Sigmoid neovagina prolapse treated with Altemeier procedure: case report and systematic review of the literature.

BACKGROUND: Bowel vaginoplasty is a surgical method for neovagina construction that, despite its advantages over other techniques, is still burdened by complications such as prolapse. The incidence of sigmoid neovagina prolapse (SNP) is difficult to determine, and there are no evidence-based recommendations for treatment. We present a case of SNP and a systematic review of previous cases. CASE: A 73-year-old woman presented with stage III prolapse of her sigmoid neovagina constructed 51 years prior. Dynamic pelvic MRI revealed that the majority of the prolapse was due to the mucosa's loss of support. Due to the presence of numerous pelvic adhesions, an alternative to the laparoscopic approach was evaluated by a multidisciplinary team which led to the patient being treated using a modification of Altemeier's procedure. SYSTEMATIC REVIEW: After PROSPERO Registration (CRD42023400677), a systematic search of Medline and Scopus was performed using specific search terms. Study metadata including patient demographics, prolapse measurements, reconstruction techniques, recurrence rates, and timing were extracted. Fourteen studies comprising 17 cases of SNP were included. Vaginal resection of the redundant sigmoid, comprising Altemeier's procedure, was the most definitive surgery, but it was also associated with recurrences in three cases. Laparoscopic sacropexy was the second most definitive surgery with no recurrence reported. CONCLUSION: Our review shows that the recurrence after correction of sigmoid neovagina prolapses is higher than previously reported. Laparoscopy colposacropexy appeared to be the best approach, but it's not always feasible. In these scenarios, a mucosal resection using the Altemeier's procedure is the most effective surgery.

Combined loss of function of two different loci of miR-15/16 drives the pathogenesis of acute myeloid leukemia.

Double knockout of the two miR-15/16 loci in mouse resulted in the development of acute myeloid leukemia (AML). This result suggested that, at least, a fraction of human AMLs could be due to a similar mechanism. We analyzed the role of the two miR-15/16 clusters in 93 myelodysplastic syndrome (MDS) patients divided in three subgroups: patients with MDS, patients with MDS before transforming into AML (MDS-T), and patients with AML evolving from MDS (MDS-AML). Then, we tested 139 AML cases and 14 different AML cell lines by assessing microRNA (miRNA) expression, target protein expression, genetic loss, and silencing. MDS-T and MDS-AML patients show a reduction of the expression of miR-15a/-15b/-16 compared to MDS patients. Each miRNA can significantly predict MDS and MDS-T groups. Then, 79% of primary AMLs show a reduced expression of miR-15a and/or miR-15b. The expression of miR-15a/-15b/-16 significantly stratified AML patients in two prognostic classes. Furthermore, 40% of AML cell lines showed a combined loss of the expression of miR-15a/-15b and overexpression of their direct/indirect targets. As potential mechanisms involved in the silencing of the two miR-15/16 loci, we identified a genetic loss of miR-15a and miR-15b and silencing of these two loci by methylation. We identified a potential driver oncogenic role in the loss of expression of both miR-15/16 clusters in the progression of MDS into AML and in AML pathogenesis. The stratification of AML patients, based on miR-15/16 expression, can lead to targeted and combination therapies for the treatment of this incurable disease.

Knockout of both miR-15/16 loci induces acute myeloid leukemia.

MicroRNAs (miRNAs) have been extensively reported to be associated with hematological malignancies. The loss of miR-15a/16-1 at chromosome 13q14 is a hallmark of most of human chronic lymphocytic leukemia (CLL). Deletion of murine miR-15a/16-1 and miR-15b/16-2 has been demonstrated to promote B cell malignancies. Here, we evaluate the biological role of miR-15/16 clusters, crossbreeding miR-15a/16-1 and miR-15b/16-2 knockout mice. Unexpectedly, the complete deletion of both clusters promoted myeloproliferative disorders in the majority of the mice by the age of 5 months with a penetrance of 70%. These mice showed a significant enlargement of spleen and abnormal swelling of lymph nodes. Flow cytometry characterization demonstrated an expanded CD11b/Gr-1 double-positive myeloid population both in spleen and in bone marrow. The transplantation of splenocytes harvested from double-KO mice into wild-type recipient mice resulted in the development of myeloproliferative disorders, as observed in the donors. In vivo, miR-15/16 cluster deletion up-regulated the expression of Cyclin D1, Cyclin D2, and Bcl-2. Taken together, our findings identify a driver oncogenic role for miR-15/16 cluster deletion in different leukocytic cell lineages.

