Biomarker Analysis Services for Melanoma
Drug R&D Solutions

Biomarker Analysis Services for Melanoma

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Alfa Cytology offers specialized biomarker analysis services dedicated to advancing Melanoma therapeutic research and drug discovery. Our comprehensive biomarker panel is designed to unravel the molecular and cellular mechanisms underlying Melanoma, providing deep insights into disease pathophysiology. Please note that all Alfa Cytology services are exclusively focused on supporting drug discovery through preclinical development stages and do not include clinical diagnostic services.

Biomarker Discovery and Identification

Effective therapeutic intervention in Melanoma begins with the discovery and identification of robust biomarkers. At Alfa Cytology, our biomarker discovery services are integral to drug development, enabling the early detection of molecular targets and pathways associated with disease progression. Our approach involves systematic screening of candidate biomarkers using advanced analytical platforms, followed by rigorous validation in preclinical models. This process ensures that only the most promising candidates are advanced for further study, supporting rational drug design and mechanism-of-action elucidation.

Multi Omics: Our multi-omics approach leverages state-of-the-art technologies, including genomics, transcriptomics, and proteomics, to provide a holistic view of biological systems relevant to Melanoma. By integrating high-throughput sequencing, gene expression profiling, and protein quantification, we identify and characterize DNA, RNA, protein, and metabolite biomarkers. This comprehensive strategy enables the mapping of key disease pathways such as the MAPK/ERK, PI3K/AKT, and immune checkpoint signaling cascades, which are central to Melanoma pathogenesis and therapeutic response.

Candidate Validation: Alfa Cytology applies robust validation strategies to confirm the relevance of candidate biomarkers to Melanoma pathophysiology. Our preliminary screening processes include quantitative and qualitative analyses of biomarker expression, mutation status, and functional activity in preclinical models. Candidates are prioritized based on criteria such as specificity for Melanoma, association with disease progression or therapeutic response, and feasibility for assay development. This ensures a focused pipeline of biomarkers for further exploration in drug discovery.

Biomarker Assay Development and Validation

Diverse Technological Platforms: We offer custom biomarker assay development tailored to the unique requirements of Melanoma research. Our technological platforms are adaptable, supporting a range of analytical needs from single-analyte detection to high-throughput multiplexed analysis. Platforms include ELISA, chemiluminescent and multiplex immunoassays, LC-MS/MS, flow cytometry, molecular diagnostic systems, and advanced histopathology imaging solutions.

Immunoassays: We utilize ELISA, chemiluminescent, and multiplex immunoassays for sensitive and specific detection of protein biomarkers relevant to Melanoma.

Mass Spectrometry: Our LC-MS/MS platforms enable precise quantification and characterization of proteins and metabolites, supporting discovery and validation of novel Melanoma biomarkers.

Flow Cytometry: Multiparametric flow cytometry is employed for cellular phenotyping, immune profiling, and detection of cell surface or intracellular biomarkers.

Molecular Diagnostics: We offer nucleic acid-based assays for mutation analysis and gene expression profiling, including qPCR and next-generation sequencing for Melanoma-associated targets.

Histopathology And Imaging: Advanced imaging and immunohistochemistry techniques are used for spatial localization and quantification of biomarker expression in tissue samples.

Rigorous Method Validation: Our method validation process adheres to industry and regulatory guidelines, encompassing assessment of accuracy, precision, sensitivity, specificity, linearity, and reproducibility. Rigorous quality control measures are implemented at every stage, including the use of reference standards, controls, and inter-assay comparisons to ensure reliable and reproducible results.

Biomarker Quantitative and Qualitative Analysis

Alfa Cytology provides quantitative analysis capabilities leveraging validated assays and high-sensitivity platforms. Our services include absolute and relative quantification of biomarker levels, enabling robust comparison across preclinical models and experimental conditions.

Sample Analysis: We handle a wide range of preclinical sample types, including cell lines, xenograft tissues, blood, and other biofluids. Standardized protocols ensure optimal sample processing, storage, and analysis. Stringent quality assurance procedures are in place to maintain sample integrity and data reliability throughout the analytical workflow.

