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海希试剂盒宣传册-英文版

Wuhan Healthy Biotechnology Co.,LTD

Brochures

Catalog

1. Company profile

2. Product introduction

3. NGS Service

4. Ordering information

Company profile

Wuhan Healthy Biotechnology Co., Ltd. was founded in 2018. Professor Shiang Huang and professional technical team, have accumulated more than fifteen years of medical special inspection technology and experience. Its purpose is to provide precise detection reagent for medical special inspection and provide perfect research reagents and services for biomedical researchers. Healthy biotechnology commany is committed to research and development, production, marketing and service of medical diagnostic and biomedical research reagent products. At present, a series of products have been completed on the platform of PCR, Q-PCR, sanger sequencing and NGS technology, including MPN diagnosis, CML curative effect and MRD monitoring, AML diagnosis and prognosis stratification, ALL diagnosis and prognosis stratification, covering the whole stage from leukemia differential diagnosis, genotyping, prognosis stratification, targeted therapy to therapeutic effect monitoring, providing one-stop service for leukemia patients. In the future, we will provide special reagents in other areas, such as infection, heredity, cardiovascular and cerebrovascular, drug metabolism, etc. We hope to help the accurate diagnosis, efficacy tracking and monitoring of diseases in these areas. In addition, while meeting the needs of special testing reagents, Healthy biotechnology will also pay attention to the research and development, production of scientific research reagents in the field of biomedicine, research technology introduction and service.

Product introduction

1. Product Advantage

2. Detection process

3. Area of Application

It is suitable for users such ashospital laboratory and third-party laboratory.

NGS services

1. AML 15 targeted NGS gene panel

Gene

Regions

Clinical significance

FLT3

FLT3-ITD

The FLT3 gene encodes III type receptor tyrosine kinase. FLT3-ITD mutations occur in 20-40% of AML patients, most commonly in patients with t (6; 9) (p23; q34) abnormalities, APL and normal chromosomes. Flt3-ITD mutation in AML patients suggests poor prognosis.

dupMLL

MLL-partial tandem duplicaiton were found in about 10% of normal karyotype AML and 90% of AML patients with 11q23 abnormalities. FLT3-ITD mutation was found in 30-40% of MLL-PTD patients. MLL-PTD may indicate poor prognosis in AML patients with normal karyotype.

IDH1

Exon4

IDH1 mutation exists in 6-9% of AML patients, and the mutation frequency is higher in NK-AML patients (8-16%). In NK-AML patients, IDH1 mutation often occurs simultaneously with NPM1 mutation. In NK-AML patients, IDH1 mutations suggest poor EFS and OS.

IDH2

Exon4

IDH2 mutation exists in 8-12% of AML patients, and the mutation frequency is higher in NK-AML patients, about 19%. The common mutations of IDH2 gene are R172 and R140, and the mutation frequency of R140 is higher. In NK-AML patients, IDH2-R140Q mutation indicates good prognosis, and IDH2-R172 indicates poor prognosis.

NPM1

Exon11

NPM1 is the most common mutation gene in AML. In adult AML with normal karyotype, NPM1 gene mutation was found in 45-64%. Forty different mutations of NPM1 have been reported. About 40% of NPM 1 mutations were accompanied by FLT3-ITD mutations. 5-15% of NPM1 mutation patients were accompanied by other chromosomal abnormalities, such as + 8, del (9q), and NPM1 patients were accompanied by abnormal proliferation of trilineage hematopoietic cells. Its clinical significance is not yet clear. NPM1 mutation without FLT3-ITD mutation suggests a good prognosis in AML patients with normal karyotype.

c-KIT

Exon8 and17

C-KIT mutations are common in t (8:21) and inv (16) AML patients, and the frequency of c-KIT mutations in inv (16) AML patients is higher, accounting for about 20%. The prognosis of AML patients with t (8; 21) (q22; q22) is worse with c-KIT gene mutation, suggesting a high risk of recurrence. The prognosis of AML patients with Inv (16) (p13.1q22) or t (16; 16) (p13.1; q22) remains controversial. However, tyrosine kinase inhibitors (TKI) are effective in the treatment of patients with c-KIT mutation.

NRAS

Exon2 and 3

NRAS mutations occur in 11-30% of AML patients, and hotspot mutations occur in codons 12, 13 and 61. NRAS mutation has no definite prognostic significance for OS, EFS and DFS in AML patients. In patients with AML with normal karyotype, both NPM1 and NRAS mutations and NPM1, Nras mutations and DNMT3A mutations were detected simultaneously, suggesting a good prognosis.

CEBPA

Exon1

CEBPA mutation was found in 7-11% of AML patients, and the mutation frequency was higher in NK-AML patients (13-15%). The patients with AML with double mutation of CEBPA suggest a good prognosis and can be used as an independent prognostic indicator.

DNMT3A

Exon2-23

DNMT3A mutation exists in 18-22% of AML patients, and the mutation frequency is higher in NK-AML patients (29-34%). R882 is the most common mutation. No NPM1 and FLT3-ITD mutations, or no NPM1 and FLT3-ITD mutations in NK-AML patients, suggesting shorter OS and DFS, poor prognosis.

PHF6

Exon2-10

PHF6 is located on the X chromosome and was first found in T-ALL. About 3% of AML had PHF6 gene mutation. The Association of PHF6 mutation with FLT3-ITD, MLL-PTD, ASXL1 mutation suggests poor prognosis in AML patients.

TET2

Exon3-11

The mutation of TET2 gene results in increased self-renewal and impaired differentiation of hematopoietic stem cells. Mutations were mainly found in MDS, MPN and other myeloid tumors. About 10% of AML had this gene mutation, and 23% of AML with normal chromosome had TET2 gene mutation. TET2 mutation indicates poor prognosis in AML patients with normal karyotype.

ASXL1

Exon12

ASXL1 gene mutations are found in MDS, CMML, AML and other myeloid tumors, and more in CMML. ASXL1 mutations are associated with FLT3-ITD, MLL-PTD and PHF6 mutations, which suggest poor prognosis in AML patients.

RUNX1

Exon2-9

RUNX1 mutation exists in 8-16% of AML patients. RUNX1 mutation often occurs with ASXL1 mutation, and rarely occurs in patients with NPM1 and CEBPA mutations. Patients with AML with RUNX1 mutation suggest shorter DFS and OS and poor prognosis.

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