tRFUniverse: A comprehensive resource for the interactive analyses of tRNA-derived ncRNAs in human cancer.

tRNA-derived ncRNAs are a heterogeneous class of non-coding RNAs recently proposed to be active regulators of gene expression and be involved in many diseases, including cancer. Consequently, several online resources on tRNA-derived ncRNAs have been released. Although interesting, such resources present only basic features and do not adequately exploit the wealth of knowledge available about tRNA-derived ncRNAs. Therefore, we introduce tRFUniverse, a novel online resource for the analysis of tRNA-derived ncRNAs in human cancer. tRFUniverse presents an extensive collection of classes of tRNA-derived ncRNAs analyzed across all the TCGA and TARGET tumor cohorts, NCI-60 cell lines, and biological fluids. Moreover, public AGO CLASH/CLIP-Seq data were analyzed to identify the molecular interactions between tRNA-derived ncRNAs and other transcripts. Importantly, tRFUniverse combines in a single resource a comprehensive set of features that we believe may be helpful to investigate the involvement of tRNA-derived ncRNAs in cancer biology.

Nutrient restriction-activated Fra-2 promotes tumor progression via IGF1R in miR-15a downmodulated pancreatic ductal adenocarcinoma.

Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease, characterized by an intense desmoplastic reaction that compresses blood vessels and limits nutrient supplies. PDAC aggressiveness largely relies on its extraordinary capability to thrive and progress in a challenging tumor microenvironment. Dysregulation of the onco-suppressor miR-15a has been extensively documented in PDAC. Here, we identified the transcription factor Fos-related antigen-2 (Fra-2) as a miR-15a target mediating the adaptive mechanism of PDAC to nutrient deprivation. We report that the IGF1 signaling pathway was enhanced in nutrient deprived PDAC cells and that Fra-2 and IGF1R were significantly overexpressed in miR-15a downmodulated PDAC patients. Mechanistically, we discovered that miR-15a repressed IGF1R expression via Fra-2 targeting. In miR-15a-low context, IGF1R hyperactivated mTOR, modulated the autophagic flux and sustained PDAC growth in nutrient deprivation. In a genetic mouse model, Mir15aKO PDAC showed Fra-2 and Igf1r upregulation and mTOR activation in response to diet restriction. Consistently, nutrient restriction improved the efficacy of IGF1R inhibition in a Fra-2 dependent manner. Overall, our results point to a crucial role of Fra-2 in the cellular stress response due to nutrient restriction typical of pancreatic cancer and support IGF1R as a promising and vulnerable target in miR-15a downmodulated PDAC.

VIRGO: visualization of A-to-I RNA editing sites in genomic sequences.

BACKGROUND: RNA Editing is a type of post-transcriptional modification that takes place in the eukaryotes. It alters the sequence of primary RNA transcripts by deleting, inserting or modifying residues. Several forms of RNA editing have been discovered including A-to-I, C-to-U, U-to-C and G-to-A. In recent years, the application of global approaches to the study of A-to-I editing, including high throughput sequencing, has led to important advances. However, in spite of enormous efforts, the real biological mechanism underlying this phenomenon remains unknown. DESCRIPTION: In this work, we present VIRGO (http://atlas.dmi.unict.it/virgo/), a web-based tool that maps Ato-G mismatches between genomic and EST sequences as candidate A-to-I editing sites. VIRGO is built on top of a knowledge-base integrating information of genes from UCSC, EST of NCBI, SNPs, DARNED, and Next Generations Sequencing data. The tool is equipped with a user-friendly interface allowing users to analyze genomic sequences in order to identify candidate A-to-I editing sites. CONCLUSIONS: VIRGO is a powerful tool allowing a systematic identification of putative A-to-I editing sites in genomic sequences. The integration of NGS data allows the computation of p-values and adjusted p-values to measure the mapped editing sites confidence. The whole knowledge base is available for download and will be continuously updated as new NGS data becomes available.

Delayed surgical management of rectovaginal fistula: a case report highlighting challenges and lessons learned.

