Biomarker Analysis Services for Neuroendocrine Cancer
Alfa Cytology offers specialized biomarker analysis services dedicated to advancing Neuroendocrine Cancer research and therapeutic development. Our comprehensive biomarker panel is designed to elucidate the complex pathophysiology of neuroendocrine tumors, supporting drug discovery from target identification through preclinical development stages. Please note that all services are strictly limited to preclinical research and drug discovery; we do not provide clinical diagnostic services.
Effective therapeutic intervention in Neuroendocrine Cancer begins with robust biomarker discovery and identification. At Alfa Cytology, our biomarker discovery services are tailored to accelerate drug development by uncovering novel molecular targets and pathways relevant to neuroendocrine tumor biology. Our screening process integrates high-throughput omics data mining, literature curation, and bioinformatics analyses to identify potential biomarkers. Rigorous validation steps, including orthogonal testing and cross-platform verification, ensure that selected candidates are reproducible and relevant for further preclinical investigation.
Multi Omics: We utilize a cutting-edge multi-omics approach, leveraging genomics, transcriptomics, proteomics, and metabolomics platforms to provide a comprehensive analysis of biological systems implicated in Neuroendocrine Cancer. Through next-generation sequencing, RNA profiling, quantitative proteomics (including mass spectrometry), and targeted metabolite analysis, we identify and characterize DNA, RNA, protein, and metabolite biomarkers. These strategies enable the elucidation of disease pathways such as hormone secretion regulation, cell proliferation, and neuroendocrine signaling, providing a holistic understanding of tumor heterogeneity and molecular drivers.
Candidate Validation: Our candidate validation and prioritization strategies employ a combination of in vitro and in silico analyses to confirm biomarker association with Neuroendocrine Cancer pathophysiology. Preliminary screening includes expression profiling across tumor and normal tissues, pathway enrichment analysis, and correlation with disease-relevant phenotypes. Promising candidates are prioritized based on criteria such as specificity, functional relevance, and detectability in accessible sample types, ensuring the translational potential of selected biomarkers for preclinical drug development.
Diverse Technological Platforms: Alfa Cytology excels in custom assay development, adapting technological platforms to meet the unique requirements of Neuroendocrine Cancer biomarker research. Our capabilities span immunoassay design, mass spectrometry method development, flow cytometry panel optimization, molecular diagnostic assay creation, and advanced histopathological imaging. These platforms are tailored for sensitivity, specificity, and scalability, supporting a wide range of research needs.
Immunoassays: We offer a suite of immunoassays including ELISA, chemiluminescent assays, and multiplex bead-based platforms for quantitative and qualitative detection of protein biomarkers.
Mass Spectrometry: Our LC-MS/MS services enable highly sensitive and specific quantification of proteins, peptides, and metabolites implicated in neuroendocrine tumor biology.
Flow Cytometry: Multiparametric flow cytometry is employed for cell surface and intracellular biomarker analysis, supporting phenotypic characterization of tumor and immune cell populations.
Molecular Diagnostics: We develop and utilize PCR-based, qPCR, and digital PCR assays for detection of gene expression, mutations, and copy number variations in biomarker genes.
Histopathology And Imaging: Our histopathology services include immunohistochemistry (IHC), immunofluorescence, and digital image analysis to localize and quantify biomarker expression in tissue specimens.
Rigorous Method Validation: All analytical methods undergo rigorous validation according to established research guidelines. Validation parameters include accuracy, precision, sensitivity, specificity, linearity, and reproducibility. Comprehensive quality control measures—such as the use of reference standards, calibration curves, and internal controls—ensure the reliability and robustness of our biomarker assays throughout preclinical studies.
Our quantitative analysis capabilities encompass absolute and relative quantification of biomarkers across diverse sample types. We employ standard curves, internal standards, and multiplexed detection to enable high-throughput, reproducible measurements crucial for comparative studies and pharmacodynamic assessments in Neuroendocrine Cancer research.
Sample Analysis: We handle a wide range of sample types, including cell lines, xenograft tissues, primary tumor samples, plasma, and serum. Our analysis protocols are optimized for each matrix, incorporating stringent sample preparation, preservation, and handling procedures. Quality measures include pre-analytical variable monitoring, sample tracking, and the use of controls to safeguard data integrity.
