Molecular diagnostics for oncology - Entrogen

Personalized therapies and monitoring of malignancies require accurate and reliable determination of genetic disorders of tumor cells. Wildtype or mutant, absence or detection of oncogenic fusion proteins may be crucial to find the appropriate therapy for the patient. Furthermore the knowledge of the genetic variation of malignant cells provide important information about progression and prognosis. 

Product overview

BREAST CANCER

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s AKT1 E17K Mutation Analysis Kit CE

E17K

50

AKTE17-RT50

EntroGen´s PIK3CA Mutation Detection Kit CE

E542K, E545K, E545Q, H1047R, H1047L

48

PI3K-RT48

EntroGen´s BRCA CompleteTM  for NGS CE

BRCA1, BRCA2

40

BRCA-NGS

COLORECTAL CANCER

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s KRAS Mutation Analysis Kit CE

Exons 2, 3, 4

50

KRAS-RT50

EntroGen´s KRAS/BRAF Mutation Analysis Kit CE

KRAS Exons 2, 3 und 4

BRAF V600E

50

KRBR-RT50

EntroGen´s RAS Mutation Analysis Kit CE

KRAS Codon 12, 13, 61, 59, 117, 146

NRAS Codon 12, 13, 61, 59, 117, 146

50

RAS-RT50

EntroGen´s NRAS Mutation Analysis Kit CE

Exon 2, 3, 4

50

NRAS-RT50

EntroGen´s AKT1 E17K Mutation Analysis Kit CE

E17K

50

AKTE17-RT50

EntroGen´s PIK3CA Mutation Detection Kit CE

E542K, E545K, E545Q, H1047R, H1047L

48

PI3K-RT48

EntroGen´s Colorectal Cancer Mutation Detection Panel CE

KRAS, NRAS, BRAF, PIK3CA, AKT1

48

CRC-RT48

GENOTYPING KIT

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s UGT1A1 Genotyping kit

UGT1A1 Polymorphism

50

EG-UG010-G50

GIST

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s GIST Mutation Screening Panel CE

KIT Exon 9, 11, 13, 17

PDGFRA Exon 18

44

GIST-RT44

LEUKEMIA

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s AML1-ETO One-Step Detection Kit CE

AML1-ETO: t(8;21)(q22;q22)

48

LEUK1-QRT24

EntroGen´s E2A-PBX1 One-Step Detection Kit CE

E2A-PBX1: t(1;19)(q23;p13)

48

LEUK2-QRT24

EntroGen´s MLL-AF4 One-Step Detection Kit CE

MLL-AF4: t(4;11)(q21;q23),

4 variants: e10-e4, e10-e5, e11-e4, e11-e5

48

LEUK3-QRT24

EnroGen´s PML-RARA bcr1,2,3 One -Step Detection Kit CE

PML-RARA bcr 1, 2, 3

48

LEUK4-QRT24

EntroGen´s TEL-AML1 One-Step Detection Kit CE

TEL-AML1: t(12;21)(p13;q22)

48

LEUK5-QRT24

EntroGen´s CBFB-MYH11 One-Step Detection Kit CE

CBFB-MYH11: Inv(16) (p13q22),

3 variants: type A, D, E

48

LEUK6-QRT24

EntroGen´s BCR-ABL P190 One-Step Detection Kit CE

e1a2

46

BCR(190)-QRT46

EntroGen´s BCR-ABL P210 One-Step Detection Kit CE

b2a2

b3a2

46

BCR(210)-QRT46

LUNG CANCER (NSCLC)

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s EGFR Mutation Detection Kit CE

Exon 18, 19, 20, 21

52

EGFR-RT52

EntroGen´s ctDNA EGFR Mutation Detection Kit CE

Exon 19, L858R, T790M

48

ctEGFR-48

EntroGen´s KRAS Mutation Analysis Kit CE

Exons 2, 3, 4

50

KRAS-RT50

EntroGen´s PIK3CA Mutation Detection Kit CE

E542K, E545K, E545Q, H1047R, H1047L

48

PI3K-RT48

EntroGen´s EML4 ALK Fusion Gene Detection Kit CE

E13;A20    

E20;A20    

E6;A20     

E6;insA20  

E14;(-49)A20             

(E2;A20)   

