Biomarker Analysis Services for Esophageal Cancer
At Alfa Cytology, we provide specialized biomarker analysis services dedicated to advancing Esophageal Cancer research and therapeutic development. Our comprehensive biomarker panel enables in-depth exploration of disease pathophysiology, supporting the discovery and validation of novel drug targets. All our services are exclusively focused on facilitating drug discovery through preclinical development stages, and do not include clinical diagnostic applications.
The foundation of effective therapeutic intervention lies in the precise identification and characterization of relevant biomarkers. Alfa Cytology’s biomarker discovery services are designed to accelerate drug development by systematically screening for molecular indicators associated with Esophageal Cancer. Our approach includes high-throughput screening, comparative analyses, and robust validation processes to ensure that only the most promising candidates advance to subsequent stages. Through iterative validation, we refine biomarker panels to support target identification, mechanism-of-action studies, and preclinical efficacy assessments.
Multi Omics: Leveraging cutting-edge -omics technologies, Alfa Cytology employs an integrated multi-omics strategy encompassing genomics, transcriptomics, proteomics, and beyond. This comprehensive approach enables the simultaneous study of DNA, RNA, protein, and metabolite biomarkers, providing a holistic view of biological systems relevant to Esophageal Cancer. By interrogating key disease pathways—such as receptor tyrosine kinase signaling (e.g., EGFR, ERBB2, MET, KIT), immune checkpoint regulation (e.g., CD274/PD-L1), angiogenesis (e.g., VEGFA, KDR), and post-transcriptional gene regulation (e.g., MIR21)—we uncover actionable insights into tumor biology and therapeutic vulnerabilities.
Candidate Validation: Our candidate validation and prioritization strategies incorporate both experimental and computational methodologies. We evaluate biomarker candidates for their association with Esophageal Cancer pathophysiology, including alterations in gene expression, protein function, and signaling pathways. Preliminary screening involves rigorous statistical and functional analyses, while prioritization criteria include biological relevance, detectability, and translational potential. Only candidates demonstrating robust association with disease mechanisms and technical feasibility progress to advanced validation stages.
Diverse Technological Platforms: Alfa Cytology offers custom assay development tailored to the unique requirements of Esophageal Cancer research. Our technological platforms are adaptable, supporting a range of analytical modalities from single-analyte to multiplexed formats. We integrate immunoassay systems, mass spectrometry, flow cytometry, molecular diagnostics, and advanced histopathology/imaging to provide comprehensive and flexible solutions for biomarker quantification and characterization.
Immunoassays: We develop and implement ELISA, chemiluminescent, and multiplex immunoassays for sensitive and specific detection of protein biomarkers, such as MUC1, VEGFA, and CD274.
Mass Spectrometry: Our LC-MS/MS platforms enable precise quantitation and structural characterization of proteins and metabolites, supporting discovery and validation of complex biomarker signatures.
Flow Cytometry: We utilize flow cytometry for high-throughput, quantitative analysis of cell-surface and intracellular markers, enabling phenotypic profiling of tumor and immune cell populations.
Molecular Diagnostics: Our molecular diagnostics capabilities include PCR, qPCR, and next-generation sequencing for detection of gene mutations (e.g., PIK3CA, EGFR, KIT), gene amplification, and microRNA expression (e.g., MIR21).
Histopathology And Imaging: We offer advanced histopathological and imaging techniques, including immunohistochemistry and in situ hybridization, for spatial localization and quantification of biomarker expression within tissue samples.
Rigorous Method Validation: All analytical methods undergo rigorous validation in accordance with established guidelines for preclinical research. We assess performance characteristics such as sensitivity, specificity, linearity, precision, and reproducibility. Robust quality control measures are implemented throughout assay development and sample analysis to ensure data integrity and reliability.
Our quantitative analysis capabilities enable accurate measurement of biomarker levels across diverse sample types. Using validated protocols and state-of-the-art instrumentation, we generate reproducible, high-quality data suitable for preclinical decision-making and exploratory research.
Sample Analysis: We handle a variety of sample types, including cell lines, primary tissues, and biofluids relevant to Esophageal Cancer models. Our analysis protocols are optimized for sample integrity, minimizing degradation and maximizing yield. Comprehensive quality assurance procedures are in place to monitor sample handling, processing, and analytical workflows.
