The Rat sarcoma virus (RAS) family of proteins, which includes the Kristen Rat sarcoma virus (KRAS), is linked to nearly one-fourth of all human cancers. KRAS mutations, in particular, are associated with Non-Small Ce...The Rat sarcoma virus (RAS) family of proteins, which includes the Kristen Rat sarcoma virus (KRAS), is linked to nearly one-fourth of all human cancers. KRAS mutations, in particular, are associated with Non-Small Cell Lung Carcinoma (NSCLC), colorectal cancer, adenocarcinomas, ovarian carcinoma, and endometrial tumors. KRAS activates 80 different signaling pathways, including Mitogen-activated protein kinases (MAPK) and Phosphoinositide 3-kinase (PI3K), and up-regulates transcription factors such as ETS like Protein (ELK), Jun Proto-Oncogene (JUN), and Myelocytomatosis (MYC), which are involved in cell differentiation, proliferation, transformation, and survival. KRAS mutations are also known to cause autocrine function, which further exacerbates the situation. In NSCLC, KRAS mutations have a strong positive correlation with the disease, particularly in patients with a smoking history. In pancreatic cancer, KRAS mutations are a dominant pathological basis, with most mutations being G12D, G12V, G13D, G13C, G13S, and G13R. These mutations serve as initial markers in tumorigenesis and are associated with poor prognosis and high mortality rates. In colorectal cancer, KRAS mutations contribute to 4/5 of cases, with cellular mechanisms involving the MAPK pathway, which resists anti-epidermal growth factor antibodies. In Low-grade Serous Ovarian Cancer (LGSOC), KRAS mutations are associated with altered signaling in the MAPK pathway and drug resistance. However, treatments such as Selumetinib, a down regulator of RAS/Rapidly Accelerated Fibrosarcoma (RAF)/Mitogen-activated protein kinase (MEK) pathways, and a combination of trametinib and buparlisib have shown promise in managing LGSOC when diagnosed early through KRAS mutation markers. Although KRAS mutations are commonly associated with many types of cancer, their use in clinical practice is limited due to the lack of accurate methods to identify them. It is needed to further isolate the KRAS mutation products and correlate the cancer-causing genes to make it a promising approach for cancer chemotherapy.展开更多
目的：使用RNA干扰技术阻断人结肠癌细胞cyclin D1的表达，检测其对细胞生长增殖的影响和机制。方法：将人结肠癌细胞株HT-29分成3组，antisense组（转染反义链组）、sense组（转染正义链组）和对照组，免疫沉淀和蛋白质印迹法观察cycli...目的：使用RNA干扰技术阻断人结肠癌细胞cyclin D1的表达，检测其对细胞生长增殖的影响和机制。方法：将人结肠癌细胞株HT-29分成3组，antisense组（转染反义链组）、sense组（转染正义链组）和对照组，免疫沉淀和蛋白质印迹法观察cyclin D1 siRNA对细胞cyclin D1蛋白质表达的影响，并对蛋白质电泳图像进行分析，MTT比色法绘制细胞生长曲线，^3H-TdR技术和流式细胞技术观测细胞周期变化。结果：反义siRNA有效抑制了cyclin Dl蛋白质表达，MTT实验显示，转染反义siRNA的细胞，生长代谢减慢，与对照组细胞差异显著（P〈0．01），而antisense组细胞24h的^3H-TdR渗入量，G0／G1期和S期细胞较对照组和sense组明显减少（^3H-TdR：1181.8±117.97 VS 1798.4±55.36，1851.4±83.46；P〈0.01;G0／G1期：79.31％ VS 60.87％，59.14％；S期：13.67％ VS 26.42％．27.93％：P〈0.01）。结论：RNA干扰技术能有效减弱cyclin D1蛋白质表达，使细胞周期受阻，并抑制结肠癌细胞的生长增殖。展开更多
AIM: To describe a new surgical technique and evaluate the early results of segmental gastrectomy (SG) with modified D2 lymph node (LN) dissection for early gastric cancer (EGC). METHODS: Fourteen patients with EGC un...AIM: To describe a new surgical technique and evaluate the early results of segmental gastrectomy (SG) with modified D2 lymph node (LN) dissection for early gastric cancer (EGC). METHODS: Fourteen patients with EGC underwent SG with modified D2 dissection from 2006 to 2008. Their operative results and postoperative courses were compared with those of 17 patients who had distal gastrectomy (DG) for EGC during the same period. RESULTS: Operating time, blood loss, and hospital stay were similar between the 2 groups. Postoperative complications developed significantly more frequently in the DG group than in the SG group. Mean number of dissected LNs per each station in the SG group was comparable with that in the DG group. Postoperative recovery of body weight was significantly better in the SG group than in the DG group. The incidence of reflux esophagitis and gastritis after surgery was less frequent in the SG group than in the DG group.CONCLUSION: SG with modified D2 LN dissection may be a new function-preserving gastrectomy that is feasible for treatment of EGC with possible LN involvement.展开更多
