Biomarker Analysis Services for Metastatic Colorectal Cancer
At Alfa Cytology, we specialize in providing advanced biomarker analysis services tailored for Metastatic Colorectal Cancer research and therapeutic development. Our comprehensive biomarker panel is specifically designed to support the understanding of disease pathophysiology, facilitating the discovery and validation of novel therapeutic targets. All services are exclusively focused on drug discovery through preclinical development stages; we do not offer or provide clinical diagnostic services.
The foundation of effective therapeutic intervention lies in the discovery and identification of robust biomarkers that reflect the molecular drivers of Metastatic Colorectal Cancer. Alfa Cytology offers a suite of biomarker discovery services that play a critical role in drug development by enabling the identification of genetic, transcriptomic, and proteomic alterations associated with tumor progression and therapy response. Our screening process involves high-throughput profiling of candidate biomarkers, followed by rigorous validation using orthogonal methods to ensure biological relevance and reproducibility.
Multi Omics: Leveraging cutting-edge -omics technologies, Alfa Cytology employs integrated genomics, transcriptomics, proteomics, and metabolomics platforms for a comprehensive study of biological systems. This multi-omics approach enables the identification and characterization of DNA mutations, RNA expression changes, protein modifications, and metabolite alterations relevant to Metastatic Colorectal Cancer. By interrogating key disease pathways such as the MAPK, PI3K/AKT, and EGFR signaling cascades, we provide deep insights into the molecular heterogeneity and therapeutic vulnerabilities of metastatic tumors.
Candidate Validation: Our candidate validation strategies combine robust experimental design with advanced data analytics to confirm the association of identified biomarkers with Metastatic Colorectal Cancer pathophysiology. Preliminary screening processes include functional assays, correlation with disease models, and cross-platform verification. Promising candidates are prioritized based on criteria such as biological plausibility, pathway involvement, prevalence in metastatic lesions, and potential for therapeutic targeting.
Diverse Technological Platforms: Alfa Cytology offers custom assay development capabilities across a range of technological platforms, ensuring adaptation to specific research requirements. Our platforms include advanced immunoassays, high-sensitivity mass spectrometry, multiparametric flow cytometry, molecular diagnostics, and digital histopathology and imaging systems—all optimized for preclinical biomarker research.
Immunoassays: We develop and optimize ELISA, chemiluminescent, and multiplex immunoassays for quantitative and qualitative detection of protein biomarkers relevant to Metastatic Colorectal Cancer.
Mass Spectrometry: Our LC-MS/MS workflows enable high-resolution, quantitative analysis of proteins, peptides, and metabolites, supporting deep profiling of tumor-associated biomolecules.
Flow Cytometry: Multiparametric flow cytometry is used for cell surface and intracellular marker analysis, facilitating the characterization of tumor and immune cell populations.
Molecular Diagnostics: We utilize PCR, qPCR, and digital PCR platforms for the detection of gene mutations, copy number variations, and gene expression changes.
Histopathology And Imaging: Custom immunohistochemistry, immunofluorescence, and digital pathology imaging are used for spatial localization and quantification of biomarkers in tissue contexts.
Rigorous Method Validation: All analytical methods undergo rigorous validation in accordance with industry guidelines, including assessment of sensitivity, specificity, linearity, reproducibility, and robustness. Quality control measures are embedded throughout the workflow to ensure data integrity and reliability, supporting the generation of reproducible and actionable research findings.
Our quantitative analysis capabilities enable accurate measurement of biomarker levels across a range of biological matrices. Advanced data processing and normalization strategies ensure consistent quantitation, supporting comparative studies and biomarker ranking for Metastatic Colorectal Cancer research.
Sample Analysis: Alfa Cytology handles a diverse array of sample types, including cell lines, tissue lysates, plasma, serum, and other relevant biological fluids. Standardized protocols are employed for sample processing, storage, and analysis, with stringent quality control at each step to maximize data reliability and minimize pre-analytical variability.