High Throughput Capabilities: Alfa Cytology offers high-throughput analytical platforms, such as multiplex immunoassays and automated sample processing, to enable rapid and efficient biomarker analysis. These approaches maximize efficiency, reduce sample volume requirements, and conserve valuable research specimens, supporting large-scale preclinical studies without compromising data quality.
| Gene Target | Biological Function | Application as a Biomarker |
|---|---|---|
| CD274 molecule (CD274) | The CD274 molecule, also known as programmed death-ligand 1 (PD-L1), is a transmembrane protein that plays a critical role in regulating immune responses. CD274 is expressed on various cell types, including antigen-presenting cells, some epithelial and endothelial cells, and a range of tumor cells. Its primary function is to bind to the programmed cell death protein 1 (PD-1) receptor on T cells, leading to the inhibition of T cell activation and proliferation. This interaction contributes to the maintenance of peripheral immune tolerance and the prevention of autoimmunity by downregulating immune responses. In the tumor microenvironment, upregulation of CD274 can facilitate immune evasion by inhibiting the anti-tumor activity of T cells. | CD274 (PD-L1) expression is widely used as a biomarker in oncology, particularly in the context of immunotherapy. Immunohistochemical assessment of CD274 expression on tumor cells and/or immune cells within the tumor microenvironment is used to help identify patients who may benefit from immune checkpoint inhibitor therapies targeting the PD-1/PD-L1 pathway. CD274 expression levels have been studied in various cancers, including non-small cell lung cancer, melanoma, and urothelial carcinoma, among others. Its expression is also investigated for potential associations with disease prognosis and therapeutic response. |
| MET proto-oncogene, receptor tyrosine kinase (MET) | The MET proto-oncogene encodes a receptor tyrosine kinase known as MET or hepatocyte growth factor receptor (HGFR). MET is primarily expressed on epithelial cells and is activated by its ligand, hepatocyte growth factor (HGF). Upon ligand binding, MET undergoes dimerization and autophosphorylation, triggering downstream signaling pathways such as the RAS-MAPK, PI3K-AKT, and STAT pathways. These signaling cascades regulate various cellular processes including proliferation, survival, motility, morphogenesis, and differentiation. MET signaling plays a critical role in embryonic development, tissue regeneration, and wound healing. Dysregulation of MET activity, through gene amplification, mutation, or overexpression, has been implicated in oncogenesis and tumor progression. | MET is utilized as a biomarker in oncology, particularly in the context of solid tumors such as non-small cell lung cancer (NSCLC), gastric cancer, and papillary renal cell carcinoma. Assessment of MET gene amplification, protein overexpression, or activating mutations can provide information relevant to tumor classification, prognosis, and potential therapeutic targeting. For example, detection of MET amplification or exon 14 skipping mutations may inform eligibility for MET-targeted therapies. Additionally, MET status is sometimes evaluated to predict resistance to certain treatments, such as EGFR inhibitors, in specific cancer types. |
| erb-b2 receptor tyrosine kinase 2 (ERBB2) | ERBB2, also known as HER2, encodes a transmembrane receptor tyrosine kinase that is a member of the epidermal growth factor receptor (EGFR) family. The protein does not have a known ligand but forms heterodimers with other EGFR family members, leading to the activation of intracellular signaling pathways such as MAPK and PI3K/AKT. These pathways regulate cell proliferation, differentiation, migration, and survival. ERBB2 plays a critical role in normal embryonic development, particularly in the nervous and cardiac systems, and is involved in the regulation of cell growth and differentiation in various tissues. | ERBB2 is used as a biomarker in oncology, most notably in breast cancer. Amplification or overexpression of ERBB2 is detected in a subset of breast cancers and is associated with specific clinicopathological features. Its status is assessed to inform prognosis and guide therapeutic decisions, including the use of targeted therapies such as monoclonal antibodies and tyrosine kinase inhibitors. ERBB2 testing is also performed in other tumor types, such as gastric and gastroesophageal junction cancers, to determine eligibility for targeted treatments. |