High Throughput Capabilities: Our high-throughput analytical platforms support multiplexed biomarker analysis, allowing simultaneous measurement of multiple targets from minimal sample volumes. This increases efficiency, conserves valuable samples, and accelerates data generation to support rapid decision-making in Melanoma research.

Key Biomarkers for Melanoma Drug Development

Gene Target Biological Function Application as a Biomarker
AKT serine/threonine kinase 2 (AKT2) AKT serine/threonine kinase 2 (AKT2) is a member of the AKT family of serine/threonine kinases, which are key regulators of multiple cellular processes. AKT2 is primarily involved in the regulation of glucose metabolism, cell survival, growth, and proliferation. It is activated downstream of phosphoinositide 3-kinase (PI3K) signaling pathways, particularly in response to insulin and other growth factors. AKT2 plays a critical role in mediating insulin signaling by promoting glucose uptake in insulin-responsive tissues such as muscle and adipose tissue. Mutations or dysregulation of AKT2 have been associated with metabolic disorders, including insulin resistance and diabetes, as well as with the development and progression of certain cancers. AKT2 has been investigated as a biomarker in several contexts. In oncology, overexpression or activating mutations of AKT2 have been observed in various tumor types, including ovarian, pancreatic, and breast cancers, and have been associated with tumor progression and poor prognosis. AKT2 expression levels and activation status are used in research settings to assess PI3K/AKT pathway activity in tumor samples. Additionally, mutations in AKT2 have been identified in rare cases of familial severe insulin resistance and diabetes, making it a potential marker for certain metabolic syndromes. Its application as a biomarker is generally focused on disease characterization, prognosis, and potentially guiding targeted therapeutic strategies.
AKT serine/threonine kinase 3 (AKT3) AKT serine/threonine kinase 3 (AKT3) is a member of the AKT family of serine/threonine protein kinases, which play critical roles in regulating a variety of cellular processes. AKT3 is involved in the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway, which influences cell survival, proliferation, metabolism, and growth. AKT3 is expressed in multiple tissues, with particularly high expression in the brain. It contributes to neuronal development and brain size regulation, and is implicated in processes such as glucose metabolism and cell cycle progression. AKT3 functions by phosphorylating a range of downstream substrates involved in apoptosis inhibition, protein synthesis, and cell growth. AKT3 expression and activity have been studied as potential biomarkers in several contexts. In oncology, altered AKT3 expression has been observed in certain cancers, including glioblastoma and melanoma, where it may be associated with tumor progression and resistance to therapy. In neurological research, AKT3 has been investigated in relation to neurodevelopmental disorders and brain tumor subtypes. Its expression levels and genetic alterations are used in research settings to characterize disease subtypes, assess prognosis, and explore therapeutic response.
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 central role in the RAS-RAF-MEK-ERK signaling pathway (also known as the MAPK/ERK pathway), which is involved in the regulation of cell division, differentiation, and survival. Upon activation by RAS, BRAF phosphorylates and activates MEK1 and MEK2, which in turn activate ERK1 and ERK2, leading to the modulation of gene expression and cellular responses. Mutations in BRAF, most notably the V600E substitution, can lead to constitutive activation of the MAPK pathway, promoting uncontrolled cell proliferation and survival. BRAF is applied as a biomarker in oncology, particularly for the detection of specific mutations such as BRAF V600E. The presence of BRAF mutations is used in the diagnosis, prognosis, and therapeutic stratification of several cancers, including melanoma, colorectal cancer, thyroid carcinoma, and non-small cell lung cancer. Identification of BRAF mutations can inform the selection of targeted therapies, such as BRAF inhibitors, and can also provide information regarding disease progression and potential resistance mechanisms.
