Solid Tumors
Solid tumors are remarkably diverse in their cellular origins and developmental stages. Comprehensive genomic profiling is needed for solid tumor specimens in order to capture their cellular and/or molecular heterogeneities.
Our pan-cancer gene panels for all solid tumors and cancer-type specific genetic tests can meet all your clinical needs for precision medicine.
PAN-CANCER GENE PANELS
GENESEEQPRIME™
A comprehensive genomic profiling panel across all solid tumors
GeneseeqPrime™ analyzes 437 cancer-related genes by next-generation sequencing. It reveals clinically actionable information for therapy selection by providing valuable insight into key oncogenic genes and drug resistance mechanisms.
WHO IS IT FOR
Patients with solid tumors seeking precision medicine
SAMPLE TYPES
Tumor tissue (FFPE block/slides, or frozen tissue)
Fine needle biopsy
Liquid biopsy (plasma and others)
All-in-one test for 437 cancer-related genes
Identifies numerous mutation types: single nucleotide variants (SNVs), insertions and deletions (indels), copy number variations (CNVs), gene fusions and large genomic rearrangements (LGR)
Assesses key biomarkers: tumor mutation burden (TMB), microsatellite instability (MSI), DNA mismatch repair (MMR) genes, homologous recombination repair (HRR) genes
GeneseeqPrime™ Report
Provides information for clinically actionable genomic alterations and their associated targeted therapy, both approved and in clinical trials
Evaluates TMB and MSI to better inform immunotherapy decisions
Predicts efficacy and toxicity of chemotherapy based on associated genetic biomarkers
Reveals potential resistance mechanism(s) to current therapies and options for alternative treatments
Assesses genetic predisposition to certain cancer types for early intervention
GeneseeqPrime™HRD
Comprehensively evaluates homologous recombination deficiency
GeneseeqPrime™HRD is a next-generation sequencing-based laboratory developed test that analyzes homologous recombination deficiency (HRD)-related genomic instabilities through a genome-wide analysis approach. It also detects genomic alterations in 437 cancer-relevant genes, including BRCA1/2 and other homologous recombination repair (HRR)-relevant genes.
WHO IS IT FOR
Patients with solid tumors seeking precision medicine, including PARP inhibitors selection, other targeted therapy options and immunotherapy
SAMPLE TYPES
Tumor tissue (FFPE block/slides, or frozen tissue)
All-in-one test
Genome-wide HRD score by assessing loss of heterozygosity (LOH), telomeric allelic imbalance (TAI), and large-scale station transitions (LST)
Genomic alterations in 437 cancer-relevant genes, including 25 HRR genes
Identifies numerous mutation types: single nucleotide variants (SNVs), insertions and deletions (indels), copy number variations (CNVs), gene fusions and large genomic rearrangements (LGR)
Assesses other key biomarkers: tumor mutation burden (TMB), microsatellite instability (MSI), DNA mismatch repair (MMR) genes, homologous recombination repair (HRR) genes
GeneseeqPrime™HRD Report
Evaluates HRD score and HRR-gene alterations to inform PARP inhibitors selection
Assesses TMB, MSI and dMMR with the option to add the PD-L1 immunohistochemistry (IHC) test to better inform immunotherapy decisions
Provides information for other clinically actionable genomic alterations and their associated targeted therapy, both approved and in clinical trials
Reveals potential resistance mechanism(s) to current therapies and options for alternative treatments
Assesses genetic predisposition to certain cancer types for early intervention
GeneseeqLite™
For all solid tumors
GeneseeqLite™ is a compact panel that targets major actionable solid tumor genes. It includes variants (POLE and POLD1) implicated in hereditary cancers, genetic alterations (ALK, ROS1, BRAF, c-MET, RET, NTRK, KRAS and HER2) seen in non-small cell lung cancer and genetic predispositions to reproductive cancers (BRCA1 /2). GeneseeqLite™, like its predecessors, GeneseeqPrime™ and GeneseeqPrime™HRD, detects DNA mismatch repair (MMR) and microsatellite instability (MSI) – hallmarks of cell’s inability to repair errors during DNA replication. Thus, relevant for determining prognosis for cancer treatments.
