Biomarker Analysis Services for Gastrointestinal Stromal Tumor
At Protheragen, we provide specialized biomarker analysis services tailored for Gastrointestinal Stromal Tumor (GIST) research and therapeutic development. Our comprehensive biomarker panel is designed to facilitate a deep understanding of GIST pathophysiology, supporting drug discovery and preclinical development efforts. Please note that all our services are exclusively focused on research and drug development applications up to the preclinical stage; we do not offer clinical diagnostic services.
The foundation of effective therapeutic intervention lies in the precise discovery and identification of disease-relevant biomarkers. Protheragen’s biomarker discovery services are integral to the early stages of drug development for GIST. We employ advanced screening technologies and systematic validation processes to identify, characterize, and prioritize biomarkers that can inform target selection, mechanism of action studies, and preclinical efficacy assessments. Our workflow encompasses initial high-throughput screening, bioinformatic analysis, and experimental validation to ensure robust candidate identification.
Multi Omics: Our approach integrates cutting-edge -omics technologies, including genomics, transcriptomics, proteomics, and metabolomics, to enable a comprehensive study of biological systems involved in Gastrointestinal Stromal Tumor. Through next-generation sequencing, quantitative PCR, mass spectrometry-based proteomics, and metabolite profiling, we identify DNA mutations, RNA expression patterns, protein modifications, and metabolite changes linked to GIST. This holistic strategy allows for the elucidation of key disease pathways, such as receptor tyrosine kinase signaling (including KIT and PDGFRA) and downstream cascades like PI3K/AKT and RAS/MAPK, relevant to GIST pathogenesis and therapeutic response.
Candidate Validation: We implement rigorous validation strategies to confirm the association of candidate biomarkers with GIST pathophysiology. Our process includes preliminary in vitro and ex vivo screening, correlation with disease models, and functional assays to assess biological relevance. Criteria for promising candidates include specificity to GIST, reproducibility across platforms, and demonstrated linkage to known disease mechanisms, such as mutations or overexpression in key receptor tyrosine kinases. Prioritization is based on analytical performance, biological significance, and translational potential for preclinical drug development.
Diverse Technological Platforms: Protheragen offers custom assay development capabilities, adapting technological platforms to meet specific project requirements in GIST research. Our platform portfolio includes immunoassay systems, mass spectrometry instrumentation, flow cytometry analyzers, molecular diagnostic tools, and advanced histopathology and imaging suites. Each platform is selected and optimized based on the biomarker modality and intended research application, ensuring flexibility and precision.
Immunoassays: We develop and deploy ELISA, chemiluminescent, and multiplex immunoassays for quantitative and qualitative protein biomarker detection, enabling sensitive analysis of targets such as KIT and PDGFRA.
Mass Spectrometry: Our LC-MS/MS capabilities support high-resolution proteomic and metabolomic profiling, facilitating the detection of post-translational modifications and low-abundance biomolecules.
Flow Cytometry: We use flow cytometry for cell surface and intracellular biomarker analysis, supporting phenotypic characterization and quantification in GIST models.
Molecular Diagnostics: Techniques such as PCR, qPCR, and next-generation sequencing allow for the detection of gene mutations, amplifications, and expression changes, particularly in genes like KIT, PDGFRA, and PIK3CA.
Histopathology And Imaging: Advanced histopathological staining and imaging modalities provide spatial and morphological assessment of biomarker expression within tissue samples, supporting translational research.
Rigorous Method Validation: All analytical methods undergo rigorous validation in accordance with established research guidelines. We assess performance characteristics including sensitivity, specificity, linearity, reproducibility, and robustness. Quality control measures are implemented at every stage, encompassing calibration, standardization, and the use of appropriate controls to ensure data integrity and reliability throughout the preclinical research process.
Our quantitative analysis capabilities enable precise measurement of biomarker levels across diverse sample types. Using validated protocols and calibration standards, we ensure accurate quantitation for comparative studies, pharmacodynamic assessments, and mechanism-of-action investigations in GIST research.
Sample Analysis: We handle a wide range of sample types, including cell lines, tissue lysates, xenograft models, and biofluids relevant to GIST. Our analysis protocols are standardized for each sample matrix, incorporating stringent quality assurance steps such as sample tracking, contamination prevention, and reproducibility checks to maintain high data quality.
