nCounter®
PanCancer Progression Panel
Helping Your Research
Cancer progression involves multiple processes and mechanisms that are highly interconnected. The nCounter PanCancer Progression Panel lets you perform multiplex gene expression analysis with 770 genes from each step in the cancer progression process including: angiogenesis, extracellular matrix remodeling (ECM), epithelial-to-mesenchymal transition (EMT) and metastasis.
- Comprehensive gene expression analysis of cancer progression
- Quantify gene expression of metastatic growth and suppressor genes
- Rapidly and easily screen samples for biomarker discovery or drug mechanism of action to support your research
- Customizable with up to 55 additional user-defined genes with Panel Plus option
Inspired by systems biology approaches to cancer research, NanoString’s 360 Series Panel Collection gives you a 360° view of gene expression by combining carefully-curated content involved in the biology of the tumor, microenvironment, and the immune response into a single holistic assay. Each panel contains the 18-gene Tumor Inflammation Signature (TIS) that measures a peripherally-suppressed, adaptive immune response and has been shown to correlate with response to checkpoint inhibitors.
360 Series Panel Collection
Gene Coverage
Processes, features and key genes included in the panel:
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PRIMARY TUMOR
↓ O2, ↑ Glycolysis -
DISTANT TUMOR
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Extracellular Matrix Remodeling
The extracellular matrix (ECM) is an assembly of proteins and sugars that surrounds cells in solid tissues, primarily providing mechanical structure to cells. The ECM must be remodeled in order to accommodate tumor growth. Tumor cells rely on the MMP and LOX gene families to change the surrounding EMC environment. Several of these remodeling genes have further roles in progression, acting as transcription factors in metastatic growth.
Genes: LOXs MMPs TIMPs ITGAs ITGBs COLs SERPINs -
Epithelial-to-Mesenchymal Transition
The epithelial-mesenchymal transition (EMT) is a process that cancer cells undergo which promotes metastatic progression. Epithelial cells are defined by their ability to laterally tether to each other in sheets using intercellular junctions, where as mesenchymal cells are more elongated for motility and rely on focal adhesions for attachment. The epithelial-mesenchymal transition (EMT) is a dynamic spectrum between these two states that can be reversible depending on the surrounding processes
Genes: ZEBs SNAIs TWISTs PRRZ1 SMADs BMI1 ESR1 GSC MITF SIP1 -
Metastasis
Metastasis is a collection of cellular processes commencing when a cell migrates from the primary tumor to successful development of a distant tumor. While all of the general processes that are not included in the major three themes have been grouped in to the term ‘metastasis’. This term includes general cell growth signaling pathways, hypoxia response, and metabolic changes. Additionally, there are a set of metastasis suppressor genes that each potential new tumor site must avoid.
Genes: HIF1A BRMS1 TXNIP MED23 DLC1 CDH1 GSN KISS1 KDM1A NME1 MTOR -
Angiogenesis
Angiogenesis is the biological process of generating new blood vessels from pre-existing vasculature. In the disease state, angiogenesis is induced quite early in cancer development, a process often referred to as turning on an “angiogenic switch.” Angiogenesis is of particular interest in cancer progression considering that distant tumors cannot grow more that 2-3 cubic mm without vasculature.
Genes: VEGFs FGFs FGFRs PDGFs ANG ANGPTs EGF HGF
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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
Tumoral and stromal hMENA isoforms impact tertiary lymphoid structure localization in lung cancer and predict immune checkpoint blockade response in patients with cancer
BACKGROUND: Tertiary Lymphoid Structures (TLS) correlate with positive outcomes in patients with NSCLC and the efficacy of immune checkpoint blockade (ICB) in cancer. The actin regulatory protein hMENA undergoes tissue-specific splicing, producing the epithelial hMENA(11a) linked to favorable prognosis in early NSCLC, and the mesenchymal hMENADeltav6 found in invasive cancer cells and pro-tumoral cancer-associated fibroblasts (CAFs).
HER2 heterogeneity and treatment response-associated profiles in HER2-positive breast cancer in the NCT02326974 clinical trial
BACKGROUND: HER2-targeting therapies have great efficacy in HER2-positive breast cancer, but resistance in part due to HER2 heterogeneity (HET) is a significant clinical challenge. We previously described that in a phase II neoadjuvant trastuzumab emtansine (T-DM1) and pertuzumab (T-DM1+P) clinical trial in early-stage HER2-positive breast cancer, none of the patients with HER2-HET tumors had pathologic complete response (pCR).
Clinically relevant molecular hallmarks of PFA ependymomas display intratumoral heterogeneity and correlate with tumor morphology
Posterior fossa type A (PF-EPN-A, PFA) ependymoma are aggressive tumors that mainly affect children and have a poor prognosis. Histopathology shows significant intratumoral heterogeneity, ranging from loose tissue to often sharply demarcated, extremely cell-dense tumor areas.
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