CD274 molecule (CD274) CD274 molecule, also known as programmed death-ligand 1 (PD-L1), is a transmembrane protein that plays a critical role in the regulation of immune responses. It is expressed on various cell types, including antigen-presenting cells, epithelial cells, and tumor cells. CD274 binds to its receptor, programmed death-1 (PD-1), which is found on activated T cells and other immune cells. This interaction inhibits T cell activation and proliferation, leading to reduced immune responses. The CD274/PD-1 pathway is a key mechanism by which peripheral tolerance is maintained and autoimmunity is prevented. In the context of cancer, tumor cells may upregulate CD274 expression to evade immune surveillance by suppressing anti-tumor T cell activity. CD274 expression is utilized as a biomarker in several clinical and research settings, particularly in oncology. Its expression levels on tumor cells or within the tumor microenvironment are commonly assessed to inform therapeutic decisions regarding immune checkpoint inhibitors targeting the PD-1/PD-L1 pathway. Immunohistochemical detection of CD274 is used to stratify patients for therapies such as anti-PD-1 or anti-PD-L1 monoclonal antibodies. Additionally, CD274 is studied as a prognostic and predictive biomarker in various malignancies, including non-small cell lung cancer, melanoma, and urothelial carcinoma.
KIT proto-oncogene, receptor tyrosine kinase (KIT) The KIT proto-oncogene, receptor tyrosine kinase (KIT), encodes a transmembrane receptor that belongs to the type III receptor tyrosine kinase family. KIT is activated by binding to its ligand, stem cell factor (SCF), triggering receptor dimerization and autophosphorylation. This activation initiates multiple intracellular signaling cascades, including the PI3K/AKT, RAS/RAF/MEK/ERK, and JAK/STAT pathways. KIT signaling plays a critical role in the regulation of cell proliferation, survival, differentiation, and migration in various cell types such as hematopoietic stem cells, melanocytes, germ cells, and interstitial cells of Cajal. KIT is used as a biomarker in several clinical and research contexts. Immunohistochemical detection of KIT protein expression is commonly employed in the diagnosis of gastrointestinal stromal tumors (GIST), where KIT positivity helps distinguish GIST from other mesenchymal tumors. Additionally, activating mutations in the KIT gene are frequently identified in GIST and certain other malignancies, and mutation analysis can inform prognosis and guide targeted therapy decisions, particularly the use of tyrosine kinase inhibitors. KIT expression and mutation status are also assessed in some cases of mast cell disease, melanoma, and acute myeloid leukemia.
NRAS proto-oncogene, GTPase (NRAS) NRAS (neuroblastoma RAS viral oncogene homolog) is a member of the RAS family of small GTPases, which function as molecular switches in intracellular signaling pathways. NRAS cycles between an active GTP-bound state and an inactive GDP-bound state, regulating cell proliferation, differentiation, and survival. Upon activation by upstream signals such as growth factors, NRAS transduces signals through pathways including the MAPK/ERK and PI3K/AKT cascades. Mutations in NRAS can result in constitutive activation, leading to uncontrolled cell growth and oncogenesis. NRAS is used as a molecular biomarker in oncology, particularly for the identification of activating mutations in various cancers, including melanoma, acute myeloid leukemia, and colorectal cancer. Detection of NRAS mutations can inform prognosis and assist in therapeutic decision-making, such as the selection or exclusion of targeted therapies. NRAS mutation status is commonly assessed in clinical molecular diagnostics to guide patient management.
interferon gamma (IFNG) Interferon gamma (IFNG) is a cytokine primarily produced by activated T lymphocytes, particularly Th1 cells, and natural killer (NK) cells. It plays a critical role in innate and adaptive immunity by promoting the activation of macrophages, enhancing antigen presentation through upregulation of major histocompatibility complex (MHC) molecules, and modulating the differentiation and function of various immune cell subsets. IFNG is involved in the defense against intracellular pathogens, such as viruses and certain bacteria, and contributes to the regulation of immune responses, including the inhibition of viral replication and the orchestration of inflammatory processes. IFNG is used as a biomarker to assess cellular immune responses, particularly in the context of infectious diseases and immune-mediated conditions. Its measurement is applied in assays such as interferon-gamma release assays (IGRAs) for the detection of latent or active Mycobacterium tuberculosis infection. Additionally, IFNG levels are monitored in research and clinical settings to evaluate immune activation, monitor response to immunotherapies, and investigate immune dysregulation in diseases such as autoimmune disorders and certain cancers.
