首页> 外文会议>International Conference on the Development of Biomedical Engineering in Vietnam >A Molecular Alteration Situations of KRAS, NEAS, BRAF, PIK3C and PTEN Loss in Colorectal Adenocarcinoma at Can The Oncology Hospital
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A Molecular Alteration Situations of KRAS, NEAS, BRAF, PIK3C and PTEN Loss in Colorectal Adenocarcinoma at Can The Oncology Hospital

机译:肿瘤医院在肿瘤医院的kras,et,braf,pik3c和Pten损失的分子改变情况

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Aim To determine the characteristics of KRAS, NRAS, BRAF, PIK3CA gene mutation and loss of PTEN expression in colorectal adenocarcinoma in Can Tho Oncology Hospital. Materials and methods A cross-sectional study included 50 cases of colorectal adenocarcinoma were diagnosed and treated at Can Tho Oncology Hospital. KRAS, NRAS, BRAF, PIK3CA mutations identified by Sanger DNA sequencing as well as evaluating the loss of PTEN protein expressed by MHC. Results and discussion Among the 50 colorectal cancer patients, we detected 17 (34%) mutations in the KRAS, NRAS (0%), BRAF 1(2%) and PIK3CA 3(6%), all of which were point mutations. Mutation frequencies at codon 12 and codon 13 were 26%. Only one patient harboured a point mutation at codon 10. The KRAS mutation frequency was significantly higher in the rectum than in the colon (26% versus 8%, p = 0.022). Other clinic-pathological features, such as gender, histological type, and grade, TNM stage, showed no positive relationship with KRAS gene mutations. The PIK3CA mutation frequency was significantly higher in the <50 years patients or female than in the group > 50 years (6% versus 0%) with p = 0.042; p = 0.036 respectively. The incidence of PTEN loss was 14%. Loss of PTEN expression, relative to regional lymph nodes metastatic and distant metastasis was statistically significant. Conclusion The KRAS mutation rates of colorectal adenocarcinoma patients in Can Tho Oncology Hospital were 34%. KRAS mutation associated with tumor location. PIK3CA mutation associated with age and gender. In 50 cases, none of NRAS mutations detected. K601E BRAF mutation is also one of several situations that cause over-activation of the BRAF protein. The rate of PTEN loss was 14% and about regional and distant metastasis.
机译:目的是确定KRA,NRA,BRAF,PIK3CA基因突变和CAN肿瘤医院癌症腺癌中PTEN表达丧失的特征。材料和方法横截面研究包括在肿瘤医院诊断和治疗50例结直肠癌腺癌。 KRA,NRAS,BRAF,由Sanger DNA测序鉴定的PIK3CA突变,以及评估MHC表达的PTEN蛋白的损失。结果与讨论50种结肠直肠癌患者,我们检测到KRA,NRA(0%),BRAF 1(2%)和PIK3CA 3(6%)中的17(34%)突变,所有这些都是点突变。密码子12和密码子13处的突变频率为26%。只有一名患者在密码子10处留下了点突变。直肠的克拉斯突变频率显着高于结肠(26%,与8%,P = 0.022)。其他临床病理特征,例如性别,组织学型和等级,TNM阶段,与KRAS基因突变没有阳性关系。 <50岁的患者或女性突变频率显着高于本组50岁(6%与0%),P = 0.042; P = 0.036分别。 PTEN损失的发病率为14%。相对于区域淋巴结转移性和远处转移的失去PTEN表达具有统计学意义。结论肿瘤医院肿瘤医院结直肠腺癌患者的KRA突变率为34%。与肿瘤位置相关的KRAS突变。与年龄和性别相关的Pik3CA突变。在50例中,没有检测到NRAS突变。 K601E BRAF突变也是导致BRAF蛋白的过度激活的几种情况之一。 PTEN损失率为14%,涉及区域和远端转移。

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