High Throughput Capabilities: Alfa Cytology’s high-throughput analytical platforms support multiplexed biomarker analysis, enabling efficient processing of large sample cohorts. These capabilities enhance productivity, conserve valuable samples, and facilitate robust data generation for preclinical studies.
| Gene Target | Biological Function | Application as a Biomarker |
|---|---|---|
| CD274 molecule (CD274) | CD274 molecule, also known as programmed death-ligand 1 (PD-L1), is a transmembrane protein that plays a key role in the regulation of immune responses. It is expressed on various cell types, including antigen-presenting cells, some non-hematopoietic cells, and many tumor cells. CD274 binds to the PD-1 receptor on T cells, leading to inhibition of T cell activation and proliferation, reduction of cytokine production, and promotion of T cell apoptosis. This interaction serves as an immune checkpoint, contributing to the maintenance of immune homeostasis and prevention of autoimmunity by limiting excessive immune responses. In the context of cancer, upregulation of CD274 on tumor cells can facilitate immune evasion by inhibiting anti-tumor T cell activity. | CD274 expression is used as a biomarker in oncology, particularly in the context of immunotherapy. Assessment of CD274 (PD-L1) levels in tumor tissue can inform clinical decisions regarding the use of immune checkpoint inhibitors targeting the PD-1/PD-L1 pathway. Immunohistochemical detection of CD274 is commonly employed to evaluate its expression in various cancers, including non-small cell lung cancer, urothelial carcinoma, and melanoma. The level of CD274 expression may be associated with the likelihood of response to therapies that block PD-1 or PD-L1, and it is often used as a companion diagnostic in this setting. |
| KIT proto-oncogene, receptor tyrosine kinase (KIT) | The KIT proto-oncogene encodes a type III receptor tyrosine kinase known as KIT (also called CD117). KIT is a transmembrane protein that binds stem cell factor (SCF), leading to receptor dimerization and autophosphorylation. This activation initiates downstream signaling pathways, including PI3K/AKT, RAS/RAF/MEK/ERK, and JAK/STAT, which regulate cellular processes such as proliferation, differentiation, survival, and apoptosis. KIT is expressed in several cell types, notably hematopoietic stem cells, melanocytes, germ cells, and interstitial cells of Cajal. Mutations or dysregulation of KIT can contribute to oncogenesis and other pathologies. | KIT is utilized as a biomarker primarily in the diagnostic evaluation of certain tumors. Immunohistochemical detection of KIT (CD117) is commonly used to identify gastrointestinal stromal tumors (GISTs), as the majority of these tumors express KIT protein. Additionally, KIT expression is assessed in other neoplasms, such as some cases of melanoma, seminoma, and acute myeloid leukemia, to aid in classification and differential diagnosis. The presence of specific KIT mutations is also used to guide targeted therapy decisions in GIST and other malignancies. |
| MET proto-oncogene, receptor tyrosine kinase (MET) | The MET proto-oncogene encodes the MET receptor tyrosine kinase, which is primarily activated by binding to its ligand, hepatocyte growth factor (HGF). Upon activation, MET initiates a cascade of intracellular signaling pathways, including the PI3K-AKT, RAS-MAPK, and STAT pathways. These signaling events regulate various cellular processes such as proliferation, survival, motility, morphogenesis, and angiogenesis. MET signaling is essential for embryonic development, tissue regeneration, and wound healing. Dysregulation of MET activity, through gene amplification, mutations, or protein overexpression, has been associated with aberrant cell growth and oncogenic transformation. | MET has been studied as a biomarker in multiple cancer types, including non-small cell lung cancer, gastric cancer, and renal cell carcinoma. Its utility as a biomarker includes assessment of MET gene amplification, protein overexpression, or activating mutations, which may provide information on prognosis or predict response to targeted therapies that inhibit MET signaling. Detection of MET alterations can be performed using techniques such as immunohistochemistry, fluorescence in situ hybridization, or next-generation sequencing. |
