Rissoidae (Mollusca, Gastropoda, Rissooidea) from taphocoenotic assemblages of the Strait of Sicily (Mediterranean Sea) with the description of two new species.

Twenty-one rissoid species have been found in four bathyal samples from the Strait of Sicily, represented exclusively by empty shells. Some of these species are shallow water dwellers, associated with algal facies, others are typical of deep-sea (bathyal-abyssal). Two species are described as new (Alvania ismar n.

WNT Oncogenic Transcription Requires MYC Suppression of Lysosomal Activity and EPCAM Stabilization in Gastric Tumors.

Background & Aims: WNT signaling is central to spatial tissue arrangement and regulating stem cell activity, and it represents the hallmark of gastrointestinal cancers. Although its role in driving intestinal tumors is well characterized, WNT's role in gastric tumorigenesis remains elusive.

Methods: We have developed mouse models to control the specific expression of an oncogenic form of β-catenin (CTNNB1) in combination with MYC activation in Lgr5 cells of the gastric antrum.

Oxidative stress enhances the therapeutic action of a respiratory inhibitor in MYC-driven lymphoma.

MYC is a key oncogenic driver in multiple tumor types, but concomitantly endows cancer cells with a series of vulnerabilities that provide opportunities for targeted pharmacological intervention. For example, drugs that suppress mitochondrial respiration selectively kill MYC-overexpressing cells. Here, we unravel the mechanistic basis for this synthetic lethal interaction and exploit it to improve the anticancer effects of the respiratory complex I inhibitor IACS-010759.

MYC and therapy resistance in cancer: risks and opportunities.

The MYC transcription factor, encoded by the c-MYC proto-oncogene, is activated by growth-promoting signals, and is a key regulator of biosynthetic and metabolic pathways driving cell growth and proliferation. These same processes are deregulated in MYC-driven tumors, where they become critical for cancer cell proliferation and survival. As other oncogenic insults, overexpressed MYC induces a series of cellular stresses (metabolic, oxidative, replicative, etc.

Polycomb group ring finger protein 6 suppresses Myc-induced lymphomagenesis.

Max is an obligate dimerization partner for the Myc transcription factors and for several repressors, such as Mnt, Mxd1-4, and Mga, collectively thought to antagonize Myc function in transcription and oncogenesis. Mga, in particular, is part of the variant Polycomb group repressive complex PRC1.6.

Targeting mitochondrial respiration and the BCL2 family in high-grade MYC-associated B-cell lymphoma.

Multiple molecular features, such as activation of specific oncogenes (e.g., MYC, BCL2) or a variety of gene expression signatures, have been associated with disease course in diffuse large B-cell lymphoma (DLBCL), although their relationships and implications for targeted therapy remain to be fully unraveled.

Integrated requirement of non-specific and sequence-specific DNA binding in Myc-driven transcription.

Eukaryotic transcription factors recognize specific DNA sequence motifs, but are also endowed with generic, non-specific DNA-binding activity. How these binding modes are integrated to determine select transcriptional outputs remains unresolved. We addressed this question by site-directed mutagenesis of the Myc transcription factor.

Low diversity or poorly explored? Mesophotic molluscs highlight undersampling in the Eastern Mediterranean.

Mesophotic assemblages are the next frontier of marine exploration in the Mediterranean Sea. Located below recreational scuba diving depths, they are difficult to access but host a diverse array of habitats structured by large invertebrate species. The Eastern Mediterranean has been much less explored than the western part of the basin and its mesophotic habitats are virtually unknown.

Revision of the Recent Alvania scabra (Philippi, 1844) complex (Mollusca, Gastropoda, Rissoidae) from the Mediterranean Sea with the description of a new species.

Herein we revise several Recent Mediterranean species of the rissoid genus Alvania Risso, 1826: Alvania scabra (Philippi, 1844), Alvania sculptilis (Monterosato, 1877), Alvania sororcula Granata-Grillo, 1877, Alvania lucinae Oberling, 1970, Alvania josefoi Oliver Templado, 2009 and Alvania scuderii Villari, 2017. They represent a rather homogeneous group of morphologically similar species, referred to as the Alvania scabra complex, which includes also some other species from the northeastern Atlantic. We designate a neotype for Rissoa scabra Philippi, 1844 and a lectotype for Rissoa oranica Pallary, 1900 to stabilize the use of the names.

Reactivation of Myc transcription in the mouse heart unlocks its proliferative capacity.

It is unclear why some tissues are refractory to the mitogenic effects of the oncogene Myc. Here we show that Myc activation induces rapid transcriptional responses followed by proliferation in some, but not all, organs. Despite such disparities in proliferative response, Myc is bound to DNA at open elements in responsive (liver) and non-responsive (heart) tissues, but fails to induce a robust transcriptional and proliferative response in the heart.

Cooperation Between MYC and β-Catenin in Liver Tumorigenesis Requires Yap/Taz.

Background And Aims: Activation of MYC and catenin beta-1 (CTNNB1, encoding β-catenin) can co-occur in liver cancer, but how these oncogenes cooperate in tumorigenesis remains unclear.

Approach And Results: We generated a mouse model allowing conditional activation of MYC and WNT/β-catenin signaling (through either β-catenin activation or loss of APC - adenomatous polyposis coli) upon expression of CRE recombinase in the liver and monitored their effects on hepatocyte proliferation, apoptosis, gene expression profiles, and tumorigenesis. Activation of WNT/β-catenin signaling strongly accelerated MYC-driven carcinogenesis in the liver.

An early Myc-dependent transcriptional program orchestrates cell growth during B-cell activation.