High Throughput Capabilities: Protheragen’s high-throughput analytical platforms, including multiplex immunoassays and automated sample processing systems, enable efficient analysis of large sample cohorts. These capabilities facilitate rapid data generation, conserve valuable samples, and support parallel assessment of multiple biomarkers, enhancing the throughput and scalability of GIST research projects.
| Gene Target | Biological Function | Application as a Biomarker |
|---|---|---|
| B-Raf proto-oncogene, serine/threonine kinase (BRAF) | The B-Raf proto-oncogene, serine/threonine kinase (BRAF), encodes a cytoplasmic serine/threonine-protein kinase that is a member of the RAF kinase family. BRAF plays a crucial role in the RAS-RAF-MEK-ERK mitogen-activated protein kinase (MAPK) signaling pathway, which is involved in the regulation of cell division, differentiation, and survival. Upon activation by RAS proteins, BRAF phosphorylates and activates MEK1 and MEK2, which in turn activate ERK1/2. This signaling cascade transmits extracellular growth signals to the nucleus, thereby influencing gene expression and cellular responses. Mutations in BRAF, particularly the V600E substitution, can result in constitutive kinase activation and aberrant MAPK pathway signaling. | BRAF is used as a molecular biomarker in several clinical contexts, primarily in oncology. Detection of BRAF mutations, especially the V600E variant, is applied in the diagnosis, prognosis, and therapeutic stratification of various cancers, including melanoma, colorectal cancer, papillary thyroid carcinoma, and non-small cell lung cancer. Identification of BRAF mutations can inform the use of targeted therapies, such as BRAF and MEK inhibitors, and may provide information regarding disease progression and response to treatment. |
| KIT proto-oncogene, receptor tyrosine kinase (KIT) | The KIT proto-oncogene, receptor tyrosine kinase (KIT), encodes a transmembrane receptor tyrosine kinase that is a member of the type III receptor tyrosine kinase family. KIT is activated by binding to its ligand, stem cell factor (SCF), which induces receptor dimerization and autophosphorylation. This activation initiates multiple downstream signaling pathways, including the PI3K/AKT, RAS/MAPK, and JAK/STAT pathways, regulating cellular processes such as proliferation, differentiation, apoptosis, and migration. KIT plays essential roles in the development and maintenance of hematopoietic stem cells, melanocytes, germ cells, and interstitial cells of Cajal. | KIT is widely utilized as a biomarker in diagnostic pathology, particularly for the identification of gastrointestinal stromal tumors (GISTs), where KIT expression is commonly detected by immunohistochemistry. In addition, KIT mutations or overexpression have been reported in several malignancies, including certain subtypes of acute myeloid leukemia, melanoma, and mast cell diseases. Assessment of KIT status can assist in tumor classification, prognosis, and may inform therapeutic decisions, especially in contexts where KIT-targeted therapies are considered. |
| MET proto-oncogene, receptor tyrosine kinase (MET) | The MET proto-oncogene encodes the receptor tyrosine kinase MET, also known as hepatocyte growth factor receptor (HGFR). MET is primarily expressed on the surface of epithelial cells and is activated by binding to its ligand, hepatocyte growth factor (HGF). Upon activation, MET undergoes autophosphorylation and initiates multiple downstream signaling cascades, including the PI3K-AKT, RAS-MAPK, and STAT pathways. These signaling events regulate diverse cellular processes such as proliferation, survival, motility, morphogenesis, and angiogenesis. MET signaling plays an essential role in embryonic development, tissue regeneration, and wound healing. Dysregulation of MET activity through gene amplification, mutations, or overexpression has been implicated in tumorigenesis and metastasis. | MET is used as a biomarker in oncology, particularly in the context of certain solid tumors. Overexpression, amplification, or activating mutations of MET have been associated with prognosis and therapeutic response in cancers such as non-small cell lung cancer (NSCLC), gastric cancer, and papillary renal cell carcinoma. Assessment of MET status can inform the selection of patients for targeted therapies, including MET inhibitors. In clinical settings, MET alterations are evaluated using techniques such as immunohistochemistry, fluorescence in situ hybridization, and next-generation sequencing. |