Background: Rectovaginal fistulas following an obstetric anal sphincter injury's repair are rare in developed country and their management could be challenging, particularly in cases of delayed repair. This study emphasizes the importance of accurately diagnosing and promptly repairing such fistulas for optimal patient well-being. Case: A 30-year-old patient presented with gas incontinence and a greenish discharge from the vagina, 6 months after delivering her baby. Examination revealed a small pinhole lesion on the posterior vaginal wall, and an endoanal ultrasound confirmed the presence of a rectovaginal fistula. Surgical repair was delayed for 9 months due to the patient's breastfeeding. The fistula was eventually repaired through a transrectal approach, with excision of the fistulous tract and closure of both the rectum and vagina. A laparoscopic protective ileostomy was also performed due to the delayed repair. However, a recurrence of the fistula was detected 8 months later, requiring a second repair. The patient underwent physiotherapy for the anal sphincter and achieved optimal sphincter function. After 6 months, the ileostomy was successfully closed, and the patient remained continent. Conclusions: This case highlights the importance of early recognition and prompt repair of rectovaginal fistulas following obstetric anal sphincter injury. Delayed repairs pose greater challenges and increase the risk of recurrence. Individualized surgical approaches, skilled pelvic floor repair, and a multidisciplinary approach are crucial for successful outcomes. This case underscores the need for careful planning and consideration of patient characteristics in the management of rectovaginal fistulas, aiming to achieve optimal outcomes and patient well-being.

HDAC1 regulates the chromatin landscape to control transcriptional dependencies in chronic lymphocytic leukemia.

Chronic lymphocytic leukemia (CLL) is a quiescent B-cell malignancy that depends on transcriptional dysregulation for survival. The histone deacetylases are transcriptional regulators whose role within the regulatory chromatin and consequence on the CLL transcriptome is poorly characterized. Here, we profiled and integrated the genome-wide occupancy of HDAC1, BRD4, H3K27Ac, and H3K9Ac signals with chromatin accessibility, Pol2 occupancy, and target expression signatures in CLL cells. We identified that when HDAC1 was recruited within super-enhancers (SEs) marked by acetylated H3K27 and BRD4, it functioned as a transcriptional activator that drove the de novo expression of select genes to facilitate survival and progression in CLL. Targeting HDACs reduced BRD4 and Pol2 engagement to downregulate the transcript and proteins levels of specific oncogenic driver genes in CLL such as BLK, a key mediator of the B-cell receptor pathway, core transcription factors such as PAX5 and IKZF3, and the antiapoptotic gene, BCL2. Concurrently, HDAC1, when recruited in the absence of SEs, repressed target gene expression. HDAC inhibition reversed silencing of a defined set of protein-coding and noncoding RNA genes. We focused on a specific set of microRNA genes and showed that their upregulation was inversely correlated with the expression of CLL-specific survival, transcription factor, and signaling genes. Our findings identify that the transcriptional activator and repressor functions of HDACs cooperate within the same tumor to establish the transcriptional dependencies essential for survival in CLL.

A plasma miRNA-based classifier for small cell lung cancer diagnosis.

Introduction: Small cell lung cancer (SCLC) is characterized by poor prognosis and challenging diagnosis. Screening in high-risk smokers results in a reduction in lung cancer mortality, however, screening efforts are primarily focused on non-small cell lung cancer (NSCLC). SCLC diagnosis and surveillance remain significant challenges. The aberrant expression of circulating microRNAs (miRNAs/miRs) is reported in many tumors and can provide insights into the pathogenesis of tumor development and progression. Here, we conducted a comprehensive assessment of circulating miRNAs in SCLC with a goal of developing a miRNA-based classifier to assist in SCLC diagnoses. Methods: We profiled deregulated circulating cell-free miRNAs in the plasma of SCLC patients. We tested selected miRNAs on a training cohort and created a classifier by integrating miRNA expression and patients' clinical data. Finally, we applied the classifier on a validation dataset. Results: We determined that miR-375-3p can discriminate between SCLC and NSCLC patients, and between SCLC and Squamous Cell Carcinoma patients. Moreover, we found that a model comprising miR-375-3p, miR-320b, and miR-144-3p can be integrated with race and age to distinguish metastatic SCLC from a control group. Discussion: This study proposes a miRNA-based biomarker classifier for SCLC that considers clinical demographics with specific cut offs to inform SCLC diagnosis.

Comparison of Maternal and Neonatal Outcomes between SARS-CoV-2 Variants: A Retrospective, Monocentric Study.