- Coverage of critical exons and fusion-related introns in 196 known actionable genes of solid tumors
- Detection of targetable gene alterations relates to targeted therapy, immunotherapy, PARP inhibitors for personalized treatment strategy
- Detection of alterations in EGFR, BRAF, ALK, RET, ROS1, KRAS, ERBB2, MET and NTRK to inform targeted therapy
- Detection of somatic and germline BRCA1/2 and homologous recombination pathway gene alterations to inform PARP inhibitor therapy
- Detection of POLD1/POLE gene, microsatellite sites, and DNA mismatch repair (MMR) genes including MLH1, MSH2, MSH6, PMS2 to comprehensively evaluate the microsatellite instability (MSI) status
- ctDNA-based liquid biopsy to monitor disease progression and predict the risk of postoperative/post-treatment tumor recurrence and metastases
- Timely assessment of drug resistance and associated mechanism(s) to guide targeted therapy
- Hereditary cancer risk assessment for early intervention
- Detection of single nucleotide variants (SNVs), small insertions and deletions (indels), gene fusion and copy number variations (CNVs)
- Helps to match patients to targeted therapy, immunotherapy, PARP inhibitor therapy and clinical trials
WHO IS IT FOR
Patients with solid tumors seeking precision medicine, including PARP inhibitors selection, other targeted therapy options and immunotherapy
SAMPLE TYPES
Tumor tissue (FFPE block/slides, or frozen tissue)
Fine needle biopsy
Liquid biopsy (plasma and others)
BRCASCAN™
A comprehensive genetic test for BRCA1/2 and other key HRR-related genes
BRCAscan™ analyzes 26 key genes in homologous recombination repair (HRR) pathways, including BRCA1/BRCA2, and ERBB2 to inform treatment decisions such as PARP inhibitors selection and assess genetic predisposition to breast, ovary, prostate and pancreatic cancers.
WHO IS IT FOR
- Individuals with a family history of BRCA1 or BRCA2 mutations
- Breast cancer patients with one or more of the following conditions:
- Early onset breast cancer diagnosed before age 45
- Family history of breast or/and ovarian cancer
- Triple negative breast cancer diagnosed at age 60 or younger
- Bilateral breast cancer diagnosed at age 50 or younger with two or more primary lesions
- HER2-negative metastatic breast cancer
- Male breast cancer patients
- Patients with advanced or recurrent ovarian cancer
- Patients with hereditary breast and ovarian cancer syndrome (HBOC)
- Patients with two or more types of cancer
- Patients with metastatic prostate cancer
- Patients with metastatic pancreatic cancer
SAMPLE TYPES
Tumor tissue (FFPE block/slides, or frozen tissue)
Fine needle biopsy
Liquid biopsy (plasma and others)
RADIOTRON™
Bringing precision medicineto radiotherapy
Radiotherapy is an important modality in treating cancer patients. Radiotron™ is a 486-gene panel for all solid tumors that is upgraded from GeneseeqPrime™ 437-gene panel. It has a total of 118 genes associated with radiosensitivity, radiotherapy tolerance and susceptibility to radiation-induced second cancer.
WHO IS IT FOR
Solid tumor patients seeking personalized drug and radiotherapy
SAMPLE TYPES
Tumor tissue (FFPE block/slides, or frozen tissue)
Fine needle biopsy
PANCARNA™
Targets 117 fusion genes in solid tumors
Fusion genes are a major driver of tumorigenesis and tumor progression. They have been continuously incorporated into international definitive guides. Fusion genes are also important in determining diagnosis and prognosis. In solid tumors, each tumor type has tumor-specific fusions as well as those that are common to several cancers.
Solid Tumor Fusion Genes
1. Gene fusion partners have widely distributed breakpoints and non-fixed hotspots
- Conventional IHC, FISH can’t distinguish between gene fusion partners
- Fusion breakpoints are widely distributed and may exist in intron regions, DNA-level detection does not provide comprehensive coverage
2. DNA testing alone may lead to missed detections
- Due to panel coverage constraints, 4-14% NSCLC patients that are negative for driver genes miss out on treatment opportunities
3. Fusion gene breakpoints detected at the DNA level cannot be used to infer functionally meaningful mRNA fusion patterns
- A considerable proportion of “gene-intergenic region” fusions detected by DNA level sequencing do not produce functional fusion transcripts at the RNA level, suggesting that some fusion genes detected by DNA cannot be used as therapeutic targets
4. Conventional RNA-Seq struggles to discern transcriptional signatures of tumor tissues on small scales
- RNA-Seq lacks sufficient sensitivity and resolution, and therefore requires higher sample quality and insufficiently detects low-abundance fusions
Pancarna™ uses targeted RNA sequencing technology to comprehensively detect gene fusions in solid tumors, with increased sensitivity and dynamic range compared to whole transcriptome RNAseq.
WHO IS IT FOR
- Patients with solid tumors who need to maximize their opportunity for targeted therapy (accompanying GeneseeqPrime™ testing)
- Patients with solid tumors whose DNA results are ‘pan-negative’ or possess non-classical fusions and require further fusion testing
- Patients with solid tumors that are difficult to diagnose using conventional methods and require further additional classification
SAMPLE TYPES
Tumor tissue (FFPE block/slides, or frozen tissue)
CANCER-TYPE SPECIFIC GENE PANELS
LET’S ACCELERATE PRECISION CANCER CARE, TOGETHER.
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