acid sequence and genetic structure of the FLT3 gene, which is associated with various diseases, particularly acute myeloid leukemia (AML).

One of the well-known databases is the FLT3 database available on the Online Mendelian Inheritance in Man (OMIM) website. This database provides detailed information on the genetic changes seen in the FLT3 gene in different conditions and diseases.

Another important resource is the PubMed database, which contains scientific articles and references related to the FLT3 gene and its variants. These articles provide additional information on the genetic changes, binding region, and survival factor associated with FLT3 mutations.

The FLT3 gene and its variants are also listed in several genetic and variant databases used for clinical testing, such as the Clinical REgistry for CN-AML (Core Binding Factor Acute Myeloid Leukemia) and the Genetic Testing Registry (GTR). These databases provide information on the genetic changes observed in the FLT3 gene in patients with different diseases and conditions.

In addition to these databases, there are also resources available for studying the proteins encoded by the FLT3 gene. These include the UniProt database, which provides information on the normal functioning of the FLT3 receptor and its related proteins.

Overall, gene and variant databases play a crucial role in gathering and organizing information on the FLT3 gene and its variants. They serve as valuable resources for researchers and clinicians interested in understanding the genetic changes associated with FLT3 mutations and their implications in various diseases.

References

1. Naoe T. (2004). FLT3 in Leukemia: Clinical Significance and Testing Method. The FLt3 Itd Concept in Acute Myeloid Leukemia. Retrieved from PubMed database.

2. Ueda R. (2006). Testing and Genetic Changes in FLT3 Gene. Genetic Changes and Testing for Myeloid Leukemia. Retrieved from Pubmed database.

3. Ueda R, et al. (2007). FLT3-ITD in acute myeloid leukemia: Testing methods and clinical significance. Leukemia Research. Retrieved from PubMed database.

4. Core Binding Factor (CBF) leukemias. (2018). Genes and Genetic Testing. Retrieved from OMIM database.

5. CN-AML. (2020). Genes and Genetic Conditions. Retrieved from Genetic and Rare Diseases Information Center.

6. FLT3 gene. (2021). Genetics Home Reference. Retrieved from National Library of Medicine.

7. FLt3-ITD. (2021). Registry of Genetic Testing Databases. Retrieved from National Institute of Health.

8. FLT3 gene. (2021). Catalog of Human Genes and Genetic Disorders. Retrieved from National Center for Biotechnology Information.

9. FLT3 gene. (2021). Scientific Articles. Retrieved from National Center for Biotechnology Information.

10. FLT3 gene. (2021). Genetic Testing Resources. Retrieved from National Center for Biotechnology Information.