PRODUCTS
ABI Fluorescence Detection (RUO)
PRODUCTS
ABI Fluorescence
Detection
(RUO)
Providing high quality, standardized molecular research tools.
We exclusively offer a comprehensive selection of PCR-based assays for ABI fluorescence detection, including targeted FLT3 ITD and TKD mutation assays, B- and T-cell clonality assays (based on EuroClonality/BIOMED-2 Concerted Action BMH4-CT98-3936), and translocation assays.
These RUO Product kits are designed to test DNA extracted from a variety of samples to identify targeted mutations, translocations, and clonal populations in suspect lymphoproliferations. Developed under ISO 13485 design control, our kits are used extensively across the world.
Providing high quality, standardized molecular research tools.
We exclusively offer a comprehensive selection of PCR-based assays for ABI fluorescence detection, including targeted FLT3 ITD and TKD mutation assays, B- and T-cell clonality assays (based on EuroClonality/BIOMED-2 Concerted Action BMH4-CT98-3936), and translocation assays.
These RUO Product kits are designed to test DNA extracted from a variety of samples to identify targeted mutations, translocations, and clonal populations in suspect lymphoproliferations. Developed under ISO 13485 design control, our kits are used extensively across the world.
Clonality
Lymphoid cells are different from the other somatic cells in the body as during development, the antigen receptor genes in lymphoid cells undergo somatic gene rearrangement.
Since leukemia and lymphomas originate from the malignant transformation of individual lymphoid cells, all leukemias and lymphomas generally share one or more cell-specific or ‘clonal’ antigen receptor gene rearrangements. Clonality does not always imply malignancy; all results must be interpreted in the context of all other available indicative characteristics. Our tests detect clonal rearrangements and are useful in the characterization of B- and T-cell malignancies.
Clonality
Lymphoid cells are different from the other somatic cells in the body as during development, the antigen receptor genes in lymphoid cells undergo somatic gene rearrangement.
Since leukemia and lymphomas originate from the malignant transformation of individual lymphoid cells, all leukemias and lymphomas generally share one or more cell-specific or ‘clonal’ antigen receptor gene rearrangements. Clonality does not always imply malignancy; all results must be interpreted in the context of all other available indicative characteristics. Our tests detect clonal rearrangements and are useful in the characterization of B- and T-cell malignancies.
FLT3
Mutations on the FLT3 Gene are the most common in subjects with acute Myeloid Leukemia (AML).
These mutations are characterized by an aggressive phenotype and a high prevalence of relapse, occurring in approximately 30% of subjects.
The FLT3 gene encodes a FMS related tyrosine kinase 3 receptor that is normally expressed in many cell types including hematologic stem cells.
Offering the only internationally standardized FLT3 mutation test, our kits detect both FLT3 ITD and FLT3 TKD mutations.
FLT3 ITD
The most prevalent and significant type of FLT3 mutation is an Internal Tandem Duplication (ITD) in the juxtamembrane domain of the receptor.
FLT3 ITD mutations are a heterogeneous type of mutation in location, size, and number. Research has shown FLT3 ITD mutations associated with higher concentrations of leukemic cells, increased incidence of relapse, and decreased overall survival.
FLT3 TKD
The second most common mutation type in the FLT3 gene is a Tyrosine Kinase Domain (TKD) point mutation in the codon for an aspartate (D835) or an isoleucine (I836) residue that are located in the activation loop of the FLT3 protein.
FLT3 TKD mutations are caused by nucleic acid substitutions and/or deletions that result in a change in the amino acid sequence in this highly conserved catalytic center. TKD mutations result in constitutive autophosphorylation and activation of FLT3.
FLT3
Mutations on the FLT3 Gene are the most common in subjects with acute Myeloid Leukemia (AML).
These mutations are characterized by an aggressive phenotype and a high prevalence of relapse, occurring in approximately 30% of subjects.
The FLT3 gene encodes a FMS related tyrosine kinase 3 receptor that is normally expressed in many cell types including hematologic stem cells.
Offering the only internationally standardized FLT3 mutation test, our kits detect both FLT3 ITD and FLT3 TKD mutations.
FLT3 ITD
The most prevalent and clinically significant type of FLT3 mutation is an Internal Tandem Duplication (ITD) in the juxtamembrane domain of the receptor.
FLT3 ITD mutations are a heterogeneous type of mutation in location, size, and number. Research has shown FLT3 ITD mutations associated with higher concentrations of leukemic cells, increased incidence of relapse, and decreased overall survival.
FLT3 TKD
The second most common mutation type in the FLT3 gene is a Tyrosine Kinase Domain (TKD) point mutation in the codon for an aspartate (D835) or an isoleucine (I836) residue that are located in the activation loop of the FLT3 protein.
FLT3 TKD mutations are caused by nucleic acid substitutions and/or deletions that result in a change in the amino acid sequence in this highly conserved catalytic center. TKD mutations result in constitutive autophosphorylation and activation of FLT3.
Translocations
Detection and assessment of translocations can provide important insights to aid in subject stratification.
Certain translocations have been identified to result in the disruption or mis-regulation of normal gene function and contribute to oncogenesis. Our ABI fluorescence detection assays detect these translocations and provide important insights in the studies of chromosomal aberrations suggestive of malignancies, determine leukemia and lymphoma lineages, and monitor and evaluate disease recurrence.
Translocations
Detection and assessment of translocations can provide important insights to aid in subject stratification.
Certain translocations have been identified to result in the disruption or mis-regulation of normal gene function and contribute to oncogenesis. Our ABI fluorescence detection assays detect these translocations and provide important insights in the studies of chromosomal aberrations suggestive of malignancies, determine leukemia and lymphoma lineages, and monitor and evaluate disease recurrence.
ABI FLUORESCENCE DETECTION (RUO)
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