BackgroundEpithelial ovarian cancer (EOC) is the deadliest gynecological malignancy, and evidence is accumulating on how molecular markers may be associated with the origin and process of EOC. Sam68 (Src-associated in mitosis, of 68 kD), is a K homology domain RNA-binding protein that has been investigated as a risk factor in multiple types of tumors. The aim of the present study was to investigate the contribution of the Sam68 gene in the pathogenesis of EOC.Material/MethodsWestern blot assay and real-time quantitative PCR methods were performed to examine Sam68 expression in EOC tissue specimens. The association of Sam68 expression with clinic-pathologic variables of EOC was evaluated. Then gain-of-function and loss-of-function strategies were adopted to examine the regulation of Sam68 on the proliferation of EOC OVCAR-3 cells using CCK-8 and colony forming assays.ResultsSam68 was overexpressed in both mRNA and protein levels in EOC tumor tissue (n=152) in an association with malignant factors of EOC such as International Federation of Gynecology and Obstetrics (FIGO) stage, residual tumor size (cm), histological grade, and lymph node metastasis. In vitro results demonstrated that Sam68 overexpression was upregulated while Sam68 knockdown downregulated the proliferation of EOC OVCAR-3 cells via regulation of cell growth and colony formation.ConclusionsSam68 was overexpressed in EOC tissue in association with such cancer malignant factors of FIGO stage, histological grade, and lymph node metastasis, and also positively regulated the proliferation of EOC cells. Our research suggests that Sam68 might accelerate cell cycle progression, and present as a prognostic marker for EOC.

Objective: Birth weight, an important indicator of fetal nutrition and degree of development, may affect the risk of subsequent leukemia. At present, little is known about the effect of birth weight on acute myeloid leukemia (AML) and whether there is a dose-dependent relationship of birth weight with acute lymphoid leukemia (ALL) and AML. To address these questions, the present work aimed to systematically investigate the relationship between birth weight and the risk of subsequent leukemia based on the current epidemiological studiesMethods: Relevant studies were systematically retrieved from electronic databases PubMed, Embase, and Cochrane Library, from inception to May 15th, 2021. Finally, 28 studies (including 21 case-control studies and 7 cohort studies) were included for the final meta-analysis. Results in cohort studies were performed by risk ratios (RRs), while those in case-control studies by odds ratios (ORs), and all results were assessed by adopting the random-effect model. Besides, a dose-dependent analysis was conducted based on the cohort studies.Results: Compared with the population with normal birth weight (NBW), the population with high birth weight (HBW) might have an increased risk of leukemia (OR 1.33, 95%CI 1.20–1.49; I2 0%). Meanwhile, low birth weight (LBW) was associated with a decreased risk of ALL, as evidenced from the pooled analysis of case-control studies (OR 0.83, 95% CI 0.75–0.92; I2 23.3%). However, relative to NBW population, the HBW population might have an increased risk of ALL (OR 1.28, 95% CI 1.20–1.35; I2 7%). There was no obvious evidence supporting the relationship between LBW and the risk of AML from the pooled analysis of case-control studies (OR, 1.11 95% CI 0.87–1.42; I2 31.7%).Conclusions: Overall, in children and young adults, HBW population may be associated with the risks of subsequent leukemia and AML relative to NBW population, but the supporting dose-dependent evidence is lacking. In addition, compared with NBW population, there is stronger evidence supporting a significantly increased risk of subsequent ALL in HBW population, and a decreased risk in LBW population in a dose-dependent manner. More prospective studies with large samples are warranted in the future to validate and complement these findings.