Improving intensity-modulated radiation therapy quality assurance by adopting statistical process control.

PURPOSE: To use statistical process control for intensity-modulated radiation therapy (IMRT) quality assurance (QA) and improve tolerance limits and action limits. METHODS: An electronic portal imaging device (EPID) was selected to verify IMRT QA. The I-chart and the exponentially weighted moving averages (EWMA) chart were used to analyze the corresponding results. RESULTS: Twenty samples were used to enable the sampling requirements for building the control limits to be met. The I-chart showed that isolated data points beyond the control limits were mainly derived from complex plans. The EWMA made predictions of systematic errors earlier than the I-chart. Systematic errors primarily originated from the dose calibration on the EPID, and recalibrating the EPID could eliminate such errors. CONCLUSION: Statistical process control is an effective tool to detect controllable and can be used in IMRT QA. After calibrating the EPID, the tolerance and action limits all improved and satisfied the requirements/recommended values of the AAPM TG-218 report.

LINC00641 induces the malignant progression of colorectal carcinoma through the miRNA-424-5p/PLSCR4 feedback loop.

OBJECTIVE: To illustrate the role of LINC00641 in inducing the malignant progression of colorectal cancer (CRC) through the miRNA-424-5p/PLSCR4 feedback loop. PATIENTS AND METHODS: LINC00641 levels in paired CRC and non-tumoral tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Its prognostic potential in CRC was assessed by Kaplan-Meier method. Changes in proliferative and migratory abilities of HCT116 and SW620 cells transfected with si-LINC00641 were evaluated by 5-Ethynyl-2'- deoxyuridine (EdU), cell counting kit-8 (CCK-8) and transwell assay. The feedback loop LINC00641/miRNA-424-5p/PLSCR4 was identified through Dual-Luciferase reporter assay and its involvement in CRC progression was finally explored by rescue experiments. RESULTS: LINC00641 was upregulated in CRC tissues, which was an unfavorable factor to the overall survival of CRC. Proliferative and migratory abilities of HCT116 and SW620 cells were inhibited by knockdown of LINC00641. LINC00641 could competitively bind miRNA-424-5p, thereby abolishing its inhibitory effect on PLSCR4 expression. Knockdown of PLSCR4 could inhibit proliferative and migratory abilities of HCT116 and SW620 cells. CONCLUSIONS: LINC00641 stimulates proliferative and migratory abilities of CRC through the miRNA-424-5p/PLSCR4 feedback loop.

[Metformin inhibits the growth of hypopharyngeal carcinoma xenografts in nude mice model].

Objective:To investigated the effect of metformin on growth inhibition of hypopharyngeal carcinoma xenograft in nude mice and to study the theoretical basis of metformin for the treatment of hypopharyngeal carcinoma in clinical.Method:①To observe the course of metformin treatment, there were no severe adverse effects among the xenograft mice. ②After 28 days treatment, the average volumes of hypopharyngeal carcinoma xenografts of the metformin treated groups were significantly low compared with that of the control group.〖JP2〗The inhibition ratio of metformin at the concentration of 40 mg/(kg•d) and 200 mg/(kg•d) to the growth of tumor was 23.30%±7.17% and 40.51%±9.25%, respectively.③The aver ageoptical density(OAD) of AMPK in tumors of the control, met40 and met200 group was 0.246±0.038, 0.262±0.046, and 0.308±0.087, respectively. The OAD of p21 was 0.288±0.065, 0.305±0.091, and 0.477±0.114, respectively. And the OAD of cyclin D1 was 1.608±0.101, 0.781±0.055, and 0.711±0.046, respectively. Both the OAD of AMPK and p21 in met40 and met200 group were observably higher than those of the control group (P< 0.05). But the OAD of cyclin D1 in met40 and met200 group were remarkably lower than the control group (P< 0.05). ④The Western Blot drawed the consistant trend variation with immunohistochemical analyses. The gray value of AMPK in tumors of the control,met40 and met200 group was 0.641±0.042, 1.124±0.085, and 1.783±0.128; The gray value of p21 was 0.474±0.027, 0.594±0.063, and 0.970±0.079; The gray value of cyclin D1 was 1.608±0.101,0.781±0.055, and 0.711±0.046.Result:①To observe the course of metformin treatment, there were no severe adverse effects among the xenograft mice. ②After 28 days treatment, the average volumes of hypopharyngeal carcinoma xenografts of the metformin treated groups were significantly low compared with that of the control group.〖JP2〗The inhibition ratio of metformin at the concentration of 40 mg/(kg•d) and 200 mg/(kg•d) to the growth of tumor was 23.30%±7.17% and 40.51%±9.25%, respectively.③The aver ageoptical density(OAD) of AMPK in tumors of the control, met40 and met200 group was 0.246±0.038, 0.262±0.046, and 0.308±0.087, respectively. The OAD of p21 was 0.288±0.065, 0.305±0.091, and 0.477±0.114, respectively. And the OAD of cyclin D1 was 1.608±0.101, 0.781±0.055, and 0.711±0.046, respectively. Both the OAD of AMPK and p21 in met40 and met200 group were observably higher than those of the control group (P< 0.05). But the OAD of cyclin D1 in met40 and met200 group were remarkably lower than the control group (P< 0.05). ④The Western Blot drawed the consistant trend variation with immunohistochemical analyses. The gray value of AMPK in tumors of the control,met40 and met200 group was 0.641±0.042, 1.124±0.085, and 1.783±0.128; The gray value of p21 was 0.474±0.027, 0.594±0.063, and 0.970±0.079; The gray value of cyclin D1 was 1.608±0.101,0.781±0.055, and 0.711±0.046.Conclusion:Metformin can suppress the growth of hypopharyngeal carcinoma xenograft in nude mice and inducing tumor cell apoptosis without any severe adverse effects.