High Throughput Capabilities: Our high-throughput analytical platforms support multiplexed biomarker analysis, enabling the simultaneous evaluation of multiple targets in limited sample volumes. This approach increases efficiency, conserves valuable research samples, and accelerates the pace of discovery in Metastatic Colorectal Cancer biomarker research.
| 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 family within the mitogen-activated protein kinase (MAPK) signaling pathway. BRAF functions as a key signal transducer by phosphorylating and activating downstream MEK1 and MEK2 kinases in response to RAS activation. This signaling cascade regulates various cellular processes, including cell growth, differentiation, and survival. BRAF activity is tightly regulated in normal physiology, and aberrant activation, often through mutation, can result in uncontrolled cell proliferation. | BRAF is used as a biomarker primarily in oncology. The presence of specific activating mutations, such as the V600E mutation, is associated with certain cancers, including melanoma, colorectal cancer, and thyroid carcinoma. Detection of BRAF mutations can inform diagnosis, prognosis, and therapeutic decision-making, particularly in selecting patients for targeted therapies that inhibit mutant BRAF kinase activity. |
| KRAS proto-oncogene, GTPase (KRAS) | KRAS (Kirsten rat sarcoma viral oncogene homolog) encodes a small GTPase that functions as a molecular switch in signal transduction pathways. It cycles between an active GTP-bound state and an inactive GDP-bound state, regulating key cellular processes such as proliferation, differentiation, and survival. Upon activation by upstream signals, such as growth factor binding to receptor tyrosine kinases, KRAS transduces signals through downstream effectors including the MAPK/ERK and PI3K/AKT pathways. Mutations in KRAS commonly result in constitutive activation of the protein, leading to uncontrolled cell growth and oncogenesis. | KRAS is widely used as a molecular biomarker in oncology, particularly in colorectal, lung, and pancreatic cancers. Detection of specific KRAS mutations, especially in codons 12 and 13, provides clinically relevant information for prognosis and for predicting response to targeted therapies. For example, the presence of activating KRAS mutations in colorectal cancer is associated with resistance to anti-EGFR monoclonal antibodies. KRAS mutation status is also utilized to stratify patients for clinical trial enrollment and to guide therapeutic decision-making. |
| MET proto-oncogene, receptor tyrosine kinase (MET) | The MET proto-oncogene encodes the MET receptor tyrosine kinase, which is primarily expressed on the surface of epithelial cells. MET serves as the receptor for hepatocyte growth factor (HGF), also known as scatter factor. Upon binding of HGF, MET undergoes dimerization and autophosphorylation, initiating a cascade of downstream signaling pathways including the PI3K/AKT, RAS/MAPK, and STAT pathways. These signaling events regulate a range of cellular processes such as proliferation, survival, motility, morphogenesis, and angiogenesis. MET signaling is critical for normal embryonic development, tissue regeneration, and wound healing. Dysregulation of MET activity, including overexpression, gene amplification, or activating mutations, has been associated with oncogenic transformation and tumor progression in several cancer types. | MET has been investigated as a biomarker in oncology, particularly in non-small cell lung cancer (NSCLC), gastric cancer, and other malignancies. Its expression levels, gene amplification, and mutation status have been evaluated in tumor tissue as potential indicators of prognosis and as predictive markers for response to targeted therapies, such as MET inhibitors. Detection of MET alterations may assist in identifying patients who could benefit from specific therapeutic interventions. Additionally, MET status has been used in clinical trials to stratify patients and guide treatment decisions. |
