MAFB/IGH融合基因t（14;20）探针
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MAFB/IGH融合基因t（14;20）探针 本试剂盒主要用于MAFB/IGH融合基因t（14;20）的检测，里面包括即用型杂交液和DAPI复染剂。 本试剂盒仅供科研使用。
- 产品描述
MAFB/IGH融合基因t(14;20)探针
广州健仑生物科技?有限公司
本司长期供应尼古丁（可替宁）检测试剂盒，其主要品牌包括美国NovaBios、广州健仑、广州创仑等进口产品，国产产品，试剂盒的实验方法是胶体金方法。
我司还有很多荧光原位杂交系列检测试剂盒以及各种FISH基因探针和染色体探针等，。
MAFB/IGH融合基因t(14;20)探针
本试剂盒主要用于AML1/ETO融合基因t(8;21)的检测，里面包括即用型杂交液和DAPI复染剂。
本试剂盒仅供科研使用。
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以下是我司出售的部分FISH产品：
| 6号染色体计数探针（绿色） |
| 8号/20q探针 |
| D13S25（13q14）探针（红色） |
| JAK2（9p24）基因断裂探针 |
| FRS2（12q15）基因探针 |
| p53/RB1/ATM/CSP12/D13S25/6/6q21/IGH基因探针(七探针 ) |
| MYC（8q24），BCL6（3q37），BCL2（18q21）探针 |
| API2/MALT1融合基因t(11;18)探针 |
| MALT1/IGH融合基因t(14;18)探针 |
| IGH融合基因（CCND1,MAF,MAFB,FGFR3）探针 |
| ALK、MET、ROS1基因探针 |
| FGFR1,PDGFRA,PDGFRB基因探针 |
| 7号/8号染色体探针 |
| 8号/17号染色体探针 |
| 8号染色体计数探针（红色） |
| D7S522（7q31）基因探针 |
| RB1(13q14)/ATM(11q22)基因探针 |
MAFB/IGH融合基因t(14;20)探针
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【公司名称】 广州健仑生物科技有限公司
【】 杨永汉
【】
【腾讯 】
【公司地址】 广州清华科技园创新基地番禺石楼镇创启路63号二期2幢101-3室
【企业文化宣传】MAFB/IGH融合基因t(14;20)探针
肿瘤细胞的基因型和表达程序与细胞的表型、肿瘤微环境的作用、肿瘤的特质、演变和治疗抵抗有关。zui近几年，肿瘤的基因组图谱之类的研究绘制了肿瘤的遗传景观、几千个肿瘤的表达形态、识别了驱动突变、并根据特定的转录图谱区分不同的亚型。但是肿瘤的遗传状态可以更为精确的进行研究，而整块组织的基因表达提供的信息是有限的，因为肿瘤程序的表达决定因素、微环境的影响以及肿瘤内基因的异质性都被整体平均了。而单细胞转录组测序可以解决这些问题，但是同时也带来了更多的花费和更多的工作量，比如需要更多的时间从新鲜的肿瘤样品当中获得单个细胞，尤其是一些罕见肿瘤。
2研究方法
? 10个IDH-A患者，流式分选肿瘤细胞，然后进行单细胞RNA-seq。6个IDH-O患者，流式分选肿瘤细胞，进行单细胞RNA-seq。
? 分析了从TCGA数据库下载的76个IDH-O91个IDH-A胶质瘤大量细胞的数据，有550个差异表达的基因。并对比了单细胞测序的结果与大量细胞测序的结果进行比较。
? DNA、RNA原位杂交。
3研究结果
? 分析IDH突变的胶质瘤标本单细胞RNA-Seq与大量细胞RNA-seq结果的差异基于细胞分群的方法：
1> 基因表达聚类分析，细胞分为胶质瘤细胞、免疫细胞和少突胶质细胞。
2> 由于胶质瘤细胞常伴有大的染色体变异，我们使用每个细胞在大的染色体区域基因表达的数据来评估CNVs，然后通过外显子测序和DNA FISH来验证CNV。使用基因表达和CNV来分类细胞的结果是*的，一共定义了5097个恶性细胞。
接下来将单细胞测序的数据与ATCG下载的大量细胞RNA-seq的数据进行比较，寻找两种肿瘤亚群基因表达的差异，并分析亚群特征性基因。
IDH-A和IDH-O因为肿瘤微环境和遗传学导致的基因表达的差异
其中一半的基因在单细胞测序中没有差异，在大量细胞测序有差异，表明非恶性细胞导致的差异基因占了一半。免疫基因和神经基因作为非恶性细胞的基因就是一些干扰因素。
? IDH-A与IDH-O恶性细胞基因表达的差异主要源于基因组的问题。
基于转录组的结果主要是有4类基因组的变异引起的，分别是1p/19q、CIC激活的基因、CIC抑制的基因和P53的靶基因。
不同肿瘤亚型的特征基因均有以上4类遗传学影响导致
? 单细胞测序显示IDH-A和IDH-O共享胶质细胞谱系
之前研究认为IDH-A和IDH-O分别以星状胶质细胞和少突胶质细胞为主。通过特征基因和PCA分析IDH-A和IDH-O胶质细胞的差异基因是很少的，他们的区别主要是因为遗传学和肿瘤微环境的差异，而并不是胶质细胞的差异。
The genotypes and expressions of tumor cells are related to the phenotype of the cells, the role of the tumor microenvironment, the characteristics and evolution of the tumor, and the resistance to treatment. In recent years, the research of tumor genome map has drawn the genetic landscape of cancer, the expression pattern of thousands of tumors, identified the driving mutation, and differentiated different subtypes according to specific transcriptional patterns. However, the genetic status of cancer can be studied more accuray, while the information provided by gene expression in whole tissue is limited, because the determinants of tumor expression, the influence of microenvironment and the heterogeneity of tumor genes are all averaged. Single cell transcriptome sequencing can solve these problems, but at the same time, it also brings more cost and more workload. For example, more time is needed to get individual cells from fresh tumor samples, especially some rare tumors.