E2;(+117)A20            

E13;(+69)A20            

E14;(-13)A20

44

ALKFG-RT46

MELANOMA

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s BRAF Mutation Analysis Kit CE

V600E/K/D/R/M/G

64

BRAFX-RT64

EntroGen´s ctDNA BRAF Mutaion Detection Kit CE

V600E/E2, D, K

48

ctBRAF-48

EntroGen´s c-Kit Mutation Detection Kit CE

Exon 9, 11, 13, 17

44

CKIT-RT44

EntroGen´s NRAS Mutation Analysis Kit CE

Exon 2, 3, 4

50

NRAS-RT50

THYROID CANCER

Mutation / Translocation / Fusion Gene

Tests

Ordering number

EntroGen´s Thyroid Cancer Fusion Gene Detection Kit CE

inv(10)(q11q21)-translocation

inv(10)(q11q11)-translocation

t(2;3)(q13;p25)-translocation

32

THRNA-RT32

EntroGen´s Thyroid Cancer Mutation Detection Kit CE

BRAF, KRAS, NRAS, HRAS

64

THDNA-RT64

SAMPLE QUALITY PRODUCTS

     
EntroGen´s Internal Quality Control Assay CE Kit for assessing the quality of DNA specimen   IQCA-RT50
EntroGen´s DNA Fragmentation Assay CE Assay for assessment of DNA sample quality   FQA-RT40

EntroGen´s Library Quantification Kit for Illumina CE

Assay for assessment of library quality for Illumina sequencing

 

LIBQ-NGS

 Chronic myelogenous leukemia

Chronic myelogenous leukemia (CML) results from a neoplastic transformation of hematopoietic stem cells. The hallmark genetic abnormality of CML is a t(9;22)(q34;q11) translocation, which was first discovered as an abnormal, small chromosome, named the ‘Philadelphia chromosome’. This translocation generates the BCR - ABL fusion gene. The discovery that BCR-ABL is required for the pathogenesis of CML, and that the tyrosine-kinase activity of ABL is essential for BCR-ABL mediated transformation, made the ABL kinase an attractive target for therapeutic intervention. Imatinib mesylate (Glivec, previously known as STI571 and CGP 57148) — a potent inhibitor of the tyrosine kinases ABL, ARG, platelet derived growth factor receptor and KIT — has been shown to selectively induce apoptosis of BCR-ABL-positive cells, and is remarkably successful in treating patients with CML. In newly diagnosed patients with CML in chronic phase, imatinib induces complete cytogenetic response in more than 80% patients. Patients with more advanced phases of CML also respond to imatinib, but this occurs much less frequently and treatment is less durable. However, there are two major obstacles to imatinib-based therapies for patients with CML. One is the persistence of BCR-ABL -positive cells — this is known as ‘residual disease’, and is detected by a sensitive reverse-transcriptase PCR assay. Suppression of the disease therefore relies on continuous imatinib therapy. The other major problem is relapse of the disease due to the emergence of resistance to imatinib. Several mechanisms of resistance have been described, the most frequent of which are the appearance of point mutations in the BCR - ABL gene that impair the drug binding (comprehensively reviewed elsewhere). The fact that the resistance to imatinib is most commonly associated with point mutations in the kinase domain of BCR-ABL further demonstrates the importance of this activity in the pathogenesis of CML. On the other hand, the persistence of BCR-ABL-positive cells in patients on imatinib therapy indicates that inhibition of the ABL kinase activity alone might not be sufficient to eradicate the leukemia cells.

CML kits

EntroGen´s BCR190-QRT46

BCR-ABL P190 (mbcr)

One-Step Detection Kit

 R  CE

46

EntroGen´s BCR210-QRT46

BCR-ABL P210 (Mbcr)

One-Step Detection Kit

 R  CE

46

 

 

 

 

 

 

 

E542K, E545K, E545Q, H1047R, H1047L