The impact of SARS-CoV-2 variants on maternal and neonatal outcomes during pregnancy is still poorly understood, and the emergence of different variants has further complicated our understanding of the virus's effects. This retrospective, monocentric study aimed to fill this knowledge gap by analyzing the outcomes of pregnant women with acute SARS-CoV-2 infection caused by the Alpha, Delta, and Omicron variants. The study, conducted between December 2020 and March 2022 at San Marco Hospital, included 313 pregnant women with confirmed SARS-CoV-2 infection. The results showed that the Delta variant was associated with a significantly higher incidence of adverse outcomes, such as premature births, maternal intensive care unit admission, intrauterine growth restriction, and small for gestational age infants. Additionally, the Delta variant was linked to lower Apgar scores, higher maternal and fetal mortality rates, and increased levels of various biomarkers indicating more severe illness. Finally, the Delta variant also presented a greater possibility of vertical transmission. These findings underscore the complexity of understanding the impact of SARS-CoV-2 on pregnancy outcomes, especially considering the distinctive characteristics of different variants. By better understanding the specific impacts of each variant, appropriate preventive measures and management strategies can be implemented to optimize maternal and neonatal outcomes.

Single-cell RNA sequencing reveals immunosuppressive myeloid cell diversity during malignant progression in a murine model of glioma.

Recent studies have shown the importance of the dynamic tumor microenvironment (TME) in high-grade gliomas (HGGs). In particular, myeloid cells are known to mediate immunosuppression in glioma; however, it is still unclear if myeloid cells play a role in low-grade glioma (LGG) malignant progression. Here, we investigate the cellular heterogeneity of the TME using single-cell RNA sequencing in a murine glioma model that recapitulates the malignant progression of LGG to HGG. LGGs show increased infiltrating CD4+ and CD8+ T cells and natural killer (NK) cells in the TME, whereas HGGs abrogate this infiltration. Our study identifies distinct macrophage clusters in the TME that show an immune-activated phenotype in LGG but then evolve to an immunosuppressive state in HGG. We identify CD74 and macrophage migration inhibition factor (MIF) as potential targets for these distinct macrophage populations. Targeting these intra-tumoral macrophages in the LGG stage may attenuate their immunosuppressive properties and impair malignant progression.

Large Gartner cyst of the posterior vaginal fornix.

International classifications of congenital anomalies do not extensively describe vaginal cysts. For this reason, clinicians who deal with such conditions can only rely on their personal or other colleague's experience, and only a few case reports are present in the literature. This paper illustrates the clinical scenario due to a particular Gartner cyst, the diagnostic workup followed for its diagnosis and its surgical management.

Stasis ulcer and hydronephrosis after severe genital prolapse: a case report.

INTRODUCTION AND IMPORTANCE: The most common complication of pelvic organ prolapse is stress urinary incontinence, whereas hydronephrosis or stasis ulcers are quite rare and typical of severe stages. The best treatment for this unusual presentation is still controversial. Here we present our approach. CASE PRESENTATION: Here we present the case of a 70-year-old White/Caucasian woman who presented to our hospital with genital procidentia lasting for 10 years that was associated with both hydronephrosis and stasis ulcers. CLINICAL FINDINGS AND INVESTIGATIONS: The Pelvic Organ Prolapse Quantitation system was used to assess the severity of the prolapse, being evaluated as stage IV with the apical compartment leading. A thorough search of the literature was conducted to find any similar cases and evaluate the best evidence treatment. INTERVENTIONS AND OUTCOMES: A no-mesh procedure comprising vaginal hysterectomy, axial apex suspension, and anterior and posterior repair with ulcerated skin removal resulted in complete resolution of both mechanical and functional symptoms. At 3- and 6-month follow-up visits, a satisfying vaginal profile without hydronephrosis was seen. The Pelvic Organ Prolapse Quantitation at 6 months follow-up was as follows: Aa -3, Ba -3, C -7; gh 2, pb 3, tvt 9; Ap -3, Bp -3. RELEVANCE AND IMPACT: Pelvic organ prolapse involves many organs and causes further complications, leading seldom to renal insufficiency and stasis ulcers. A temporary solution to the obstruction can be achieved by utilizing a pessary, but this device cannot be applied when a stasis ulcer has been previously established. The use of mesh for pelvic floor repair is controversial, but a previous vaginal ulcer may represent a contraindication. A complete evaluation and a challenging surgery may allow the recovery of complicated and severe pelvic organ prolapse. Native tissue pelvic repair gives no erosion postsurgical risk, which is the typical complication of the prosthesis.

Disparities in Lung Cancer: miRNA Isoform Characterization in Lung Adenocarcinoma.

