SurExam Bio Technology Co.

Guangzhou, China

SurExam Bio Technology Co.

Guangzhou, China

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Patent
Surexam Bio Technology Co. | Date: 2017-08-09

This disclosure relates to a circulating tumour cell typing and identification kit, comprising a capture probe, an amplification probe, and a labeled probe for each marker gene mRNA, wherein the marker gene mRNA comprises the following two types: at least two epithelial cell marker gene mRNAs selected from the group consisting of EPCAM, E-cadherin, CEA, KRT5, KRT7, KRT17, and KRT20 mRNAs; and, at least two mesenchymal cell marker gene mRNAs selected from the group consisting of VIMENTIN, N-cadherin, TWIST1, AKT2, ZEB2, ZEB1, FOXC1, FOXC2, SNAI1, and SNAI2 mRNAs. This disclosure prevents false-positive results caused by, for example, possible presence of a number of non-neoplastic epithelial cells in peripheral blood, introduction of normal epithelial cells during blood sampling, and the like. Accordingly, it may be assured that cells detected with epithelial cell marker genes and/or mesenchymal cell marker genes are indeed circulating tumour cells, further improving accuracy and reliability of the detection resutls.


PubMed | Shanghai JiaoTong University, SurExam Bio Technology Co., Southern Medical University, Chongqing Medical University and 2 more.
Type: | Journal: Oncotarget | Year: 2016

Circulating tumor cells (CTCs) with phenotypic hallmarks of epithelial-mesenchymal transition (EMT) reportedly contribute to tumor metastasis in different cancer types. We therefore evaluated the expression of EMT markers in CTCs obtained from a large cohort of Chinese patients with colorectal cancer (CRC) and investigated their clinical relevance. The CanPatrolTM CTC enrichment technique was used to isolate and classify CTCs. CTCs were detected in 1046 of 1203 patients (86.9%), and three phenotypes were identified based on the expression of epithelial and mesenchymal markers: epithelial CTCs, biophenotypic (epithelial/mesenchymal) CTCs, and mesenchymal CTCs. Total CTC numbers positively correlated with both clinical stage and lymph node metastasis and distant metastasis. Furthermore, both biophenotypic and mesenchymal, but not epithelial, CTCs, correlated with the above parameters, suggesting CTCs displaying a mesenchymal phenotype denote more aggressive disease and metastatic potential. This is the first study to demonstrate a significant correlation between CTCs displaying a mesenchymal phenotype and both clinical stage and metastasis in a large cohort of patients with CRC. Our findings suggest that assessment of not only epithelial, but also mesenchymal markers in CTC analyses may offer valuable assistance for tumor staging and metastasis evaluation in patients with CRC.


Zhang L.,Peking Union Medical College | Yang H.,SurExam Bio Technology Co. | Xu J.,SurExam Bio Technology Co.
Current Drug Metabolism | Year: 2011

The association between gene expression and clinical characteristics of non-small cell lung cancer (NSCLC) are uncovered. These genes are critical elements in carcinoma physiological processes, including DNA synthesis, DNA repair and mitosis. Genes such as ERCC1, RRM1, TYMS, TUBB3 and STMN1 are predictive biomarker candidates for chemotherapy sensitivity in patients with NSCLC. Suitable gene expression analyzing technology is key factor for the personalize medicine to become a reality. This mini-review will describe and discuss critically on most currently widely used gene expression analyzing technologies, involving immunohistochemistry (IHC), reverse-transcription quantitative PCR (RT-qPCR) and branch-DNA technology (bDNA). © 2011 Bentham Science Publishers Ltd.


Ren G.-J.,Peking Union Medical College | Zhao Y.-Y.,Peking Union Medical College | Zhu Y.-J.,Peking Union Medical College | Xiao Y.,Peking Union Medical College | And 3 more authors.
Chinese Medical Journal | Year: 2011

Background Molecular targeted drugs is now widely used in non-small cell lung cancer (NSCLC) clinical treatment. Icotinib hydrochloride is a new type of oral epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs). In this study, we examined the role of EGFR, K-RAS, B-RAF somatic mutations and EGFR mRNA expression in tumor specimens from advanced NSCLC patients as predicators of the efficacy of icotinib hydrochloride. Methods We analyzed tumor paraffin-embedded specimens, which were obtained from 14 of 40 patients with advanced NSCLC who enrolled in the stage I clinical trial of icotinib hydrochloride. Somatic mutations were evaluated by mutant-enriched liquidchip (MEL) technology, and EGFR mRNA expression was measured by branched DNA liquidchip (MBL) technology. Results In the 14 specimens, seven patients showed EGFR mutations, exon 19 deletion (3/7) and exon 21 point mutation (4/7); and two patients showed K-RAS mutation. No mutations in EGFR exon 20 or B-RAF were detected. In patients with EGFR mutation, one patient developed progress disease (PD), three patients had stable disease (SD), two patients had partial responses (PR) and one patient had a complete response (CR). In patients with wild-type EGFR, four patients had PD, three patients acquired SD, and none had PR/CR (P=0.0407). EGFR mutations were associated with better progress-free survival (PFS) (141 days vs. 61 days) but without a statistically significant difference (P=0.8597), and median overall survival (OS) (≥449 days vs. 140 days). EGFR mRNA expression levels were evaluated (three high, eight moderate, one low, and two that can not be measured due to insufficient tumor tissue) and no statistically significant relationships was observed with response, PFS or OS. Conclusions The EGFR mutation rate was consistent with that reported in the Asian population, so the MEL technology is reliable for measuring EGFR mutation with high throughput and rapidity. EGFR exon 19 deletions and exon 21 point mutation are predictive biomarkers for response to icotinib hydrochloride as second line treatment or above.