mitogen-activated protein kinase 1 (MAPK1) Mitogen-activated protein kinase 1 (MAPK1), also known as ERK2, is a serine/threonine kinase that plays a central role in the MAPK/ERK signaling pathway. This pathway transduces extracellular signals into intracellular responses, regulating diverse cellular processes such as proliferation, differentiation, survival, and development. MAPK1 is activated via phosphorylation by upstream kinases (MEK1/2) in response to growth factors, cytokines, and other stimuli. Once activated, MAPK1 phosphorylates a variety of cytoplasmic and nuclear substrates, including transcription factors, thereby influencing gene expression and cellular fate decisions. MAPK1 expression and activation status (e.g., phosphorylation levels) have been investigated as biomarkers in several contexts, particularly in oncology. Altered MAPK1 activity has been associated with tumor progression, prognosis, and response to targeted therapies in cancers such as melanoma, colorectal cancer, and lung cancer. Measurement of MAPK1 and its phosphorylated form can provide information on pathway activation, which may aid in disease characterization and therapeutic monitoring.
tumor protein p53 (TP53) Tumor protein p53 (TP53) encodes a transcription factor that plays a central role in regulating the cell cycle, DNA repair, apoptosis, and senescence. Under conditions of cellular stress, such as DNA damage, TP53 is stabilized and activated, leading to transcription of genes involved in cell cycle arrest, DNA repair pathways, or initiation of programmed cell death. This function is critical for maintaining genomic stability and preventing the propagation of damaged DNA. TP53 is often referred to as the 'guardian of the genome' due to its role in preventing oncogenic transformation. TP53 is widely studied as a biomarker in oncology. Mutations in TP53 are among the most common genetic alterations observed in human cancers. The presence of TP53 mutations, as well as abnormal expression or accumulation of the p53 protein, has been associated with tumor development, progression, and response to therapy. Analysis of TP53 status is utilized in research and clinical settings for cancer diagnosis, prognosis, and in some cases, to help guide therapeutic decisions. Detection methods include immunohistochemistry for protein expression and molecular assays for genetic alterations.
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 inner surface of blood vessels. VEGFA binds to specific tyrosine kinase receptors (mainly VEGFR-1 and VEGFR-2) on endothelial cells, activating signaling pathways that promote new blood vessel formation and increase vascular permeability. VEGFA also plays roles in embryonic development, wound healing, and the response to hypoxia by enhancing blood supply to tissues. VEGFA is frequently measured as a biomarker in various clinical and research contexts. Its expression levels in blood or tissue samples are used to assess angiogenic activity, particularly in oncology, where elevated VEGFA is often associated with tumor growth and metastasis due to increased neovascularization. VEGFA is also monitored in ophthalmology, especially in conditions such as age-related macular degeneration and diabetic retinopathy, where pathological angiogenesis is a feature. Additionally, VEGFA levels have been investigated in cardiovascular diseases and inflammatory disorders as an indicator of vascular involvement.

Partner with Alfa Cytology to Advance Innovation

Explore Research Opportunities with Alfa Cytology. Our biomarker research services provide comprehensive analytical capabilities to support Melanoma drug discovery and preclinical development. We offer expertise in biomarker discovery, multi-omics integration, assay development, and quantitative analysis, all tailored to the exploratory and research-driven needs of our partners. Please note that all biomarkers discussed are research targets only and are not presented as validated or mandatory for any specific application. Our focus is strictly on preclinical research, and we maintain a commitment to scientific objectivity throughout our collaborations.

Connect with Alfa Cytology to discuss your Melanoma biomarker research needs. We welcome opportunities for scientific collaboration and knowledge exchange in the spirit of exploratory research. Our team is dedicated to supporting your preclinical studies with technical expertise and objective analysis.

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