Experimental Study and Clinical Observation on the Improvement Effect of Lienal Polypeptide on Blood Toxicity and Immune Injury Induced by Radiotherapy.

Aims: To investigate the immune and gastrointestinal functional effects of lienal polypeptide (LP) treatment in tumor-bearing mice and carcinoma patients receiving radiotherapy (RT), and to detect hematological indicators and T lymphocyte subsets. Methods: Tumor-bearing mice were randomly divided into five groups: the control group, the RT group, the RT+LP-L (1.7 mg/kg, low dosage of LP) group, the RT+LP-M (5.2 mg/kg, middle dosage of LP) group, and the RT+LP-H (10.4 mg/kg, high dosage of LP) group. In addition, carcinoma patients were randomly divided into two groups. The observation group was given LP during RT, and the control group was only treated with RT. We then compared the myelosuppression, gastrointestinal reactions, and clinical efficacy among groups. Results: In the animal experiments, compared with the control group, the number of leukocytes and lymphocytes of the mice in the "RT" group decreased (p < 0.05). Animals receiving LP evidenced a dose-response curve with regard to the number of leukocytes and lymphocytes that was proportional to the LP dose, increased (p < 0.05). Flow cytometric analyses showed that LP treatment of the mice increased the numbers of CD3+, and CD4+ T cells and theCD4+/CD8+ ratio. In our clinical study, the Radiation Therapy Oncology Group (RTOG)/European Organization for Research and Treatment of Cancer (EORTC) criteria were used for measuring myelosuppression and gastrointestinal reactions. The RTOG/EORTC grade 3 or 4 inhibition rate of leukocytes, granulocytes, hemoglobin, platelets, and gastrointestinal toxic effects in the observation group were significantly lower than that in the control group (p < 0.05). Conclusion: LP can improve the hematopoietic and immune function of RT-treated mice and reduce the hematological and gastrointestinal toxicity of patients treated with RT and improve the quality of life.

Identification of abnormal nuclear and mitochondrial genes in esophageal cancer cells.

The present study aimed to detect the mutation characteristics of mitochondrial DNA (mtDNA) in Eca109 of Ec9706 cells, and to investigate their association with the nuclear genome (nDNA), thus providing a basis for gene targeting therapies for esophageal squamous cell carcinoma (ESCC). In vitro­cultured Ec9706 and Eca109 cells were analyzed the changes of single­nucleotide polymorphisms (SNPs), insertions/deletions (INDELs), copy number varia-tion, and structure variation (SV) of their genome by high­throughput sequencing. The loci with SV on chromosome 1­12 of the two ESCC cell lines were ≥5% of the mtDNA, but SV on chromosome 13­22, X and Y was ≤3%; >40% of loci exhibited gain or loss; intergenic loci with INDEL changes and SNP features accounted for the majority of mutations. The affected genes encoded proteins including nDNA­encoding intra­mitochondrial­transporting proteins, ATP energy generation­associated proteins and mitochondrial electron respiratory chain proteins, and these proteins were all nucleus­encoded mitochondrial proteins. The transcription, duplication, and translation of the abnormally expressed mtDNA in Ec9706 and Eca109 cells were closely associated with disorders of nuclear DNA products.