Virus-modified paraspeckle-like condensates are hubs for viral RNA processing and their formation drives genomic instability.

The nucleus is a highly organised yet dynamic environment containing distinct membraneless nuclear bodies. This spatial separation enables a subset of components to be concentrated within biomolecular condensates, allowing efficient and discrete processes to occur which regulate cellular function. One such nuclear body, paraspeckles, are comprised of multiple paraspeckle proteins (PSPs) built around the architectural RNA, NEAT1_2.

Dysregulation of the DRAIC/SBK1 Axis Promotes Lung Cancer Progression.

Long non-coding RNAs (lncRNAs) are key regulators of cellular processes that underpin cancer development and progression. DRAIC is a migration inhibitor that has been linked with lung adenocarcinoma progression; however, its mechanisms remain to be studied. Several bioinformatics tools were used to explore the role of DRAIC in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC).

Meta-analysis of RNA interaction profiles of RNA-binding protein using the RBPInper tool.

Motivation: Recent RNA-centric experimental methods have significantly expanded our knowledge of proteins with known RNA-binding functions. However, the complete regulatory network and pathways for many of these RNA-binding proteins (RBPs) in different cellular contexts remain unknown. Although critical to understanding the role of RBPs in health and disease, experimentally mapping the RBP-RNA interactomes in every single context is an impossible task due the cost and manpower required.

The Hippo pathway transcription factors YAP and TAZ play HPV-type dependent roles in cervical cancer.

Human papillomaviruses (HPVs) cause most cervical cancers and an increasing number of anogenital and oral carcinomas, with most cases caused by HPV16 or HPV18. HPV hijacks host signalling pathways to promote carcinogenesis. Understanding these interactions could permit identification of much-needed therapeutics for HPV-driven malignancies.

Platelet-derived microvesicles isolated from type-2 diabetes mellitus patients harbour an altered miRNA signature and drive MDA-MB-231 triple-negative breast cancer cell invasion.

The underlying causes of breast cancer are diverse, however, there is a striking association between type 2 diabetes and poor patient outcomes. Platelet activation is a common feature of both type 2 diabetes and breast cancer and has been implicated in tumourigenesis through a multitude of pathways. Here transcriptomic analysis of type 2 diabetes patient-derived platelet microvesicles revealed an altered miRNA signature compared with normoglycaemic control patients.

Cumulative incidence and risk factors for cutaneous squamous cell carcinoma metastases in organ transplant recipients: The Skin Care in Organ Transplant Patients in Europe-International Transplant Skin Cancer Collaborative metastases study, a prospective multicenter study.

Introduction: Solid organ transplant recipients (SOTRs) are believed to have an increased risk of metastatic cutaneous squamous cell carcinoma (cSCC), but reliable data are lacking regarding the precise incidence and associated risk factors.

Methods: In a prospective cohort study, including 19 specialist dermatology outpatient clinics in 15 countries, patient and tumor characteristics were collected using standardized questionnaires when SOTRs presented with a new cSCC. After a minimum of 2 years of follow-up, relevant data for all SOTRs were collected.

Transcriptomic analysis of cutaneous squamous cell carcinoma reveals a multigene prognostic signature associated with metastasis.

Background: Metastasis of cutaneous squamous cell carcinoma (cSCC) is uncommon. Current staging methods are reported to have sub-optimal performances in metastasis prediction. Accurate identification of patients with tumors at high risk of metastasis would have a significant impact on management.

Decosus: An R Framework for Universal Integration of Cell Proportion Estimation Methods.

The assessment of the cellular heterogeneity and abundance in bulk tissue samples is essential for characterising cellular and organismal states. Computational approaches to estimate cellular abundance from bulk RNA-Seq datasets have variable performances, often requiring benchmarking matrices to select the best performing methods for individual studies. However, such benchmarking investigations are difficult to perform and assess in typical applications because of the absence of gold standard/ground-truth cellular measurements.

Dysregulation of the miR-30c/DLL4 axis by circHIPK3 is essential for KSHV lytic replication.

Non-coding RNA (ncRNA) regulatory networks are emerging as critical regulators of gene expression. These intricate networks of ncRNA:ncRNA interactions modulate multiple cellular pathways and impact the development and progression of multiple diseases. Herpesviruses, including Kaposi's sarcoma-associated herpesvirus, are adept at utilising ncRNAs, encoding their own as well as dysregulating host ncRNAs to modulate virus gene expression and the host response to infection.

ACSNI: An unsupervised machine-learning tool for prediction of tissue-specific pathway components using gene expression profiles.

Determining the tissue- and disease-specific circuit of biological pathways remains a fundamental goal of molecular biology. Many components of these biological pathways still remain unknown, hindering the full and accurate characterization of biological processes of interest. Here we describe ACSNI, an algorithm that combines prior knowledge of biological processes with a deep neural network to effectively decompose gene expression profiles (GEPs) into multi-variable pathway activities and identify unknown pathway components.

The Genomic Landscape of Actinic Keratosis.

Actinic keratoses (AKs) are lesions of epidermal keratinocyte dysplasia and are precursors for invasive cutaneous squamous cell carcinoma (cSCC). Identifying the specific genomic alterations driving the progression from normal skin to skin with AK to skin with invasive cSCC is challenging because of the massive UVR-induced mutational burden characteristic at all stages of this progression. In this study, we report the largest AK whole-exome sequencing study to date and perform a mutational signature and candidate driver gene analysis on these lesions.