Lu H.Y.,Zhejiang Cancer Hospital | Sun W.Y.,Zhejiang Cancer Hospital | Chen B.,Zhejiang Cancer Hospital | Zhang Y.P.,Zhejiang Cancer Hospital | And 5 more authors.
Neoplasma | Year: 2012

To know the incidence of epidermal growth factor receptor (EGFR) mutations in small cell lung cancer (SCLC) patients who received surgical resection in mailand China. xTAG technology was used to detect the EGFR exon 19 and exon 21 mutations of 40 patients with SCLC who received surgical treatment in Zhejiang Cancer Hospital from 1998 to 2010. 2 of 40 cases were found with mutations in exon 19 of the EGFR gene. The mutation in exon 19 of the EGFR gene is in a female and non smoking patient which pathology is SCLC combined adenocarcinoma, and the other is male and smoking patient which pathology is SCLC combined squamous cell carcinoma. The EGFR mutation is rare in SCLC patients, and EGFR mutation might occur more often in combined SCLCs than conventional patients.


Li S.,Peking Union Medical College | Li L.,Peking Union Medical College | Zhu Y.,Air Force General Hospital | Huang C.,Peking Union Medical College | And 15 more authors.
British Journal of Cancer | Year: 2014

Background:Determining the somatic mutations of epidermal growth factor receptor (EGFR)-pathway networks is the key to effective treatment for non-small cell lung cancer (NSCLC) with tyrosine kinase inhibitors (TKIs).The somatic mutation frequencies and their association with gender, smoking history and histology was analysed and reported in this study.Methods:Five thousand one hundred and twenty-five NSCLC patients' pathology samples were collected, and EGFR, KRAS, BRAF and PIK3CA mutations were detected by multiplex testing. The mutation status of EGFR, KRAS, BRAF and PIK3CA and their association with gender, age, smoking history and histological type were evaluated by appropriate statistical analysis.Results:EGFR, KRAS, BRAF and PIK3CA mutation rates revealed 36.2%, 8.4%, 0.5% and 3.3%, respectively, across the 5125 pathology samples. For the first time, evidence of KRAS mutations were detected in two female, non-smoking patients, age 5 and 14, with NSCLC. Furthermore, we identified 153 double and coexisting mutations and 7 triple mutations. Interestingly, the second drug-resistant mutations, T790M or E545K, were found in 44 samples from patients who had never received TKI treatments.Conclusions: EGFR exons 19, 20 and 21, and BRAF mutations tend to happen in females and non-smokers, whereas KRAS mutations were more inclined to males and smokers. Activating and resistant mutations to EGFR-TKI drugs can coexist and 'second drug-resistant mutations', T790M or E545K, may be primary mutations in some patients. These results will help oncologists to decide candidates for mutation testing and EGFR-TKI treatment. © 2014 Cancer Research Uk.


PubMed | Fujian Medical University and SurExam Bio Technology Co.
Type: Journal Article | Journal: The Journal of international medical research | Year: 2015

To investigate the associations between 1-adrenergic receptor (ADRB1) and cytochrome P450 2D6 (CYP2D6) gene polymorphisms and -blocker treatment outcomes in patients with hypertension.Chinese patients with essential hypertension were treated with the -blocker metoprolol and followed up for 12 weeks. xTAG liquid-chip technology was used for CYP2D6 100 C > T and ADRB1 1165G > C genotyping. Associations between gene polymorphisms and antihypertensive therapy outcomes were assessed by generalized linear model fitting. A decrease of 10 mmHg in systolic blood pressure indicated an effective treatment outcome.A total of 93 patients were included in the study. Mutant allele frequencies of 61.29% and 58.60% were obtained for ADRB1 and CYP2D6, respectively. There was no significant interaction between the effects of ADRB1 and CYP2D6 gene polymorphisms on treatment outcome. Patients homozygous for the mutant ADRB1 genotype (CC) had better treatment outcomes than those heterozygous for the mutation (GC). Interestingly, -blocker treatment duration was an independent factor associated with treatment outcome.The ADRB1 1165G > C gene polymorphism and -blocker treatment duration are independent factors associated with -blocker treatment outcome. These findings suggest that the selection of antihypertensive therapy should take into consideration the patients genotype.


