Management of dyslipidemia after allogeneic hematopoietic stem cell transplantation.

Dyslipidemia is one of the complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT), and it is often underestimated and undertreated. Dyslipidemia in allo-HSCT recipients has been confirmed to be associated with endocrine dysfunction, acute and chronic graft-versus-host disease (aGVHD and cGVHD), immunosuppressive agent application, etc. However, few studies have illustrated the accurate molecular signaling pathways involved in dyslipidemia, and there are no standard guidelines for dyslipidemia management after HSCT. This review will discuss the pathogenesis of dyslipidemia, especially the association with aGVHD and/or cGVHD. Comprehensive treatment methods for dyslipidemia after HSCT will also be summarized.

Dyslipidemia in the First 100 days and the Association with Acute Graft-versus-host Disease after Allogeneic Stem Cell Transplantation: A Single-center Retrospective Study in China.

Dyslipidemia is a common complication after allogeneic hematopoietic stem cell transplantation (allo-HSCT). The interaction between post-transplant hyperlipidemia and acute graft-versus-host disease (aGVHD) is uncertain. In this study, we performed a retrospective study to explore the relationship between dyslipidemia and aGVHD and the potential mechanism of aGVHD on dyslipidemia in 147 recipients who underwent allo-HSCT. The lipid profiles, transplantation details, and other laboratory data of the subjects were collected in the first 100 days post-transplantation. Our results indicated 63 patients with new-onset hypertriglyceridemia and 39 patients with new-onset hypercholesterolemia. A total of 57 (38.8%) patients developed aGVHD after transplantation. In a multifactorial analysis, aGVHD was an independent factor in the development of dyslipidemia in recipients (P < 0.05). After transplantation, the median LDL-C level of patients with aGVHD was 3.04 mmol/L (standard deviation value (SD): 1.36 mmol/L, 95% confidence interval (CI): 2.62, 3.45 mmol/L), and the LDL-C level in patients without aGVHD was 2.51 mmol/L (SD: 1.38 mmol/L, CI: 2.67, 3.40 mmol/L) (P < 0.05). Female recipients had higher lipid levels than males (P < 0.05). LDL levels (≥ 3.4 mmol/L) post-transplant were an independent risk factor for the development of aGVHD (OR = 0.311, P < 0.05). In conclusion, larger sample studies are anticipated to confirm our preliminary result, and an accurate mechanism between lipid metabolism and aGVHD needs to be determined in the future.

Suppression of MAL gene expression is associated with colorectal cancer metastasis.

Mal, T-cell differentiation protein (MAL) is a candidate tumor suppressor gene that functions in membrane trafficking processes in polarized epithelial cells. The aim of the present study was to determine its clinical significance in colorectal cancer (CRC). The RNA and protein expression levels of MAL in 30 colorectal specimens were detected by semi-quantitative polymerase chain reaction and immunohistochemistry analysis. Statistical analysis was performed using SPSS software. The RNA level of MAL was significantly downregulated in the CRC tissues compared with the adjacent healthy tissue (P<0.05). MAL was only positively expressed in 20% of the CRC tissues, but in 66.7% of the adjacent tissues, as determined by immunohistochemistry analysis. The expression of the MAL RNA transcript exhibited a positive correlation with protein expression. The expression levels of MAL were significantly associated with different tumor-node-metastasis stages and lymph node metastasis (P<0.05), but not with age, gender, tumor site, differentiation status and pathological type (P>0.05). Suppression of MAL expression was significantly correlated with metastasis in CRC. The present study indicated that MAL may function as an anti-metastasis factor and represent a potential biomarker for malignant colorectal tumors.