EntroGen, Inc. products

EntroGen NGS Targeted Hotspot Panel is a comprehensive pan-cancer assay designed to detect clinically relevant hotspot mutations in solid tumors.  Utilizing a robust next-generation sequencing (NGS) platform, labs are able to simultaneously analyze several different tumor types by batching up to 12 samples on a single run*.  NGS Targeted Hotspot Panel (THSP) is compatible with fresh frozen, and formalin fixed paraffin embedded (FFPE) samples. This assay features high sensitivity and throughput detecting clinically relevant hotspot variants down to 5% with minimal DNA input.  With its comprehensive, streamlined workflow, THSP is designed to be seamlessly integrated into any lab.  Laboratories with specific challenges, such as low disease specific sample volumes, are able to batch various sample types together and accelerate tumor profiling.

EntroGen RNA Fusion Gene Panel is a complete next generation sequencing (NGS) solution for detecting 307 clinically relevant fusions over 23 genes.

PIK3CA Mutations and CancerThe PIK3CA gene encodes the p110a subunit of phosphatidyl 3-kinase, a lipid kinase involved in cell growth, proliferation, motility and survival. It has a central role in the PI3K-AKT-mTOR pathway. Somatic mutations in the PIK3CA gene have been implicated in the pathogenesis of several cancers, including colon cancer, gliomas, gastric cancer, breast cancer, endometrial cancer, and lung cancer. PIK3CA mutations commonly occur in exon 9, which encodes the helical domain and exon 20, which encodes the kinase domain.

BRCA Complete Expanded Panel is a complete next generation sequencing (NGS) solution for detecting clinically relevant BRCA1 and BRCA2 mutations along with extended coverage of CHEK2, PALB2, RAD51C and TP53.

The KRAS gene encodes a small GTPase that plays a key role in transducing signals from the epidermal growth factor receptor (EGFR) to downstream effectors. KRAS mutations have been commonly found in several types of human malignancies, such as metastatic colorectal cancer (mCRC), lung adenocarcinoma and thyroid cancer. The most common mutations are found in codons 12, 13 and 61. Several studies have demonstrated that tumors carrying any of these mutant forms of the KRAS gene are less likely to respond to anti-EGFR antibody therapy.

The KRAS gene encodes a small GTPase that plays a key role in transducing signals from the epidermal growth factor receptor (EGFR) to downstream effectors. KRAS mutations have been commonly found in several types of human malignancies, such as metastatic colorectal cancer (mCRC), lung adenocarcinoma and thyroid cancer. The most common mutations are found in codons 12, 13 and 61. Several studies have demonstrated that tumors carrying any of these mutant forms of the KRAS gene are less likely to respond to anti-EGFR antibody therapy. The American Society of Clinical Oncology (ASCO) recently released its first Provisional Clinical Opinion (PCO) suggesting that all patients to be administered anti-EGFR monoclonal antibody therapy (e.g. cetuximab, panitumumab and erlotnib) should be screened for KRAS mutations. Recent studies have also shown that not all mCRC patients with wild-type KRAS tumors respond to anti-EGFR therapy. 

Isocitrate dehydrogenase 1 and 2 (IDH1/2) are key enzymes in cellular metabolism, epigenetic regulation, redox states, and DNA repair. Mutations in IDH1/2 can lead to the development and/or progression of various types of cancer including secondary glioblastomas and acute myeloid leukemias (AML).  IDH1/2 mutations are linked to abnormal histone and DNA methylation which may cause altered stem cell differentiation and eventual tumorigenesis. The unique features of IDH1/2 mutations make them good biomarkers and promising drug targets.

Many hematologic malignancies carry characteristic chromosomal translocations believed to play an important role in the pathogenesis of these tumors. Chromosomal translocations found in leukemias and lymphomas either fuse enhancer/promoter regions of one gene to another, causing aberrant expression, or by fusing a part of one gene to that of another, resulting in disruption of the normal function of the native genes involved in the translocation, or by gaining new oncogenic functions that promote proliferation and tumorigenesis.Detection of fusion gene transcript expression to assess minimal residual disease (MRD) has been established as an independent prognostic indicator for treatment stratification and patient outcome in many leukemias. Molecular monitoring of patients enables clinicians to initiate therapy at the point of molecular relapse, which has been demonstrated to be beneficial in comparison to therapy adjustments at clinical relapse.