| epidermal growth factor receptor (EGFR) | Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein and a member of the ErbB family of receptor tyrosine kinases. It is encoded by the EGFR gene located on chromosome 7p11.2. EGFR is activated by binding of specific ligands, such as epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-α), leading to receptor dimerization and autophosphorylation of intracellular tyrosine residues. This activates downstream signaling pathways, including the RAS-RAF-MEK-ERK and PI3K-AKT pathways, which regulate cellular processes such as proliferation, differentiation, migration, and survival. | EGFR is used as a biomarker in various cancers, most notably non-small cell lung cancer (NSCLC), colorectal cancer, and head and neck squamous cell carcinoma. Detection of EGFR protein expression, gene amplification, or specific activating mutations can inform prognosis and guide therapeutic decisions, particularly regarding the use of EGFR-targeted therapies such as tyrosine kinase inhibitors or monoclonal antibodies. EGFR status assessment is also utilized to predict response or resistance to these targeted 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) family of receptor tyrosine kinases. ERBB2 lacks a known ligand but can form heterodimers with other EGFR family members, such as EGFR (ERBB1), ERBB3, and ERBB4. Upon dimerization, ERBB2 undergoes autophosphorylation on specific tyrosine residues in its intracellular domain, activating downstream signaling pathways including the PI3K/AKT and MAPK pathways. These pathways regulate diverse cellular processes such as proliferation, differentiation, survival, and migration. ERBB2 plays a critical role in normal embryonic development and tissue homeostasis, but its overexpression or amplification is associated with aberrant cell growth and oncogenesis. | ERBB2 is utilized as a biomarker primarily in oncology, most notably in breast cancer. Overexpression or gene amplification of ERBB2 is detected in a subset of breast carcinomas and is associated with specific clinical characteristics, including an increased risk of disease progression. ERBB2 status is assessed using immunohistochemistry (IHC) and in situ hybridization (ISH) techniques to guide clinical decision-making. The identification of ERBB2 overexpression or amplification informs the selection of targeted therapies, such as monoclonal antibodies and tyrosine kinase inhibitors, which are designed to inhibit ERBB2-mediated signaling. |
| kinase insert domain receptor (KDR) | The kinase insert domain receptor (KDR), also known as vascular endothelial growth factor receptor 2 (VEGFR-2), is a receptor tyrosine kinase primarily expressed on endothelial cells. KDR functions as a key mediator of the effects of vascular endothelial growth factor (VEGF), playing a central role in the regulation of angiogenesis, vasculogenesis, and endothelial cell proliferation, migration, and survival. Upon binding to VEGF ligands, KDR undergoes dimerization and autophosphorylation, initiating intracellular signaling cascades that promote the formation of new blood vessels and maintain vascular integrity. | KDR expression and alterations have been utilized as biomarkers in various clinical and research contexts, particularly in oncology and cardiovascular disease. In cancer, KDR is assessed to evaluate tumor angiogenesis, as increased KDR expression is associated with active neovascularization in several tumor types. Additionally, KDR status may be used to stratify patients for anti-angiogenic therapies targeting the VEGF pathway. In other settings, circulating levels of soluble KDR or genetic variants in the KDR gene have been investigated as potential indicators of disease progression or therapeutic response. |
| microRNA 21 (MIR21) | MicroRNA 21 (MIR21) is a small non-coding RNA molecule that regulates gene expression primarily through binding to the 3' untranslated regions (UTRs) of target messenger RNAs (mRNAs), leading to their degradation or translational repression. MIR21 is widely expressed in various tissues and is involved in the regulation of numerous cellular processes, including proliferation, apoptosis, differentiation, and migration. It functions as a post-transcriptional regulator of multiple genes, such as PTEN, PDCD4, and TPM1, which are implicated in cell cycle control and apoptosis. MIR21 is notably associated with modulating pathways related to cell survival and inflammation. | MIR21 has been studied as a biomarker in a range of clinical contexts, particularly in oncology. Elevated levels of MIR21 have been consistently observed in tissue and circulating samples from patients with various cancers, including breast, lung, colorectal, and pancreatic cancers. Its expression levels have been assessed for potential utility in cancer diagnosis, prognosis, and monitoring of disease progression or therapeutic response. Additionally, MIR21 has been investigated as a biomarker in non-malignant conditions, such as cardiovascular and inflammatory diseases, due to its involvement in relevant cellular pathways. |
