Solid tumor panel

Genetic testing for solid tumors associated with somatic mutations

Genetic testing can give us the mutational profile of the solid tumor and this will in turn allow you to make better diagnostic decisions and define optimal therapeutic approaches.

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  1. Detecting Solid Tumor Mutations

Solid tumor panel – somatic mutation testing

Solid tumors are diseases characterized by the formation of an abnormal mass of tissue. They can be benign or malignant. Many solid tumors contain high numbers of somatic mutations, genetic changes that are not inherited but rather created within the tumor itself.

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Mapping the individual genetic landscape of solid tumors

Somatic mutations in many different genes have been found in breast cancer cells. Variants in BRCA1 and BRCA2 genes which are known to be responsible for the inherited breast and ovarian cancer syndrome are also found in sporadic cancer. As carriers for these variants profit from a targeted therapy somatic analysis of these genes is also recommended in cases where there is no family history for inherited breast cancer syndrome. Other genes found with sequence variations and evidence for an impact on prognosis or treatment are AKT1, PIK3CA, PTEN, CDK4, CDK6, CDK6, RB1 and TP53.

Colorectal cancer (CRC) is a heterogeneous disease that is common in both men and women. In addition to lifestyle and environmental risk factors, gene defects can contribute to an inherited predisposition to CRC. A comprehensive study that sequenced more than 13,000 genes in a series of CRCs found that tumors accumulate an average of approximately 90 mutant genes with two-thirds relevant to CRC. In addition, each tumor studied had a distinct mutational gene signature. Somatic mutations in the genes BRAF, NRAS, KRAS, AKT1, PTEN, PIK3CA and SMAD4 have been found with altered progression and prognosis.

Melanoma is considered to be one of the most aggressive and treatment-resistant of all human cancers. It starts in melanocytes, which are cells found in the outermost layer of skin. Melanocytes make a brown pigment called melanin. Melanin protects the deeper layers of skin (the dermis and subcutis layers) from the harmful effects of the sun. Melaomas are found with an increasing incidence. In addition to the inherited melanoma syndrome gene, mutations in BRAF, CTNNB1, GNA11, GNAQ, KIT, MEK1 (MAP2K1) and NRAS can be found in approximately 70% of all melanomas including sporadic cases. In addition, mutations have also been described in melanoma. Genes with somatic mutations that participate in melanoma pathology are most commonly BRCA2, CDKN2A, CDK4 and TP53.

The genetic basis for neuroblastoma is not yet well understood. As sequence variation, ALK mutations have been identified. ALK mutations have been detected in 6–9% of tumor samples (Chen et al. 2008; George et al. 2008; Janoueix-Lerosey et al. 2008). There has also been some work published on the roles of ATRX mutations (Cheung et al. 2012). ATRX mutations are associated with patient age: younger patients’ tumors are less likely to harbor ATRX mutations (Cheung et al. 2012). Development of targeted therapeutics has focused on ALK.

Environmental exposures, smoking and genetic susceptibility are contributing factors to the lung cancer risk. Adenocarcinomas in patients who have never smoked frequently contain mutations within the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene, and those patients often respond to tyrosine kinase inhibitor drugs such as gefitinib and erlotinib, but usually develop drug resistance. Conversely, KRAS mutations are more common in individuals with a history of cigarette use and are associated with resistance to EGFR-tyrosine-kinase inhibitors.

Gastric cancer is the fourth most common cancer worldwide and the second leading cause of global cancer deaths. The identification of germline E-cadherin (CDH1) mutations in families with hereditary diffuse gastric cancer provided an early insight into the initial changes that promote gastric tumorogenesis and established the CDH1 gene as a tumor suppressor. Frequently mutated genes in the gastric cancer also include TP53, PIK3CA and ARID1A. In addition, the prevalence genetic screening confirmed mutations in FAT4, a cadherin family gene, in 5% of gastric cancers and FAT4 genomic deletions in 4% of gastric tumors. Frequent mutations in chromatin remodeling genes (ARID1A, MLL3 and MLL) also occur in 47% of the gastric cancers.

Downloads for solid tumor panel

  • One pager - Colorectal cancer solid tumor panel

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  • One pager - Lung cancer solid tumor panel

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When to suggest the solid tumor panel

The solid tumor panel can be recommended for the following patients:

  • Individuals with solid tumors where a mutational profile from multiple genes will affect diagnosis disease stratification, prognosis or treatment options.

Scientific articles on somatic mutations

The goals of somatic testing of solid tumors are to identify:

  • The individual genetic landscape of the tumor by assessing multiple gene targets simultaneously
  • Actionable variants within the genes known to be associated with response or resistance to specific cancer therapies
  • Variants that may help to determine the prognosis for patients with solid tumors
  • So far unknown variants in well described tumor genes which might be used for targeted therapies
  • To finally establish a diagnosis that will reassure both patient and physician about the occurring health problem, in order to inform and to tailor the best therapeutic strategy for the patient

Benefits of solid tumorigenic testing:

  • Covers 63 of the most important genes and associated mutations with 96% coverage of the coding regions
  • Detects most actionable mutations with clear clinical relevance; EGFR/MAPK and PI3K pathways
  • Enables rapid eligibility identification and patient stratification for clinical trials
  • Allows longitudinal and serial molecular monitoring throughout the clinical trial process
  • Does not require special shipping or storage provisions
  • Employs expert analysis from a CLIA-certified lab

CENTOGENE´s solid tumor panel offers:

  • Solid tumor panel includes the following genes: ABL1, AKT1, ALK, APC, AR, ARID1A, ASXL1, ATM, AXL, BRAF, CDH1, CDK4, CDKN2A, CTNNB1, DDR2, EGFR, ERBB2, FGFR1, FGFR2, FGFR3, FGFR4, GNA11, GNAQ, GNAS, HRAS, IDH1, IDH2, JAK2, JAK3, KDM6A, KDR, KIT, KRAS, MAP2K1, MET, MLH1, MLL, MLL2, MLL3, MTOR, NF1, NOTCH1, NRAS, NTRK3, PDGFRA, PDGFRB, PIK3CA, PIK3R1, PTCH1, PTEN, PTPN11, RB1, RET, ROS1, SMAD4, SMARCA4, SMARCB1, SMO, STK11, TP53, TSHR, TSC1, VHL
  • The panel covers 96% of coding regions of all 63 tumor suppressor genes and oncogenes
  • Mean coverage depth of >1,000x
  • The turnaround time for the panel is ten working days

Sample requirements

  • Ten sections of 5–10µm thickness from the FFP tissue with areas of enriched tumor clearly marked accompanied with pathology report and oncology report in case of a relapse testing

or

  • 1 µg of DNA from tumor-enriched section

and

  • 1 ml of EDTA blood or 1 µg DNA from normal tissue (for example: buccal swab) as a recommended control

Sequencing platform

  • Solid tumor panel utilizes NGS sequencing on Ion Proton Platform

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