Despite the development of targeted therapeutics, immunotherapy, and strategies for early detection, lung cancer carries a high mortality. Further, significant racial disparities in outcomes exist for which the molecular drivers have yet to be fully elucidated. The growing field of Epitranscriptomics has introduced a new layer of complexity to the molecular pathogenesis of cancer. RNA modifications can occur in coding and non-coding RNAs, such as miRNAs, possibly altering their gene regulatory function. The potential role for such modifications as clinically informative biomarkers remains largely unknown. Here, we concurrently profiled canonical miRNAs, shifted isomiRs (templated and non-templated), and miRNAs with single-point modification events (RNA and DNA) in White American (W) and Black or African American (B/AA) lung adenocarcinoma (LUAD) patients. We found that while most deregulated miRNA isoforms were similar in W and B/AA LUAD tissues compared to normal adjacent tissues, there was a subgroup of isoforms with deregulation according to race. We specifically investigated an edited miRNA, miR-151a-3p with an A-to-I editing event at position 3, to determine how its altered expression may be associated with activation of divergent biological pathways between W and B/AA LUAD patients. Finally, we identified distinct race-specific miRNA isoforms that correlated with prognosis for both Ws and B/AAs. Our results suggested that concurrently profiling canonical and non-canonical miRNAs may have potential as a strategy for identifying additional distinct biological pathways and biomarkers in lung cancer.

Synergistic apoptotic effect of miR-183-5p and Polo-Like kinase 1 inhibitor NMS-P937 in breast cancer cells.

MicroRNAs (miRNAs) are small noncoding RNAs that act as endogenous regulatory molecules targeting specific mRNAs for translational repression. Studies of breast cancer genomics indicate that breast cancer subtypes are distinguished and regulated by specific sets of miRNAs which affect activities such as tumor initiation, progression, and even drug response. Polo-like Kinase 1 (PLK1) is widely considered to be a proto-oncogene due to its increased expression in multiple tumor types, as well as its crucial role in regulating mitosis. Pharmacological inhibition of PLK1 can reduce tumor volume and induce tumor cell death in solid and hematologic malignancies. This prompted us to investigate how PLK1 inhibition with the target-specific inhibitor NMS-P937 would impact breast cancer cells, and how miRNAs may influence the overall response of these cells to this inhibition. We found that miR-183-5p targets PLK1 gene, effectively reducing its protein expression. Such miRNA-driven regulation of PLK1 expression sensitizes breast cancer cells to NMS-P937, resulting in synergistically increased apoptosis. We also show that the miRNA-regulated reduction of PLK1 influences the expression of apoptosis-related key proteins and possibly inducing further indirect PLK1 downmodulation through a DNMT1-p53 axis. These results suggest a potential biologically significant link between the expression of miR-183-5p and the efficacy of PLK1-specific inhibitors in breast cancer cells. Our work further elucidates how miR-183-5p regulates PLK1 gene while also enhancing NMS-P937 effect in breast cancer. Future studies assessing the role of miR-183-5p as a novel biomarker for anti-PLK1 chemotherapy agents are warranted.

Transcriptome Analysis of Human Endogenous Retroviruses at Locus-Specific Resolution in Non-Small Cell Lung Cancer.

Lung cancer is the second most commonly diagnosed cancer and the leading cause of cancer deaths worldwide. Among its subtypes, lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) are the most common, accounting for more than 85% of lung cancer diagnoses. Despite the incredible efforts and recent advances in lung cancer treatments, patients affected by this condition still have a poor prognosis. Therefore, novel diagnostic biomarkers are needed. Recently, a class of transposable elements called human endogenous retroviruses (HERVs) has been found to be implicated in cancer development and later employed as novel biomarkers for several tumor types. In this study, we first ever characterized the expression of HERVs at genomic locus-specific resolution in both LUAD and LUSC cohorts available in The Cancer Genome Atlas (TCGA). Precisely, (i) we profiled the expression of HERVs in TCGA-LUAD and TCGA-LUSC cohorts; (ii) we identified the dysregulated HERVs in both lung cancer subtypes; (iii) we evaluated the impact of the dysregulated HERVs on signaling pathways using neural network-based predictions; and (iv) we assessed their association with overall survival (OS) and relapse-free survival (RFS). In conclusion, we believe this study may help elucidate another layer of dysregulation that occurs in lung cancer involving HERVs, paving the way for identifying novel lung cancer biomarkers.

Pan-Cancer Analysis of Canonical and Modified miRNAs Enhances the Resolution of the Functional miRNAome in Cancer.