| mucin 1, cell surface associated (MUC1) | Mucin 1 (MUC1) is a transmembrane glycoprotein expressed on the apical surface of most glandular epithelial cells. It plays a protective role by forming a physical barrier against pathogens and particulates, and it contributes to lubrication and hydration of mucosal surfaces. MUC1 is involved in cell signaling, modulation of immune responses, and maintenance of epithelial integrity. The extracellular domain of MUC1 is heavily glycosylated, which is important for its barrier and signaling functions. Alterations in glycosylation and expression patterns of MUC1 have been observed in various physiological and pathological conditions. | MUC1 is utilized as a biomarker primarily in oncology, particularly in the detection and monitoring of epithelial-derived cancers such as breast, ovarian, pancreatic, and lung cancers. Aberrant expression and glycosylation of MUC1 are associated with malignant transformation and tumor progression. Assays detecting MUC1 or its glycoforms (such as CA15-3 and CA27.29) are commonly used in clinical practice for monitoring disease status, evaluating treatment response, and detecting recurrence in certain cancer types. |
| 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 phosphatidylinositol 3-kinase (PI3K). PI3K is a lipid kinase that phosphorylates phosphatidylinositol-4,5-bisphosphate (PIP2) to generate phosphatidylinositol-3,4,5-trisphosphate (PIP3), a secondary messenger involved in intracellular signaling. Activation of PI3K leads to the recruitment and activation of downstream signaling proteins, including AKT, which regulate diverse cellular processes such as cell growth, proliferation, survival, metabolism, and motility. PIK3CA plays a central role in mediating signals from growth factor receptors and other cell surface receptors, contributing to the regulation of normal cellular physiology. | PIK3CA is frequently mutated in various human cancers, including breast, colorectal, endometrial, and other tumor types. The presence of specific PIK3CA mutations, particularly in exons 9 and 20, has been associated with oncogenic activation of the PI3K/AKT signaling pathway. Detection of PIK3CA mutations is used in oncology to characterize tumors at the molecular level. These mutations can inform prognosis and may be considered in the selection of targeted therapies, such as PI3K inhibitors, in certain clinical contexts. PIK3CA mutation status is also utilized in clinical trials to stratify patients or assess therapeutic response. |
| vascular endothelial growth factor A (VEGFA) | Vascular endothelial growth factor A (VEGFA) is a key signaling protein involved in the regulation of angiogenesis, the process by which new blood vessels form from pre-existing vasculature. VEGFA primarily acts by binding to specific tyrosine kinase receptors (mainly VEGFR-1 and VEGFR-2) on the surface of endothelial cells, stimulating their proliferation, migration, and survival. This protein plays an essential role in both physiological processes, such as embryonic development and wound healing, and in pathological conditions, including tumor growth and ocular neovascular disorders. VEGFA also increases vascular permeability and contributes to the remodeling of blood vessels. | VEGFA has been utilized as a biomarker in various clinical and research contexts. Elevated levels of VEGFA in blood, tissue, or other biological fluids have been associated with several diseases characterized by abnormal angiogenesis, including certain cancers, age-related macular degeneration, diabetic retinopathy, and rheumatoid arthritis. Measurement of VEGFA concentrations can provide information on disease presence, progression, or response to anti-angiogenic therapies. It is also used in clinical trials to monitor the pharmacodynamic effects of drugs targeting the VEGF pathway. |
Explore Research Opportunities with Alfa Cytology. Our biomarker research services provide a robust platform for exploratory studies in Esophageal Cancer, offering advanced analytical capabilities and comprehensive multi-omics profiling. Please note that all biomarkers discussed are research targets only; we do not claim any as validated or mandatory markers. Our work is focused exclusively on preclinical research stages, maintaining scientific objectivity throughout the discovery and development process.
We invite you to engage with Alfa Cytology for collaborative discussions on biomarker research in Esophageal Cancer. Let’s explore new scientific possibilities together, focusing on preclinical research and knowledge exchange in this rapidly evolving field.
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