BackgroundTraditional Chinese medicine (TCM) has been widely applied for cancer care in China. There have been a large number of controlled clinical studies published in Chinese literature, yet no systematic searching and analysis has been done. This study summarizes the current evidence of controlled clinical studies of TCM for cancer.MethodsWe searched all the controlled clinical studies of TCM therapies for all kinds of cancers published in Chinese in four main Chinese electronic databases from their inception to November 2011. We bibliometrically analyzed the included studies and assessed the reporting quality.ResultsA total of 2964 reports (involving 253,434 cancer patients) including 2385 randomized controlled trials and 579 non-randomized controlled studies were included. The top seven cancer types treated were lung cancer, liver cancer, stomach cancer, breast cancer, esophagus cancer, colorectal cancer and nasopharyngeal cancer by both study numbers and case numbers. The majority of studies (72%) applied TCM therapy combined with conventional treatment, whilst fewer (28%) applied only TCM therapy in the experimental groups. Herbal medicine was the most frequently applied TCM therapy (2677 studies, 90.32%). The most frequently reported outcome was clinical symptom improvement (1667 studies, 56.24%) followed by biomarker indices (1270 studies, 42.85%), quality of life (1129 studies, 38.09%), chemo/radiotherapy induced side effects (1094 studies, 36.91%), tumor size (869 studies, 29.32%) and safety (547 studies, 18.45%). Completeness and adequacy of reporting appeared to improve with time.ConclusionsData from controlled clinical studies of TCM therapies in cancer treatment is substantial, and different therapies are applied either as monotherapy or in combination with conventional medicine. Reporting of controlled clinical studies should be improved based on the CONSORT and TREND Statements in future. Further studies should address the most frequently used TCM therapy for common cancers and outcome measures should address survival, relapse/metastasis and quality of life.

Epigenetic modifications affect the differentiation of T cell subsets and the pathogenesis of autoimmune diseases, but many mechanisms of epigenetic regulation of T cell differentiation are unclear. Here we show reduced expression of the transcription factor RFX1 in CD4 + T cells from patients with systemic lupus erythematosus, which leads to IL-17A overexpression through increased histone H3 acetylation and decreased DNA methylation and H3K9 tri-methylation. Conditional deletion of Rfx1 in mice exacerbates experimental autoimmune encephalomyelitis and pristane-induced lupus-like syndrome and increases induction of Th17 cells. In vitro, Rfx1 deficiency increases the differentiation of naive CD4 + T cells into Th17 cells, but this effect can be reversed by forced expression of Rfx1. Importantly, RFX1 functions downstream of STAT3 and phosphorylated STAT3 can inhibit RFX1 expression, highlighting a non-canonical pathway that regulates differentiation of Th17 cells. Collectively, our findings identify a unique role for RFX1 in Th17-related autoimmune diseases.

Background Reduced 18 F-fluorodeoxyglucose-positron emission tomography (FDG-PET) brain metabolism was recognized as a biomarker of neurodegeneration in the recently proposed ATN framework for Alzheimer’s disease (AD) biological definition. However, accumulating evidence suggested it is an independent biomarker, which is denoted as “F” in the very study. Methods A total of 551 A+T+ individuals from the Alzheimer’s Disease Neuroimaging Initiative database were recruited and then further divided into four groups based on the biomarker positivity as 132 A+T+N−F−, 102 A+T+N−F+, 113 A+T+N+F−, and 204 A+T+N+F+. Frequency distributions of the groups were compared, as well as the clinical progression [measured by the longitudinal changes in cognition and brain structure, and mild cognitive impairment (MCI) to AD dementia conversion] between every pair of F+ and F− groups. Results The prevalence of A+T+N+F+ profile was 66.24% in clinically diagnosed AD dementia patients; similarly, the majority of individuals with reduced FDG-PET were AD dementia subjects. Among the 551 individuals that included, 537 had at least one follow-up (varied from 1 to 8 years). Individuals in F+ groups performed worse and dropped faster in Mini-Mental State Examination scale and had faster shrinking middle temporal lobe than those in F− groups (all p < 0.05). Moreover, in MCI patients, reduced FDG-PET exerted 2.47 to 4.08-fold risk of AD dementia progression compared with those without significantly impaired FDG-PET (both p < 0.001). Conclusions Based on the analyses, separating FDG-PET from “N” biomarker to build the ATN(F) system is necessary and well-founded. The analysis from this study could be a complement to the original ATN framework for AD’s biological definition. Electronic supplementary material The online version of this article (10.1186/s13195-019-0512-1) contains supplementary material, which is available to authorized users.

To assess plasma phosphorylated tau181 (p-tau181) as a progression biomarker in Alzheimer’s disease (AD), we examined longitudinal plasma p-tau181 of 1184 participants (403 cognitively normal (CN), 560 patients with mild cognitive impairment (MCI), and 221 with AD dementia) from Alzheimer’s Disease Neuroimaging Initiative (ADNI). The plasma p-tau level was increased at baseline for MCI and AD dementia (mean: CN, 15.4 pg/mL; MCI, 18.4 pg/mL; AD dementia, 23.7 pg/mL; P < 0.001) and increased significantly over time at preclinical (Aβ-positive CN), prodromal (Aβ-positive MCI), and dementia (Aβ-positive dementia) stage of AD. A longitudinal increase of plasma p-tau181 was associated with abnormal cerebrospinal fluid biomarker levels (low Aβ42, high phosphorylated tau, and high total tau, all P < 0.001), amyloid accumulation (P < 0.001) and hypometabolism (P = 0.002) on positron emission tomography, atrophy in structure imaging (small hippocampal (P = 0.030), middle temporal (P = 0.008), and whole brain (P = 0.027) volume, and large ventricular volume (P = 0.008)), and deteriorated cognitive performance (global cognition and memory, language, executive function, and visuospatial function, all P < 0.050) at baseline. Furthermore, longitudinal plasma p-tau181 correlated with concurrent changes of nearly all these AD-related hallmarks and faster increase in plasma p-tau181 correlated with faster worsening cognition in all diagnostic groups. Importantly, most associations remained significant in Aβ-positive group and became non-significant in Aβ-negative group. Longitudinal analyses of plasma p-tau181 suggest its potential as a noninvasive biomarker to track disease progression in AD and to monitor effects of disease-modifying therapeutics in clinical trials.