| kinase insert domain receptor (KDR) | Kinase insert domain receptor (KDR), also known as vascular endothelial growth factor receptor 2 (VEGFR-2), is a type III receptor tyrosine kinase predominantly expressed on endothelial cells. KDR serves as a principal receptor for vascular endothelial growth factor A (VEGF-A) and mediates the majority of VEGF-induced responses in endothelial cells. Upon ligand binding, KDR undergoes dimerization and autophosphorylation, triggering downstream signaling pathways such as the MAPK, PI3K/AKT, and PLCγ pathways. These cascades promote endothelial cell proliferation, migration, survival, and increased vascular permeability, collectively contributing to angiogenesis and vasculogenesis. KDR is essential for normal embryonic vascular development and plays a significant role in physiological and pathological neovascularization. | KDR expression and activation status have been utilized as biomarkers in several clinical and research contexts. In oncology, increased KDR expression in tumor vasculature has been associated with tumor angiogenesis and progression. Measurement of KDR levels in tumor tissue, circulating endothelial cells, or plasma has been explored as an indicator of angiogenic activity and as a potential tool for assessing response to anti-angiogenic therapies targeting the VEGF pathway. Additionally, KDR has been investigated as a prognostic and predictive marker in various malignancies, including colorectal, lung, and renal cancers, as well as in certain non-malignant conditions characterized by abnormal angiogenesis. |
| ret proto-oncogene (RET) | The RET proto-oncogene encodes a receptor tyrosine kinase that is integral to the development of neural crest-derived cell lineages. RET is activated by binding of glial cell line-derived neurotrophic factor (GDNF) family ligands in conjunction with GFRα co-receptors. Upon activation, RET initiates intracellular signaling cascades, including the RAS/MAPK, PI3K/AKT, and JAK/STAT pathways, which regulate processes such as cell proliferation, differentiation, migration, and survival. RET plays a critical role in embryonic development, especially in the formation of the enteric nervous system and the kidneys. | RET serves as a biomarker in oncology, particularly in the context of thyroid carcinomas and non-small cell lung cancer (NSCLC). Rearrangements, mutations, or fusions involving RET can be detected in medullary thyroid carcinoma (MTC), papillary thyroid carcinoma (PTC), and a subset of lung adenocarcinomas. The identification of RET alterations is used to inform diagnosis, guide therapeutic decisions, and predict response to targeted kinase inhibitor therapies. Molecular testing for RET gene status is utilized in clinical settings for tumor characterization and selection of patients for RET-targeted treatments. |
| somatostatin receptor 1 (SSTR1) | Somatostatin receptor 1 (SSTR1) is a member of the G protein-coupled receptor (GPCR) family that binds somatostatin, a peptide hormone involved in the inhibition of endocrine and exocrine secretions. Upon ligand binding, SSTR1 mediates the inhibitory effects of somatostatin by reducing intracellular cyclic AMP (cAMP) levels and modulating calcium and potassium channel activity. This leads to decreased hormone secretion, cell proliferation, and neurotransmission. SSTR1 is expressed in various tissues, including the brain, gastrointestinal tract, and pancreas, and participates in the regulation of physiological processes such as neurotransmission, cell growth, and hormone release. | SSTR1 expression has been investigated in various tumor types, including neuroendocrine tumors, pituitary adenomas, and certain cancers of the gastrointestinal tract. The presence or relative abundance of SSTR1 in tumor tissue can be assessed by immunohistochemistry or molecular techniques, and may provide information relevant to tumor characterization and potential responsiveness to somatostatin analog-based therapies. SSTR1, along with other somatostatin receptor subtypes, is also considered in the context of imaging modalities that utilize radiolabeled somatostatin analogs for tumor localization. |
| somatostatin receptor 2 (SSTR2) | Somatostatin receptor 2 (SSTR2) is a G protein-coupled receptor that binds to the peptide hormone somatostatin. Upon ligand binding, SSTR2 mediates the inhibitory effects of somatostatin on hormone secretion and cell proliferation by activating inhibitory G proteins (Gi/o), which in turn inhibit adenylyl cyclase activity and decrease intracellular cAMP levels. SSTR2 activation also modulates ion channel activity and downstream signaling pathways, leading to reduced secretion of hormones such as growth hormone, insulin, and glucagon. SSTR2 is expressed in various tissues, including the brain, gastrointestinal tract, and endocrine organs. | SSTR2 is utilized as a biomarker for the identification and characterization of neuroendocrine tumors (NETs), including gastroenteropancreatic NETs and pituitary adenomas. Its expression is assessed by immunohistochemistry or molecular imaging techniques, such as somatostatin receptor scintigraphy and positron emission tomography (PET) using radiolabeled somatostatin analogs. Detection of SSTR2 can assist in tumor localization, selection of patients for somatostatin analog therapy, and monitoring of disease progression or response to treatment. |
