Recent studies have demonstrated the existence of intratumoral microorganisms. However, the role of intratumoral microbes in the development of ovarian cancer and their interaction with the tumor microenvironment are largely unknown.

The existence of microbiome in human tumors has been determined widely, but evaluating the contribution of intratumoral bacteria and fungi to tumor immunity and prognosis from a pan-cancer perspective remains absent. We designed an improved microbial analysis pipeline to reduce interference from host sequences, complemented with integration analysis of intratumoral microbiota at species level with clinical indicators, tumor microenvironment, and prognosis across cancer types. We found that intratumoral microbiota is associated with immunophenotyping, with high-immunity subtypes showing greater bacterial and fungal richness compared to low-immunity groups. We also noted that the combination of fungi and bacteria demonstrated promising prognostic value across cancer types. We, thus, present The Cancer Microbiota (TCMbio), an interactive platform that provides the intratumoral bacteria and fungi data, and a comprehensive analysis module for 33 types of cancers. This led to the discovery of clinical and prognostic significance of intratumoral microbes.

The burgeoning field of oncobiome research declared that members of the intratumoral microbiome besidesHelicobacter pyloriexisted in tumor tissues and participated in the occurrence and development of gastric cancer, and the methylation of host DNA may be a potential target of microbes and their metabolites. Current research focuses mostly on species composition, but the functional genes of the members of the microbiota are also key to their interaction with the host.

Increasing evidence suggests a correlation between changes in the composition of gut microbiota and sleep-related phenotypes. However, it remains uncertain whether these associations indicate a causal relationship. The genome-wide association study summary statistics data of gut microbiota (n = 18,340) was downloaded from the MiBioGen consortium and the data of sleep-related phenotypes were derived from the UK Biobank, the Medical Research Council-Integrative Epidemiology Unit, Jones SE, the FinnGen consortium. To test and estimate the causal effect of gut microbiota on sleep traits, a two-sample Mendelian randomization (MR) approach using multiple methods was conducted. A series of sensitive analyses, such as horizontal pleiotropy analysis, heterogeneity test, MR Steiger directionality test and “leave-one-out” analysis as well as reverse MR analysis, were conducted to assess the robustness of MR results. The genus Anaerofilum has a negative causal effect on getting up in the morning (odd ratio = 0.977, 95% confidence interval: 0.965–0.988, p = 7.28 × 10⁻⁵). A higher abundance of order Enterobacteriales and family Enterobacteriaceae contributed to becoming an “evening person”. Six and two taxa were causally associated with longer and shorter sleep duration, respectively. Specifically, two SCFA-produced genera including Lachnospiraceae UCG004 (odd ratio = 1.029, 95% confidence interval = 1.012–1.046, p = 6.11 × 10⁻⁴) and Odoribacter contribute to extending sleep duration. Two obesity-related genera such as Ruminococcus torques (odd ratio = 1.024, 95% confidence interval: 1.011–1.036, p = 1.74 × 10⁻⁴) and Senegalimassilia were found to be increased and decreased risk of snoring, respectively. In addition, we found two risk taxa of insomnia such as the order Selenomonadales and one of its classes called Negativicutes. All of the sensitive analysis and reverse MR analysis results indicated that our MR results were robust. Our study revealed the causal effect of gut microbiota on sleep and identified causal risk and protective taxa for chronotype, sleep duration, snoring and insomnia, which has the potential to provide new perspectives for future mechanistic and clinical investigations of microbiota-mediated sleep abnormal patterns and provide clues for developing potential microbiota-based intervention strategies for sleep-related conditions.

Epidemiological studies have linked obesity to the onset of puberty, while its causality and the potential metabolite mediators remain unclear. We employed a two-sample Mendelian randomization (MR) design to evaluate the causal effects of obesity on puberty onset and its associated diseases including type 2 diabetes (T2D) and cardiovascular diseases (CVDs). The potential mediators in this pathway were further explored using a two-step MR design. The robustness of our findings was evaluated using sensitivity analyses. Our MR results revealed that childhood obesity/BMI were causally associated with an increased Tanner stage in girls, younger age at menarche, and increased risk of adulthood T2D and CVD. However, neither childhood BMI nor obesity had a causal effect on the Tanner stage in boys. Mediation analysis further indicated that increased creatine served as a mediator for the causal pathway from childhood obesity/BMI to the Tanner stage of girls, while early puberty onset in girls played a mediating role in the pathway linking childhood obesity to increased risk of adulthood T2D and CVD. This study indicated that the risk of early puberty onset in girls and its associated health issues can be potentially reduced by preventing childhood obesity. The involvement of creatine in this process needs to be further validated and explored.