| discoidin domain receptor tyrosine kinase 2 (DDR2) | Discoidin domain receptor tyrosine kinase 2 (DDR2) is a receptor tyrosine kinase that is activated by binding to fibrillar collagens. Upon ligand binding, DDR2 undergoes autophosphorylation and initiates downstream signaling pathways that regulate various cellular processes, including cell adhesion, proliferation, migration, and extracellular matrix remodeling. DDR2 plays a significant role in tissue development, wound healing, and maintenance of connective tissue integrity. It is expressed in mesenchymal cells such as fibroblasts and chondrocytes, and contributes to the regulation of collagen turnover and matrix organization. | DDR2 expression and mutation status have been studied as potential biomarkers in several pathological conditions. In oncology, DDR2 alterations have been investigated in certain subtypes of lung squamous cell carcinoma and other cancers, where they may be associated with tumor progression and response to targeted therapies. Additionally, DDR2 has been explored as a marker in fibrotic diseases, given its involvement in extracellular matrix remodeling. Its expression levels may provide information relevant to disease characterization or progression in these contexts. |
| epidermal growth factor receptor (EGFR) | Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein that belongs to the receptor tyrosine kinase (RTK) family. Upon binding with its specific ligands, such as epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), EGFR undergoes dimerization and autophosphorylation of its intracellular tyrosine kinase domain. This activation triggers multiple downstream signaling pathways, including the RAS-RAF-MEK-ERK and PI3K-AKT cascades, which regulate key cellular processes such as proliferation, differentiation, survival, and migration. EGFR signaling plays a critical role in normal cellular physiology and tissue homeostasis, as well as in the development and maintenance of epithelial tissues. | EGFR is utilized as a biomarker in several clinical and research settings, particularly in oncology. Its expression levels, gene amplification, and the presence of specific activating mutations (such as exon 19 deletions and L858R substitution in exon 21) are assessed in various cancers, most notably non-small cell lung cancer (NSCLC). EGFR status can inform prognosis and guide therapeutic decisions, including the selection of patients for targeted therapies with EGFR tyrosine kinase inhibitors (TKIs) or monoclonal antibodies. Additionally, EGFR expression and mutation analysis are employed in the context of resistance mechanisms to targeted agents and in monitoring disease progression. |
| fibroblast growth factor receptor 1 (FGFR1) | Fibroblast growth factor receptor 1 (FGFR1) is a transmembrane receptor tyrosine kinase that belongs to the FGFR family. It primarily binds members of the fibroblast growth factor (FGF) family, leading to receptor dimerization and autophosphorylation of intracellular tyrosine residues. Upon activation, FGFR1 initiates multiple downstream signaling cascades, including the RAS-MAPK, PI3K-AKT, PLCγ, and STAT pathways. These pathways regulate a range of cellular processes such as proliferation, differentiation, migration, and survival. FGFR1 plays essential roles in embryonic development, angiogenesis, and tissue homeostasis. | FGFR1 has been studied as a biomarker in several cancer types, including breast cancer, lung cancer, and glioblastoma. Its gene amplification, overexpression, or mutations have been associated with tumor development and progression. FGFR1 status is investigated for its potential to inform prognosis, predict response to targeted therapies (such as FGFR inhibitors), and assist in patient stratification in clinical studies. Assessment of FGFR1 alterations may be performed using techniques such as fluorescence in situ hybridization (FISH), immunohistochemistry, or next-generation sequencing. |
| insulin like growth factor 1 receptor (IGF1R) | Insulin-like growth factor 1 receptor (IGF1R) is a transmembrane tyrosine kinase receptor that is activated primarily by its ligands, insulin-like growth factor 1 (IGF-1) and, to a lesser extent, IGF-2. Upon ligand binding, IGF1R undergoes autophosphorylation and initiates intracellular signaling cascades, notably the PI3K/AKT and MAPK pathways. These pathways regulate a range of cellular processes, including cell growth, differentiation, survival, and metabolism. IGF1R signaling plays a critical role in normal growth and development, and is also involved in tissue repair and maintenance. Dysregulation or overexpression of IGF1R has been implicated in the pathogenesis of several diseases, particularly various cancers, where it can contribute to enhanced proliferation, resistance to apoptosis, and metastasis. | IGF1R has been investigated as a biomarker in oncology, particularly for its association with tumor progression, prognosis, and response to targeted therapies. Elevated expression or activation of IGF1R has been observed in multiple tumor types, including breast, lung, and colorectal cancers, and has been correlated with poor clinical outcomes in certain contexts. Measurement of IGF1R expression levels or activation status is used in research settings to stratify patients, assess disease aggressiveness, and predict potential responsiveness to IGF1R-targeted therapies. Additionally, IGF1R is studied as a pharmacodynamic marker in clinical trials evaluating IGF1R inhibitors. |