| epidermal growth factor receptor (EGFR) | Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein that belongs to the ErbB family of receptor tyrosine kinases. Upon binding of its ligands, such as epidermal growth factor (EGF) or transforming growth factor-alpha (TGF-α), EGFR undergoes dimerization and autophosphorylation of specific tyrosine residues in its intracellular domain. This activation initiates multiple downstream signaling cascades, including the RAS-RAF-MEK-ERK and PI3K-AKT pathways, which regulate cellular processes such as proliferation, differentiation, survival, and migration. EGFR plays a critical role in normal cellular homeostasis and development, particularly in epithelial tissues. | EGFR is used as a biomarker in oncology, particularly in non-small cell lung cancer (NSCLC), colorectal cancer, and head and neck squamous cell carcinoma. Assessment of EGFR protein expression, gene amplification, or the presence of specific activating mutations can inform prognosis and guide targeted therapy decisions. For example, the detection of activating mutations in the EGFR gene is associated with sensitivity to EGFR tyrosine kinase inhibitors in NSCLC. Additionally, EGFR overexpression or amplification may correlate with disease progression and response to certain therapeutic agents. |
| erb-b2 receptor tyrosine kinase 2 (ERBB2) | The erb-b2 receptor tyrosine kinase 2 (ERBB2), also known as HER2, is a member of the epidermal growth factor receptor (EGFR/ERBB) family of receptor tyrosine kinases. ERBB2 does not have a known ligand but functions through heterodimerization with other ERBB family members, leading to activation of intracellular signaling pathways such as the MAPK and PI3K/AKT pathways. These cascades regulate cellular processes including proliferation, differentiation, and survival. Overexpression or amplification of ERBB2 can result in aberrant signaling that contributes to oncogenic transformation and tumor progression. | ERBB2 is commonly used as a biomarker in oncology, particularly in breast cancer. Its protein overexpression or gene amplification is assessed to aid in the classification of breast tumors and to inform therapeutic decision-making, including the use of targeted therapies such as trastuzumab. ERBB2 status is also evaluated in other malignancies, such as gastric and gastroesophageal junction cancers, to guide treatment strategies. |
| mucin 1, cell surface associated (MUC1) | Mucin 1 (MUC1) is a transmembrane glycoprotein expressed on the apical surface of most glandular epithelial cells. Its extracellular domain is heavily O-glycosylated, contributing to the formation of a protective mucous barrier on epithelial surfaces. MUC1 plays a role in cell signaling, modulation of cell adhesion, and protection against pathogens by limiting microbial access to epithelial cells. Additionally, MUC1 is involved in intracellular signaling pathways that influence cell proliferation, differentiation, and survival. | MUC1 is widely studied as a biomarker in oncology, particularly in epithelial-derived cancers such as breast, ovarian, pancreatic, and lung cancers. Aberrant overexpression and altered glycosylation of MUC1 are frequently observed in malignant tissues compared to normal tissues. These changes facilitate its detection in tissue samples and body fluids, supporting its use in cancer diagnosis, prognosis, and disease monitoring. MUC1 is also utilized as a target in immunohistochemical assays and in the development of certain therapeutic strategies. |
| 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 that phosphorylate phosphatidylinositol-4,5-bisphosphate (PIP2) to generate phosphatidylinositol-3,4,5-trisphosphate (PIP3), which serves as a secondary messenger in intracellular signaling pathways. The PI3K/AKT signaling cascade regulates diverse cellular processes, including cell growth, proliferation, survival, metabolism, and motility. PIK3CA activity is tightly controlled under physiological conditions, and its dysregulation can lead to aberrant activation of downstream signaling pathways. | PIK3CA is frequently mutated in various human cancers, including breast, colorectal, endometrial, and ovarian cancers. Detection of somatic mutations in PIK3CA, particularly hotspot mutations in exons 9 and 20, is used in molecular profiling to characterize tumor subtypes and to inform targeted therapeutic strategies. In certain contexts, the presence of activating PIK3CA mutations has been associated with sensitivity or resistance to specific targeted therapies, such as PI3K inhibitors and other agents affecting the PI3K/AKT/mTOR pathway. Additionally, PIK3CA mutation analysis is utilized in the selection of patients for clinical trials and in the assessment of prognosis in some cancer types. |