基金Supported by the National Natural Science Foundation of China (No. 81603342)the Guangdong Provincial Key Laboratory of Traditional Chinese Medicine Informatization (No. 2021B1212040007)+5 种基金the Guangdong Basic and Applied Basic Re-search Foundation (No. 2022A1515012641No. 2024A1515012948)the Guangdong Provincial Bureau of Traditional Chinese Medi-cine Research Project (No. 20221107)the Guangzhou Science and Technology Projects (No. 2024A03J0154No. 2023B01J1004)the Foshan “Summit Plan” of Building High-Level Hospitals。
文摘The Rat sarcoma virus (RAS) family of proteins, which includes the Kristen Rat sarcoma virus (KRAS), is linked to nearly one-fourth of all human cancers. KRAS mutations, in particular, are associated with Non-Small Cell Lung Carcinoma (NSCLC), colorectal cancer, adenocarcinomas, ovarian carcinoma, and endometrial tumors. KRAS activates 80 different signaling pathways, including Mitogen-activated protein kinases (MAPK) and Phosphoinositide 3-kinase (PI3K), and up-regulates transcription factors such as ETS like Protein (ELK), Jun Proto-Oncogene (JUN), and Myelocytomatosis (MYC), which are involved in cell differentiation, proliferation, transformation, and survival. KRAS mutations are also known to cause autocrine function, which further exacerbates the situation. In NSCLC, KRAS mutations have a strong positive correlation with the disease, particularly in patients with a smoking history. In pancreatic cancer, KRAS mutations are a dominant pathological basis, with most mutations being G12D, G12V, G13D, G13C, G13S, and G13R. These mutations serve as initial markers in tumorigenesis and are associated with poor prognosis and high mortality rates. In colorectal cancer, KRAS mutations contribute to 4/5 of cases, with cellular mechanisms involving the MAPK pathway, which resists anti-epidermal growth factor antibodies. In Low-grade Serous Ovarian Cancer (LGSOC), KRAS mutations are associated with altered signaling in the MAPK pathway and drug resistance. However, treatments such as Selumetinib, a down regulator of RAS/Rapidly Accelerated Fibrosarcoma (RAF)/Mitogen-activated protein kinase (MEK) pathways, and a combination of trametinib and buparlisib have shown promise in managing LGSOC when diagnosed early through KRAS mutation markers. Although KRAS mutations are commonly associated with many types of cancer, their use in clinical practice is limited due to the lack of accurate methods to identify them. It is needed to further isolate the KRAS mutation products and correlate the cancer-causing genes to make it a promising approach for cancer chemotherapy.
文摘目的：使用RNA干扰技术阻断人结肠癌细胞cyclin D1的表达，检测其对细胞生长增殖的影响和机制。方法：将人结肠癌细胞株HT-29分成3组，antisense组（转染反义链组）、sense组（转染正义链组）和对照组，免疫沉淀和蛋白质印迹法观察cyclin D1 siRNA对细胞cyclin D1蛋白质表达的影响，并对蛋白质电泳图像进行分析，MTT比色法绘制细胞生长曲线，^3H-TdR技术和流式细胞技术观测细胞周期变化。结果：反义siRNA有效抑制了cyclin Dl蛋白质表达，MTT实验显示，转染反义siRNA的细胞，生长代谢减慢，与对照组细胞差异显著（P〈0．01），而antisense组细胞24h的^3H-TdR渗入量，G0／G1期和S期细胞较对照组和sense组明显减少（^3H-TdR：1181.8±117.97 VS 1798.4±55.36，1851.4±83.46；P〈0.01;G0／G1期：79.31％ VS 60.87％，59.14％；S期：13.67％ VS 26.42％．27.93％：P〈0.01）。结论：RNA干扰技术能有效减弱cyclin D1蛋白质表达，使细胞周期受阻，并抑制结肠癌细胞的生长增殖。
文摘AIM: To describe a new surgical technique and evaluate the early results of segmental gastrectomy (SG) with modified D2 lymph node (LN) dissection for early gastric cancer (EGC). METHODS: Fourteen patients with EGC underwent SG with modified D2 dissection from 2006 to 2008. Their operative results and postoperative courses were compared with those of 17 patients who had distal gastrectomy (DG) for EGC during the same period. RESULTS: Operating time, blood loss, and hospital stay were similar between the 2 groups. Postoperative complications developed significantly more frequently in the DG group than in the SG group. Mean number of dissected LNs per each station in the SG group was comparable with that in the DG group. Postoperative recovery of body weight was significantly better in the SG group than in the DG group. The incidence of reflux esophagitis and gastritis after surgery was less frequent in the SG group than in the DG group.CONCLUSION: SG with modified D2 LN dissection may be a new function-preserving gastrectomy that is feasible for treatment of EGC with possible LN involvement.