| kinase insert domain receptor (KDR) | The kinase insert domain receptor (KDR), also known as vascular endothelial growth factor receptor 2 (VEGFR-2), is a type III receptor tyrosine kinase primarily expressed on endothelial cells. KDR plays a central role in mediating the effects of vascular endothelial growth factor (VEGF), a key regulator of vasculogenesis and angiogenesis. Upon binding VEGF, KDR undergoes dimerization and autophosphorylation, initiating intracellular signaling cascades that promote endothelial cell proliferation, migration, survival, and increased vascular permeability. Through these mechanisms, KDR is essential for embryonic blood vessel formation and the regulation of vascular homeostasis in adults. | KDR expression and activation status have been investigated as biomarkers in several clinical contexts, particularly in oncology and cardiovascular research. In cancer, KDR is evaluated as a marker of tumor angiogenesis, with its expression levels in tumor tissue or circulating endothelial cells being associated with tumor progression and prognosis in certain malignancies. Additionally, KDR is used to monitor the pharmacodynamic effects of anti-angiogenic therapies that target the VEGF signaling pathway. In other settings, such as preeclampsia and certain vascular disorders, KDR levels have been studied as indicators of endothelial dysfunction or abnormal angiogenic activity. |
| phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) | Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA) encodes the p110α catalytic subunit of class IA phosphoinositide 3-kinases (PI3Ks). PI3Ks are lipid kinases involved in the phosphorylation of phosphatidylinositol-4,5-bisphosphate (PIP2) to generate phosphatidylinositol-3,4,5-trisphosphate (PIP3). This reaction is a key step in the PI3K/AKT signaling pathway, which regulates diverse cellular processes including cell growth, proliferation, survival, metabolism, and motility. PIK3CA is activated by various receptor tyrosine kinases and G protein-coupled receptors, and its activity is tightly regulated in normal physiology. | PIK3CA is frequently mutated in a variety of human cancers, including breast, colorectal, endometrial, and other solid tumors. These somatic mutations, particularly in specific hotspots (e.g., E545K, H1047R), are associated with constitutive activation of the PI3K/AKT pathway. Detection of PIK3CA mutations is utilized to aid in tumor classification, prognostic assessment, and to inform targeted therapy selection, such as the use of PI3K inhibitors in certain cancer types. Additionally, PIK3CA mutation status may be assessed in liquid biopsies for monitoring disease progression or therapeutic response. |
| platelet derived growth factor receptor alpha (PDGFRA) | Platelet derived growth factor receptor alpha (PDGFRA) is a cell surface receptor tyrosine kinase that belongs to the type III receptor tyrosine kinase family. It binds members of the platelet-derived growth factor (PDGF) family, leading to receptor dimerization and autophosphorylation. This activation triggers downstream signaling pathways, including the PI3K-AKT, RAS-MAPK, and PLCγ pathways, which regulate cellular processes such as proliferation, differentiation, migration, and survival. PDGFRA is expressed in various cell types, including mesenchymal cells, and plays a key role in embryonic development, wound healing, and tissue homeostasis. | PDGFRA is utilized as a biomarker in several clinical and research settings. Its expression and mutation status are assessed in gastrointestinal stromal tumors (GISTs), where PDGFRA mutations can inform diagnosis, prognosis, and therapeutic decision-making, particularly regarding the use of tyrosine kinase inhibitors. PDGFRA is also evaluated in other malignancies and non-neoplastic conditions for its association with disease characterization and progression. |
Explore Research Opportunities with Protheragen. Our biomarker research services offer an extensive suite of capabilities for the exploratory analysis and characterization of biomarkers in Gastrointestinal Stromal Tumor. We provide advanced technologies and scientific expertise for research use only, supporting drug discovery and preclinical development. Please note that all biomarkers discussed are research targets only; we do not claim any biomarker as validated or mandatory for any application. Our focus remains on preclinical research, maintaining scientific objectivity throughout our collaborative projects.
We invite you to connect with Protheragen to discuss exploratory biomarker research in Gastrointestinal Stromal Tumor. Let’s collaborate to advance scientific knowledge and accelerate preclinical discovery—our team is ready to support your research objectives with professionalism and technical expertise.
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