Epitranscriptomic studies of miRNAs have added a new layer of complexity to the cancer field. Although there is fast-growing interest in adenosine-to-inosine (A-to-I) miRNA editing and alternative cleavage that shifts miRNA isoforms, simultaneous evaluation of both modifications in cancer is still missing. Here, we concurrently profiled multiple miRNA modification types, including A-to-I miRNA editing and shifted miRNA isoforms, in >13,000 adult and pediatric tumor samples across 38 distinct cancer cohorts from The Cancer Genome Atlas and The Therapeutically Applicable Research to Generate Effective Treatments data sets. The differences between canonical miRNAs and the wider miRNAome in terms of expression, clustering, dysregulation, and prognostic standpoint were investigated. The combination of canonical miRNAs and modified miRNAs boosted the quality of clustering results, outlining unique clinicopathologic features among cohorts. Certain modified miRNAs showed opposite expression from their canonical counterparts in cancer, potentially impacting their targets and function. Finally, a shifted and edited miRNA isoform was experimentally validated to directly bind and suppress a unique target. These findings outline the importance of going beyond the well-established paradigm of one mature miRNA per miRNA arm to elucidate novel mechanisms related to cancer progression. SIGNIFICANCE: Modified miRNAs may act as cancer biomarkers and function as allies or antagonists of their canonical counterparts in gene regulation, suggesting the concurrent consideration of canonical and modified miRNAs can boost patient stratification.

The MicroRNA Family Gets Wider: The IsomiRs Classification and Role.

MicroRNAs (miRNAs or miRs) are the most characterized class of non-coding RNAs and are engaged in many cellular processes, including cell differentiation, development, and homeostasis. MicroRNA dysregulation was observed in several diseases, cancer included. Epitranscriptomics is a branch of epigenomics that embraces all RNA modifications occurring after DNA transcription and RNA synthesis and involving coding and non-coding RNAs. The development of new high-throughput technologies, especially deep RNA sequencing, has facilitated the discovery of miRNA isoforms (named isomiRs) resulting from RNA modifications mediated by enzymes, such as deaminases and exonucleases, and differing from the canonical ones in length, sequence, or both. In this review, we summarize the distinct classes of isomiRs, their regulation and biogenesis, and the active role of these newly discovered molecules in cancer and other diseases.

Detecting and Characterizing A-To-I microRNA Editing in Cancer.

Adenosine to inosine (A-to-I) editing consists of an RNA modification where single adenosines along the RNA sequence are converted into inosines. Such a biochemical transformation is catalyzed by enzymes belonging to the family of adenosine deaminases acting on RNA (ADARs) and occurs either co- or post-transcriptionally. The employment of powerful, high-throughput detection methods has recently revealed that A-to-I editing widely occurs in non-coding RNAs, including microRNAs (miRNAs). MiRNAs are a class of small regulatory non-coding RNAs (ncRNAs) acting as translation inhibitors, known to exert relevant roles in controlling cell cycle, proliferation, and cancer development. Indeed, a growing number of recent researches have evidenced the importance of miRNA editing in cancer biology by exploiting various detection and validation methods. Herein, we briefly overview early and currently available A-to-I miRNA editing detection and validation methods and discuss the significance of A-to-I miRNA editing in human cancer.

MiREDiBase, a manually curated database of validated and putative editing events in microRNAs.

MicroRNAs (miRNAs) are regulatory small non-coding RNAs that function as translational repressors. MiRNAs are involved in most cellular processes, and their expression and function are presided by several factors. Amongst, miRNA editing is an epitranscriptional modification that alters the original nucleotide sequence of selected miRNAs, possibly influencing their biogenesis and target-binding ability. A-to-I and C-to-U RNA editing are recognized as the canonical types, with the A-to-I type being the predominant one. Albeit some bioinformatics resources have been implemented to collect RNA editing data, it still lacks a comprehensive resource explicitly dedicated to miRNA editing. Here, we present MiREDiBase, a manually curated catalog of editing events in miRNAs. The current version includes 3,059 unique validated and putative editing sites from 626 pre-miRNAs in humans and three primates. Editing events in mature human miRNAs are supplied with miRNA-target predictions and enrichment analysis, while minimum free energy structures are inferred for edited pre-miRNAs. MiREDiBase represents a valuable tool for cell biology and biomedical research and will be continuously updated and expanded at https://ncrnaome.osumc.edu/miredibase .