Upon activation, lymphocytes exit quiescence and undergo substantial increases in cell size, accompanied by activation of energy-producing and anabolic pathways, widespread chromatin decompaction, and elevated transcriptional activity. These changes depend upon prior induction of the Myc transcription factor, but how Myc controls them remains unclear. We addressed this issue by profiling the response to LPS stimulation in wild-type and c-myc-deleted primary mouse B-cells.

MYC in Germinal Center-derived lymphomas: Mechanisms and therapeutic opportunities.

The rearrangement of immunoglobulin loci during the germinal center reaction is associated with an increased risk of chromosomal translocations that activate oncogenes such as MYC, BCL2 or BCL6, thus contributing to the development of B-cell lymphomas. MYC and BCL2 activation are initiating events in Burkitt's (BL) and Follicular Lymphoma (FL), respectively, but can occur at later stages in other subtypes such as Diffuse Large-B Cell Lymphoma (DLBCL). MYC can also be activated during the progression of FL to the transformed stage.

p53 Loss in Breast Cancer Leads to Myc Activation, Increased Cell Plasticity, and Expression of a Mitotic Signature with Prognostic Value.

Loss of p53 function is invariably associated with cancer. Its role in tumor growth was recently linked to its effects on cancer stem cells (CSCs), although the underlying molecular mechanisms remain unknown. Here, we show that c-myc is a transcriptional target of p53 in mammary stem cells (MaSCs) and is activated in breast tumors as a consequence of p53 loss.

Catalogue of the primary types of marine molluscan taxa described by Tommaso Allery Di Maria, Marquis of Monterosato, deposited in the Museo Civico di Zoologia, Roma.

We have compiled a complete list of new marine molluscan taxa introduced by Tommaso Allery Di Maria, Marquis of Monterosato (1841-1927). The dates of publication of every single work have been checked against available evidence, and an updated bibliography is also presented. Finally, the type material of all marine taxa expected to be in the collection Monterosato (presently preserved in the Museo Civico di Zoologia in Rome) has been searched in the main collection, and all retrieved specimens have been catalogued.

Therapeutic synergy between tigecycline and venetoclax in a preclinical model of / double-hit B cell lymphoma.

High-grade B cell lymphomas with concurrent activation of the and oncogenes, also known as double-hit lymphomas (DHL), show dismal prognosis with current therapies. activation sensitizes cells to inhibition of mitochondrial translation by the antibiotic tigecycline, and treatment with this compound provides a therapeutic window in a mouse model of -driven lymphoma. We now addressed the utility of this antibiotic for treatment of DHL.

Transcriptional integration of mitogenic and mechanical signals by Myc and YAP.

Mammalian cells must integrate environmental cues to determine coherent physiological responses. The transcription factors Myc and YAP-TEAD act downstream from mitogenic signals, with the latter responding also to mechanical cues. Here, we show that these factors coordinately regulate genes required for cell proliferation.

Integrative analysis of RNA polymerase II and transcriptional dynamics upon MYC activation.

Overexpression of the MYC transcription factor causes its widespread interaction with regulatory elements in the genome but leads to the up- and down-regulation of discrete sets of genes. The molecular determinants of these selective transcriptional responses remain elusive. Here, we present an integrated time-course analysis of transcription and mRNA dynamics following MYC activation in proliferating mouse fibroblasts, based on chromatin immunoprecipitation, metabolic labeling of newly synthesized RNA, extensive sequencing, and mathematical modeling.

FunChIP: an R/Bioconductor package for functional classification of ChIP-seq shapes.

Summary: Chromatin Immunoprecipitation followed by sequencing (ChIP-seq) generates local accumulations of sequencing reads on the genome ("peaks"), which correspond to specific protein-DNA interactions or chromatin modifications. Peaks are detected by considering their total area above a background signal, usually neglecting their shapes, which instead may convey additional biological information. We present FunChIP, an R/Bioconductor package for clustering peaks according to a functional representation of their shapes: after approximating their profiles with cubic B-splines, FunChIP minimizes their functional distance and classifies the peaks applying a k-mean alignment and clustering algorithm.

Opposing macrophage polarization programs show extensive epigenomic and transcriptional cross-talk.

Stimulation of macrophages with interferon-γ (IFN-γ) and interleukin 4 (IL-4) triggers distinct and opposing activation programs. During mixed infections or cancer, macrophages are often exposed to both cytokines, but how these two programs influence each other remains unclear. We found that IFN-γ and IL-4 mutually inhibited the epigenomic and transcriptional changes induced by each cytokine alone.

Genome-wide analysis of p53-regulated transcription in Myc-driven lymphomas.

The tumour suppressor p53 is a transcription factor that controls cellular stress responses. Here, we dissected the transcriptional programmes triggered upon restoration of p53 in Myc-driven lymphomas, based on the integrated analysis of p53 genomic occupancy and gene regulation. p53 binding sites were identified at promoters and enhancers, both characterized by the pre-existence of active chromatin marks.

X-box Binding Protein 1 Regulates Unfolded Protein, Acute-Phase, and DNA Damage Responses During Regeneration of Mouse Liver.

Background & Aims: Liver regeneration after partial hepatectomy (PH) increases the protein folding burden at the endoplasmic reticulum of remnant hepatocytes, resulting in induction of the unfolded protein response. We investigated the role of the core unfolded protein response transcription factor X-box binding protein 1 (XBP1) in liver regeneration using genome-wide chromatin immunoprecipitation analysis.

Methods: We performed studies with C57Bl6-J (control) and interleukin 6-knockout mice.