A Phase 1/2 Study of EG-70 as an Intravesical Administration to Patients With BCG Unresponsive Non-Muscle Invasive Bladder Cancer (NMIBC) and High-Risk NMIBC Patients Who Are BCG Naïve or Received Incomplete BCG Treatment

This study will evaluate the safety and efficacy of intravesical administration of EG-70 in the bladder and its effect on bladder tumors in patients with NMIBC.
This study study consists of two phases; a Phase 1 dose-escalation to establish safety and recommended the phase 2 dose, followed by a Phase 2 study to establish how effective the treatment is.
The Study will include patients with NMIBC with Cis for whom BCG therapy is unresponsive and patients with NMIBC with Cis who are BCG-naïve or inadequately treated.

Start Date22 Apr 2021

Sponsor / Collaborator

enGene, Inc.

100 Clinical Results associated with IL-12R x RIG-I

100 Translational Medicine associated with IL-12R x RIG-I

0 Patents (Medical) associated with IL-12R x RIG-I

Literatures (Medical) associated with IL-12R x RIG-I

01 Jan 2022·The Immunogenetics of Dermatologic DiseasesQ4 · MEDICINE

The Immunogenetics of Psoriasis

Q4 · MEDICINE

Article

Author: Cinotti, Elisa ; Rubegni, Pietro ; Trovato, Emanuele

Psoriasis vulgaris is a chronic immune-mediated dermatological condition, resulting from an interaction between environmental triggers and genetic susceptibilities. Alteration in the production of the inflammatory mediators plays a pivotal part in the pathogenesis of the disease. Genes encoding the mediators of these inflammatory pathways can dictate susceptibility to psoriasis. These genes have a wide range of functions that involve innate immunity (IFIH1, TRAF3IP2, CARD14, c-REL, DDX58), antigen presentation (HLA-Cw6), T-cells development, maturation, and polarization (RUNX1, RUNX3, STAT3), cytokine signaling (IL12Bp40, IL23Ap19, IL23R, JAK2), and immune regulators (TNIP1, TNFAIP3, IL36RN, SOCS1, ZC3H12C, NFKBIA). The risk alleles of these genes can contribute to the overall state of susceptibility to psoriasis by lowering the threshold of the innate immune response that can eventually provoke the pathogenic adaptive immune responses capable of inducing psoriasis. The investigations on genetic associations of psoriasis may allow the discovery of new diseases modifying targets and possibly open a path for the advancement of personalized medicine. They also allow us to discover new aspects of human skin biology.

01 May 2021·Brain PathologyQ1 · MEDICINE

NanoString technology distinguishes anti‐TIF‐1γ⁺ from anti‐Mi‐2⁺ dermatomyositis patients

Q1 · MEDICINE

Article

Author: Koll, Randi ; Schänzer, Anne ; Schneider, Udo ; Eede, Pascale ; Freitag, Kiara ; Froehlich, Waltraud ; Radke, Josefine ; Benveniste, Olivier ; Allenbach, Yves ; Heinzeling, Lucie ; Stenzel, Werner ; Goebel, Hans‐Hilmar ; Preusse, Corinna

AbstractDermatomyositis (DM) is a systemic idiopathic inflammatory disease affecting skeletal muscle and skin, clinically characterized by symmetrical proximal muscle weakness and typical skin lesions. Recently, myositis‐specific autoantibodies (MSA) became of utmost importance because they strongly correlate with distinct clinical manifestations and prognosis. Antibodies against transcription intermediary factor 1γ (TIF‐1γ) are frequently associated with increased risk of malignancy, a specific cutaneous phenotype and limited response to therapy in adult DM patients. Anti‐Mi‐2 autoantibodies, in contrast, are typically associated with classic DM rashes, prominent skeletal muscle weakness, better therapeutic response and prognosis, and less frequently with cancer. Nevertheless, the sensitivity of autoantibody testing is only moderate, and alternative reliable methods for DM patient stratification and prediction of cancer risk are needed. To further investigate these clinically distinct DM subgroups, we herein analyzed 30 DM patients (n = 15 Mi‐2+ and n = 15 TIF‐1 γ+) and n = 8 non‐disease controls (NDC). We demonstrate that the NanoString technology can be used as a very sensitive method to clearly differentiate these two clinically distinct DM subgroups. Using the nCounter PanCancer Immune Profiling Panel™, we identified a set of significantly dysregulated genes in anti‐TIF‐1γ+ patient muscle biopsies including VEGFA, DDX58, IFNB1, CCL5, IL12RB2, and CD84. Investigation of type I IFN‐regulated transcripts revealed a striking type I interferon signature in anti‐Mi‐2+ patient biopsies. Our results help to stratify both subgroups and predict, which DM patients require an intensified diagnostic procedure and might have a poorer outcome. Potentially, this could also have implications for the therapeutic approach.

01 Nov 2015·Journal of AutoimmunityQ1 · MEDICINE

The immunogenetics of Psoriasis: A comprehensive review

Q1 · MEDICINE

Review

Author: Krueger, James G ; Bowcock, Anne M ; Harden, Jamie L

Psoriasis vulgaris is a common, chronic inflammatory skin disease with a complex etiology involving genetic risk factors and environmental triggers. Here we describe the many known genetic predispositions of psoriasis with respect to immune genes and their encoded pathways in psoriasis susceptibility. These genes span an array of functions that involve antigen presentation (HLA-Cw6, ERAP1, ERAP2, MICA), the IL-23 axis (IL12Bp40, IL23Ap19, IL23R, JAK2, TYK2), T-cell development and T-cells polarization (RUNX1, RUNX3, STAT3, TAGAP, IL4, IL13), innate immunity (CARD14, c-REL, TRAF3IP2, DDX58, IFIH1), and negative regulators of immune responses (TNIP1, TNFAIP3, NFKBIA, ZC3H12C, IL36RN, SOCS1). The contribution of some of these gene products to psoriatic disease has also been revealed in recent years through targeting of key immune components, such as the Th17/IL-23 axis which has been highly successful in disease treatment. However, many of the genetic findings involve immune genes with less clear roles in psoriasis pathogenesis. This is particularly the case for those genes involved in innate immunity and negative regulation of immune specific pathways. It is possible that risk alleles of these genes decrease the threshold for the initial activation of the innate immune response. This could then lead to the onslaught of the pathogenic adaptive immune response known to be active in psoriatic skin. However, precisely how these various genes affect immunobiology need to be determined and some are speculated upon in this review. These novel genetic findings also open opportunities to explore novel therapeutic targets and potentially the development of personalized medicine, as well as discover new biology of human skin disease.

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