Xu J.,Chinese Academy of Sciences | He J.,SurExam Bio. Technology Co. | Yang H.,SurExam Bio. Technology Co. | Luo X.,SurExam Bio. Technology Co. | And 5 more authors.
Cancer Biomarkers | Year: 2011

The prevalence of EGFR, KRAS, BRAF and PIK3CA somatic mutations in 861 randomly selected Chinese patients with non-small cell lung cancer (NSCLC) was assayed by the SurPlex®-xTAG70plex platform and analyzed. The results showed that the occurrence rates were 41.0, 8.0, 0.7 and 3.7%, respectively. The mutation rates significantly correlated with gender, histology and smoking history. The EGFR exon 19, 20 and 21 mutations were higher in females compared to males (p< 0.001, exon 19 and 21; p=0.018, exon 20), higher in adenocarcinomas compared to other forms of lung cancers (p< 0.001, exon 19 and 21; p=0.035, exon 20), and higher in non-smokers compared to smokers (p< 0.001, exon 19 and 21; p=0.029, exon 20). Conversely, the KRAS mutations were higher in males compared to females (p=0.004), higher in adenocarcinomas compared to other forms of lung cancers (p< 0.001), and higher in smokers compared to non-smokers (p< 0.001). The PIK3CA mutation rate was lower in adenocarcinomas compared to other forms of lung cancers (p=0.003). © 2011/2012 - IOS Press and the authors. All rights reserved.


Wu S.,SurExam Bio Technology Co. | Zhu Z.,SurExam Bio Technology Co. | He J.,SurExam Bio Technology Co. | Luo X.,SurExam Bio Technology Co. | And 2 more authors.
Clinical Chemistry and Laboratory Medicine | Year: 2010

Background: Somatic mutations in the KRAS gene have been reported to confer drug resistance to epidermal growth factor receptor tyrosine kinase inhibitors and some monoclonal antibodies. However, current DNA mutation detection technologies are primarily DNA sequencing-based and not high throughput, nor sensitive enough to meet clinical needs. Methods: A mutant-enriched PCR method was designed by introducing a unique restriction enzyme site to the PCR product. This allowed the wild-type KRAS sequence to be selectively removed by restriction enzyme digestion before application to the Luminex liquidchip system. Results: A total of 100 copies of mutant KRAS DNA fragment mixed with 1×105 copies of the wild-type KRAS DNA could be detected to achieve a sensitivity of 0.1%. This technology is currently used for clinical testing of KRAS somatic mutations for the purpose of pharmacogenomic evaluation. Serum samples from 109 patients with non-small cell lung cancer were tested and 34 mutations were detected (34/109). The formalin-fixed and paraffin-embedded samples from 60 patients with colorectal cancer were tested and 19 mutations were detected (19/60). Conclusions: A novel, qualitative, sensitive, reliable and high throughput liquidchip technology has been developed for detecting KRAS mutations using clinical serum and formalin-fixed and paraffin-embedded samples. © 2010 by Walter de Gruyter Berlin New York.


Wu S.,SurExam Bio Technology Co. | Liu Z.,SurExam Bio Technology Co. | Liu S.,SurExam Bio Technology Co. | Lin L.,SurExam Bio Technology Co. | And 2 more authors.
Clinical Chemistry and Laboratory Medicine | Year: 2014

Background: Enumeration and characterization of circulating tumor cells (CTCs) can provide information on patient prognosis and treatment efficacy. However, CTCs are rare, making their isolation a major technological challenge. We developed a technique for enrichment, and subsequent characterization of CTCs based on efficient depletion of human leukocytes. Methods: The technique (CanPatrolTM CTC enrichment) we developed is based on red blood cell lysis to remove erythrocytes, followed by depletion of CD45+ leukocytes using a magnetic bead separation method, and subsequent isolation of CTCs by virtue of their larger size, compared with leukocytes. We also demonstrated that fluorescence in situ hybridization (FISH) and genetic abnormalities analysis could be performed on the isolated CTCs. Results: The spiking experiments showed that the average efficacy of leukocytes depletion was 99.98% and the average tumor cells recovery was not lower than 80%. FISH could be used to perform ALK gene rearrangement analysis on the collected NCI-H2228 cells, and EGFR Exon 19 deletion was detected by PCR-based analysis in isolated HCC827 cells. The in vivo feasibility of this technique had been demonstrated in patients with non-small cell lung cancer, breast, colon, and esophageal cancers. CTCs were detected in 13 of 59 blood samples. Tumor microemboli was also detected in three breast cancer samples. Conclusions: The technique we developed allowed isolation and characterization of circulating epithelial tumor cells that do not express classical epithelial antigens. This potentially leads to a more accurate enumeration of the number of CTCs and is suitable for application to a broad range of cancers.

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