nCounter® PanCancer
Immune Profiling Panel
Helping Your Research
Perform multiplex gene expression analysis in human or mouse with 770 genes from different immune cell types, common checkpoint inhibitors, CT antigens, and genes covering both the adaptive and innate immune response. The panel measures many features of the immune response to facilitate rapid development of clinical actionable gene expression profiles in the context of cancer immunotherapy.
- Comprehensive profiling of the immune response optimized for immuno-oncology research
- Identify tumor-infiltrating lymphocytes (TILs) for the tumor microenvironment
- Assess mechanistic pathway activity for single or combination studies
- Customizable with up to 55 additional user-defined genes with Panel Plus option
- Multi-analyte analysis with Vantage 3D™ Assays

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Product Information
360 Series Product Comparison
Fully-annotated gene lists in Excel format are available for each of the 360 Panels. The table below compares the biology coverage of the 360 Panels across the tumor, microenvironment, and the immune response to that of the PanCancer Panels Collection.
Publications
Combined MEK and JAK/STAT3 pathway inhibition effectively decreases SHH medulloblastoma tumor progression.
Medulloblastoma (MB) is the most common primary malignant pediatric brain cancer. We recently identified novel roles for the MEK/MAPK pathway in regulating human Sonic Hedgehog (SHH) MB tumorigenesis.
Immune suppression in the tumor-draining lymph node corresponds with distant disease recurrence in patients with melanoma.
Immune checkpoint blockade (ICB) using anti-PD-1/PD-L1 and anti-CTLA-4 antibodies significantly enhances survival in metastatic melanoma patients and has recently been shown to prolong relapse-free survival in stage III and high-risk stage II melanoma patients ( Eggermont et al. , 2018; Luke et al.
Multidimensional Immunophenotyping of Intraductal Papillary Mucinous Neoplasms Reveals Novel T Cell and Macrophage Signature.
Background: Intraductal papillary mucinous neoplasms (IPMN) are the only radiographically identifiable precursor to pancreatic adenocarcinoma, yet little is known about how these lesions progress to cancer. Inflammation has been associated with dysplastic progression; however, the cause and composition of this inflammation remains poorly characterized.
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