| platelet derived growth factor receptor alpha (PDGFRA) | Platelet derived growth factor receptor alpha (PDGFRA) is a cell surface receptor tyrosine kinase that binds members of the platelet-derived growth factor (PDGF) family. Upon ligand binding, PDGFRA undergoes dimerization and autophosphorylation, initiating intracellular signaling cascades such as the PI3K/AKT, RAS/MAPK, and PLCγ pathways. These signaling events regulate various cellular processes including proliferation, differentiation, migration, and survival, particularly in mesenchymal cells. PDGFRA plays critical roles during embryonic development, tissue repair, and angiogenesis. | PDGFRA is used as a biomarker in several clinical and research contexts. Its expression and mutation status are evaluated in certain cancers, such as gastrointestinal stromal tumors (GIST), where specific PDGFRA mutations can inform diagnosis and guide therapeutic decisions. Additionally, PDGFRA immunohistochemistry is utilized to help distinguish between tumor subtypes and to assess disease prognosis in some settings. |
| ret proto-oncogene (RET) | The RET proto-oncogene encodes a receptor tyrosine kinase that is part of the cadherin superfamily. RET is primarily involved in the development of the nervous system and the kidneys. It mediates signaling by binding to members of the glial cell line-derived neurotrophic factor (GDNF) family ligands in conjunction with GFRα co-receptors. Upon ligand binding, RET undergoes dimerization and autophosphorylation, activating downstream signaling pathways such as RAS/MAPK, PI3K/AKT, and JAK/STAT. These pathways regulate cell proliferation, differentiation, migration, and survival, particularly in neural crest-derived cells and urogenital tissues. | RET serves as a biomarker in several clinical contexts, most notably in oncology. Activating mutations and gene rearrangements involving RET are identified in medullary thyroid carcinoma, papillary thyroid carcinoma, and certain lung adenocarcinomas. Detection of RET mutations or fusions is used to inform diagnosis, prognostication, and therapeutic decision-making, including the selection of targeted RET inhibitors. RET status can also aid in the identification of hereditary cancer syndromes, such as multiple endocrine neoplasia type 2 (MEN2). |
| vascular endothelial growth factor A (VEGFA) | Vascular endothelial growth factor A (VEGFA) is a key signaling protein involved in vasculogenesis and angiogenesis. It primarily stimulates the proliferation, migration, and survival of endothelial cells, which line the interior surface of blood vessels. VEGFA binds to specific tyrosine kinase receptors, mainly VEGFR-1 and VEGFR-2, on endothelial cells, triggering intracellular signaling cascades that promote the formation of new blood vessels from pre-existing vasculature. This process is essential for normal embryonic development, wound healing, and the menstrual cycle. Additionally, VEGFA increases vascular permeability and plays a role in inflammatory responses. | VEGFA is utilized as a biomarker in various clinical and research contexts due to its involvement in angiogenesis. Elevated levels of VEGFA have been observed in several pathological conditions characterized by abnormal blood vessel growth, such as cancer, age-related macular degeneration, diabetic retinopathy, and rheumatoid arthritis. Measurement of VEGFA in blood, tissue, or other biological samples can provide information about disease presence, progression, or response to anti-angiogenic therapies. In oncology, VEGFA levels are often assessed to monitor tumor angiogenesis and evaluate the effectiveness of treatments targeting the VEGF pathway. |
Explore Research Opportunities with Alfa Cytology. Our biomarker research services offer comprehensive support for the discovery, characterization, and preclinical validation of novel biomarkers in Metastatic Colorectal Cancer. All biomarkers discussed are research targets only; we do not claim any biomarker as validated or mandatory for any application. Our focus is strictly on exploratory and preclinical research, maintaining scientific objectivity and supporting the advancement of drug discovery programs.
We invite you to discuss collaborative biomarker research opportunities with Alfa Cytology. Our team is committed to scientific collaboration and knowledge exchange in the exploratory field of biomarker analysis for Metastatic Colorectal Cancer. Connect with us to explore how our expertise can support your research objectives.
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Metastatic Colorectal Cancer
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