RESUMO
BACKGROUND: Many studies have reported the presence of Positive Regulatory/Su(var)3-9, Enhancer-of-zeste and Trithorax Domain 2 (PRDM2) downregulation in cancer. However, its potential as a diagnostic biomarker is still unclear. Hence, a systematic review and meta-analysis were conducted to address this issue. INTRODUCTION: As of 2018, cancer has become the second leading cause of death worldwide. Thus, cancer control is exceptionally vital in reducing mortality. One such example is through early diagnosis of cancer using tumor biomarkers. Having a function as a tumor suppressor gene (TSG), PRDM2 has been linked with carcinogenesis in several solid tumor. This study aims to assess the relationship between PRDM2 downregulation and solid tumor, its relationship with clinicopathological data, and its potential as a diagnostic biomarker. This study also aims to evaluate the quality of the studies, data reliability and confidence in cumulative evidence. MATERIALS & METHODS: A protocol of this study is registered at the International Prospective Register of Systematic Reviews (PROSPERO) with the following registration number: CRD42019132156. PRISMA was used as a guideline to conduct this review. A comprehensive electronic search was performed from inception to June 2019 in Pubmed, Cochrane Library, ProQuest, EBSCO and ScienceDirect. Studies were screened and included studies were identified based on the criteria made. Finally, data synthesis and quality assessment were conducted. RESULTS: There is a significant relationship between PRDM2 downregulation with solid tumor (RR 4.29, 95% CI [2.58-7.13], P < 0.00001). The overall sensitivity and specificity of PRDM2 downregulation in solid tumors is 84% (95% CI [39-98%]) and 86% (95% CI [71-94%]), respectively. There is a low risk of bias for the studies used. TSA results suggested the presence of marked imprecision. The overall quality of evidence for this study is very low. DISCUSSION: We present the first meta-analysis that investigated the potential of PRDM2 downregulation as a diagnostic biomarker in solid tumor. In line with previous studies, our results demonstrated that PRDM2 downregulation occurs in solid tumor. A major source of limitation in this study is the small number of studies. CONCLUSIONS: Our review suggested that PRDM2 is downregulated in solid tumor. The relationship between PRDM2 downregulation and clinicopathological data is still inconclusive. Although the sensitivity and specificity of PRDM2 downregulation are imprecise, its high values, in addition to the evidence that suggested PRDM2 downregulation in solid tumor, hinted that it might still have a potential to be used as a diagnostic biomarker. In order to further strengthen these findings, more research regarding PRDM2 in solid tumors are encouraged.
RESUMO
Sleep disruption is a key clinical issue in the dementias but the sleep phenotypes of these diseases remain poorly characterised. Here we addressed this issue in a proof-of-principle study of 67 patients representing major syndromes of frontotemporal dementia (FTD) and Alzheimer's disease (AD), in relation to 25 healthy older individuals. We collected reports on clinically-relevant sleep characteristics - time spent overnight in bed, sleep quality, excessive daytime somnolence and disruptive sleep events. Difficulty falling or staying asleep at night and excessive daytime somnolence were significantly more frequently reported for patients with both FTD and AD than healthy controls. On average, patients with FTD and AD retired earlier and patients with AD spent significantly longer in bed overnight than did healthy controls. Excessive daytime somnolence was significantly more frequent in the FTD group than the AD group; AD syndromic subgroups showed similar sleep symptom profiles while FTD subgroups showed more variable profiles. Sleep disturbance is a significant clinical issue in major FTD and AD variant syndromes and may be even more salient in FTD than AD. These preliminary findings warrant further systematic investigation with electrophysiological and neuroanatomical correlation in major proteinopathies.
