Effect of lipid metabolism disorder on liver function in patients with malignant tumors after chemotherapy: a case-control study.

BACKGROUND: This study aims to investigate the effect of lipid metabolism disorder on liver function in patients with malignant tumors after chemotherapy. METHOD: A total of 428 patients with malignant tumors with normal liver function in our hospital between May 2013 to June 2018 were divided into an observation group (lipid metabolism disorder, n = 265) and control group (normal lipid metabolism, n = 163). The lipid metabolism levels and liver damage of the two groups were compared before and after chemotherapy. RESULTS: No significant differences in age, gender, body mass index, tumor types, history of surgery, levels of alanine aminotransferase (ALT; an indicator of liver function), and chemotherapy regimen were observed between the two groups. However, the observation group showed increased levels of total cholesterol (P = 0.000), triglycerides (P = 0.000), and low-density lipoprotein (P = 0.01), as well as decreased levels of high-density lipoprotein (P = 0.000) before chemotherapy compared with the control group. Furthermore, patients with lipid metabolism disorders were more likely to develop abnormal liver function after chemotherapy. Moreover, mixed lipid metabolism disorder was more likely to cause severe liver damage after chemotherapy. Additionally, the number of patients with lipid metabolism disorders after chemotherapy (n = 367) was significantly increased compared with before chemotherapy (n = 265) (P < 0.01), indicating that chemotherapy might induce or aggravate an abnormal lipid metabolism. CONCLUSIONS: After receiving chemotherapy, patients with malignant tumors presenting lipid metabolism disorders are more prone to liver damage and lipid metabolism disorders than patients with a normal lipid metabolism.

Histone demethylase KDM2A promotes tumor cell growth and migration in gastric cancer.

Histone demethylase KDM2A has been reported to be dysregulated in lung cancer. However, its function in gastric cancer remains poorly understood. Here, it was found that the expression level of KDM2A was increased in gastric cancer tissues. Moreover, forced expression of KDM2A in gastric cancer cells promoted cell growth and migration, while the knockdown expression of KDM2A inhibited the tumorigenicity of gastric cancer cells. Mechanistically, KDM2A regulated the growth and motility of gastric cancer cells through downregulating the expression of programmed cell death 4 (PDCD4), a known tumor suppressor in the progression of gastric cancer. Taken together, our study suggested that upregulation of KDM2A was very important in the progression of gastric cancer, and KDM2A might be a promising therapeutic target.

Plasma cfDNA for the Diagnosis and Prognosis of Colorectal Cancer.

Objective: To evaluate the value of cell-free DNA (cfDNA) for the diagnosis and prognosis of colorectal cancer (CRC). Methods: Peripheral blood specimens of 120 CRC patients and 90 healthy volunteers (as a control cohort) were extracted. A quantitative real-time polymerase chain reaction (qRT-PCR) was performed to determine the cfDNA expression. Following correlation analyses for cfDNA and clinical endpoints, a receiver operator characteristic (ROC) curve was established to assess the sensitivity and specificity of cfDNA, CEA, VEGF, and CA125 and for evaluating the disease-free survival (DFS) of patients. Results: The plasma cfDNA level of colorectal cancer patients was significantly higher than that of healthy subjects (P < 0.05), and after chemotherapy, cfDNA level was significantly lower than that before chemotherapy (P < 0.05). CA125/CEA/VEGF expression significantly correlated with cfDNA level, but not with cfDNA integrity. There was also a significant correlation between tumor differentiation and the cfDNA level. cfDNA has a higher ROC value than the current tumor biomarkers. Survival analysis showed that the DFS of the low cfDNA expression group was longer (29.99 ± 0.78 months) than that of the high cfDNA expression group (27.66 ± 1.05 months, P=0.031). Conclusion: The blood cfDNA is associated with the pathological features of CRC clinical cases and represents a possible indicator for CRC diagnosis and prognosis.

Novel intergenic KIF5B-MET fusion variant in a patient with gastric cancer: A case report.

BACKGROUND: MET fusion is a key driver mutation, but it is rare in gastric cancer (GC). Several MET (hepatocyte growth factor receptor) inhibitors have been approved for the treatment of MET-positive patients, but the tumor response is heterogeneous. With the development of next-generation sequencing, diverse MET fusion partner genes have been identified. We herein report a fusion variant involving KIF5B-MET in GC. CASE SUMMARY: After thoracoscopic inferior lobectomy plus lymph node dissection under general anesthesia, a "tumor within a tumor" was found in the lung tumor tissue of a 64-year-old non-smoking male patient. Combining the medical history and the results of enzyme labeling, the focal area was considered to be GC. To seek potential therapeutic regimens, an intergenic region between KIF5B and MET fusion was identified. This fusion contains a MET kinase domain and coil-coiled domains encoded by KIF5B exons 1-25, which might drive the oncogenesis. CONCLUSION: Our finding could extend the spectrum and genomic landscape of MET fusions in GC and favor the development of personalized therapy.