Vantage 3D RNA Panels are a collection of focused gene expression panels addressing specific topics of interest in the field of cancer research. Vantage 3D RNA Panels are designed for use with Vantage 3D Protein and SNV assays and include 192 genes per panel with the ability to add an additional 24 custom targets.
This panel focuses on the acquired immune system cells that help to identify and develop memory to invading pathogens. The panel will aid in examining the process by which the adaptive immune response is initiated, including markers of T-cell and B-cell activation, subpopulations, and key signaling molecules. Some gene content also relates to antigen presentation and checkpoint genes.
The innate immune system includes cell types that mount the early response to invading pathogens and are required to create a robust adaptive immune response. This arm of the immune system involves natural killer cells, mast cells, eosinophils, basophils, macrophages, neutrophils, and dendritic cells. Innate immune genes involved in host response, bacterial sensing, inflammation, Toll-like receptor signaling, and related cytokines are included in this panel.
Altered tumor metabolism is widely recognized as the “Forgotten Hallmark” that allows for the tumor cell to thrive and proliferate. Cancer metabolism has many facets, from aerobic glycolysis and glucose uptake to energy consumption. This panel includes genes from these various areas.
The JAK/STAT pathway relays cellular cues into an intracellular transcription response. The pathway is crucial to immune response, as many of its receptors bind to cytokines. This panel includes cytokines, cytokine receptors, and key targets in the JAK/STAT signaling pathway, as well as related targets from the PI3K/AKT pathway and mTOR pathway
In addition to the 109 cell typing genes from the PanCancer Immune Profiling Panel, the cellular profiling panel includes an additional 40 genes to give a more in-depth view of immune cell populations. Also included are markers for cells that interact with the immune system including endothelial, smooth muscle, fibroblast, and stromal cells.
The Wnt signaling pathway regulates the developmental processes of cell fate and plays a role in tumorigenesis and progression. Wnt signaling comprises three pathways: the canonical pathway and two non-canonical pathways, planar cell polarity (PCP) and a calcium ion-dependent pathway. The canonical pathway is dependent on beta-catenin and regulates the cell cycle, cell growth, and proliferation. This panel includes the Wnt signaling ligands and receptors as well as other auxiliary signaling molecules for regulation, proteolysis, cell migration, cell cycle, adhesion, and EMT/metastasis.
Exposure to specific agents (such as reactive oxygen species, methylating agents, etc.) and even normal physiological processes all damage DNA. Cells must repair DNA damage to prevent mutations from propagating into cancer and accumulating. This panel includes the genes involved in major DNA damage repair pathways including base excision repair, nucleotide excision repair, mismatch repair, translesion synthesis, and other repair processes. Additional genes from apoptosis and cell cycle pathways are included.
The MAPK and PI3K pathways control key cellular processes in development, homeostasis, and disease. A variety of extracellular signals converge on these pathways, leading to the expression of genes controlling multiple cellular and tissue-level functions. Seminal publications focused on MAPK and PI3K research and signature development were collated and scored to develop a curated gene set measuring transcriptional activity of these key pathways. This panel represents the diverse set of biological functions that the MAPK and PI3K pathways modulate as crucial mediators of biological activity.
Despite diversity in cell of origin and other clinical features, hematologic malignancies share a core set of pathways and processes that drive tumorigenesis, such as MAPK, MYC signaling, NF-κB, PI3K-AKT, and B cell and T cell receptor signaling. Additionally, dysregulation of cytokines, apoptosis, the DNA damage response, and epigenetic factors are frequently observed. Seminal publications focused on hematologic oncology research and signature development were collated and scored to develop a curated gene set that measures these conserved and crucial pathways underlying hematologic malignancies.
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