| somatostatin receptor 3 (SSTR3) | Somatostatin receptor 3 (SSTR3) is a member of the G protein-coupled receptor (GPCR) family that binds somatostatin, a peptide hormone involved in the inhibition of endocrine and exocrine secretions. SSTR3 is primarily coupled to the inhibition of adenylyl cyclase via Gi/o proteins, leading to decreased intracellular cyclic AMP (cAMP) levels. It is expressed in various tissues, including the brain, pituitary, and pancreas, and plays a role in regulating neurotransmission, hormone secretion, and cell proliferation. SSTR3 is also implicated in the modulation of synaptic plasticity and neuronal signaling, and has been localized to primary cilia in certain cell types, suggesting a role in ciliary signaling pathways. | SSTR3 expression has been investigated in the context of neuroendocrine tumors and certain brain tumors, where it may be used to characterize tumor subtypes or assess receptor status. Detection of SSTR3 can aid in understanding tumor biology and may inform the selection of patients for therapies targeting somatostatin receptors, such as somatostatin analogs or radiolabeled ligands. Immunohistochemical analysis of SSTR3 is used in research to evaluate its distribution in normal and neoplastic tissues. |
| somatostatin receptor 4 (SSTR4) | Somatostatin receptor 4 (SSTR4) is a member of the G protein-coupled receptor (GPCR) family that binds somatostatin, a peptide hormone involved in the regulation of endocrine and nervous system function. Upon ligand binding, SSTR4 mediates inhibitory effects on the secretion of various hormones and neurotransmitters by activating intracellular signaling pathways, primarily through inhibition of adenylyl cyclase and reduction of cyclic AMP levels. SSTR4 is expressed in multiple tissues, including the brain, gastrointestinal tract, and immune cells, and has been implicated in modulating neurotransmission, cell proliferation, and immune responses. | SSTR4 expression has been investigated as a potential biomarker in several contexts, including neuroendocrine tumors, certain cancers, and inflammatory conditions. Detection of SSTR4 by immunohistochemistry or molecular assays can assist in the characterization of tumor subtypes and may inform research on somatostatin analog-based diagnostic imaging or therapeutic strategies. Its expression profile can also contribute to studies exploring receptor distribution in normal and diseased tissues. |
| somatostatin receptor 5 (SSTR5) | Somatostatin receptor 5 (SSTR5) is a member of the G protein-coupled receptor (GPCR) family that binds somatostatin, a peptide hormone involved in the regulation of endocrine and nervous system function. Upon ligand binding, SSTR5 mediates inhibitory signaling pathways that suppress the secretion of several hormones, including growth hormone, insulin, and glucagon. This receptor is expressed in various tissues, such as the pituitary, pancreas, and gastrointestinal tract, where it modulates cellular proliferation, neurotransmission, and hormone release. SSTR5 activation typically leads to inhibition of adenylyl cyclase activity, reduction of cyclic AMP levels, and modulation of ion channel activity, contributing to its regulatory effects. | SSTR5 expression has been utilized as a biomarker in neuroendocrine tumors, including pituitary adenomas and gastroenteropancreatic neuroendocrine tumors. Its detection can aid in tumor characterization and may inform the selection of patients for somatostatin analog-based therapies, as these analogs preferentially bind to somatostatin receptors, including SSTR5. Additionally, SSTR5 status can be assessed through immunohistochemistry or molecular imaging techniques to support diagnostic and therapeutic decision-making in certain tumor types. |
Explore Research Opportunities with Alfa Cytology. Our biomarker research services for Neuroendocrine Cancer leverage advanced technologies and a comprehensive panel of research targets to support exploratory drug discovery and preclinical development. Please note that all biomarkers discussed are research targets only; we do not claim any as validated or mandatory for clinical or regulatory use. Our focus remains on early-stage, preclinical research, and we maintain scientific objectivity throughout all collaborative projects.
We invite you to connect with Alfa Cytology to discuss exploratory biomarker research in Neuroendocrine Cancer. Our team is dedicated to scientific collaboration and knowledge exchange, supporting innovative research without making claims regarding biomarker validation or necessity. Let’s advance neuroendocrine oncology together through objective, preclinical investigation.
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Neuroendocrine Cancer
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