2 research methods
10 IDH-A with flow cytometry in tumor cells, and single cell RNA-seq. In 6 IDH-O patients, the flow cytometry was used to separate the tumor cells, and the single cell RNA-seq was performed.
Analyzed 76 IDH-O91 IDH-A glioma downloaded from the TCGA database of data, there are 550 differentially expressed genes. Compared with the results of a large number of cell sequencing, the results of single cell sequencing were compared.
DNA, RNA in situ hybridization.
3 research results
The difference analysis of IDH mutation in glioma samples and a large number of single cell RNA-Seq cell RNA-seq cell clustering method based on the results of:
1> gene expression clustering analysis, the cells are divided into glioma cells, immune cells and oligodendrocytes.
2>, because glioma cells are often accompanied by large chromosomal aberrations, we use the data of gene expression of each cell in large chromosome regions to evaluate CNVs, and then verify CNV by exon sequencing and DNA FISH. The results of using gene expression and CNV to classify cells were consistent, and 5097 malignant cells were defined.
Next, we compare the data of single cell sequencing with the data from a large number of cell RNA-seq data downloaded by ATCG. We find the difference of gene expression between two kinds of tumor subsets and analyze the characteristic genes of subpopulations.
Differences in gene expression caused by IDH-A and IDH-O because of tumor microenvironment and genetics
Half of the genes were not different in single cell sequencing, and there were differences in a large number of cell sequencing, indicating that half of the differential genes were caused by non malignant cells. The genes of immune and neurogenes as non malignant cells are some of the interfering factors.
The difference IDH-A and IDH-O gene expression in malignant cells mainly derived from the genome.
The results based on the transcriptional group are mainly caused by the variation of 4 genomes, which are 1p/19q, CIC activated genes, CIC suppressed genes and P53 target genes.
The characteristic genes of different tumor subtypes have 4 types of genetic influence
Single cell sequencing showed that IDH-A and IDH-O shared glial lineage
Previous research showed that IDH-A and IDH-O are star and oligodendrocytes. The difference genes between IDH-A and IDH-O glial cells were very few through the analysis of characteristic genes and PCA. Their difference is mainly due to the difference between genetics and tumor microenvironment, but not the difference of glial cells.
