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Immunological Variables Associated to ICI Toxicity in Cancer Patients

ABSTRACT: This is a monocentric, prospective, pilot study that will enrol 435 subjects with solid tumours that are treated with immune checkpoint inhibitor(s) (ICI) alone or in combination with chemotherapy or targeted therapy. For enrolled subjects, clinical and laboratory evaluations will be performed and reported at different time points: * Early (4-6 weeks after treatment start) * Midtime (8-11 weeks after treatment start) * Late (13-18 weeks after treatment start) * At the occurrence of immune-related adverse events (irAEs), clinical and laboratory evaluation will be performed at two principal time points: * For the 1st time of any grade 1 or 2 irAE if the subject developed it. * For the 1st time of any grade 3 or 4 irAE if the subject developed it.

DISEASE(S): Gastrointestinal Neoplasms,Carcinoma,Melanoma,Small Cell Lung Cancer,Gastrointestinal Cancer,Small Cell Lung Carcinoma,Non Small Cell Lung Cancer,Mesothelioma,Bladder Cancer,Msi-h Colorectal Cancer,Merkel Cell Carcinoma,Breast Cancer,Non-melanoma Skin Cancer,Lung Neoplasms,Carcinoma, Merkel Cell,Head And Neck Cancer,Mesothelioma, Malignant,Renal Cell Carcinoma,Hepatocellular Carcinoma

PROVIDER: 2736653 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Project description:A number of human neurodegenerative diseases result from the expansion of a glutamine repeat within the disease-causing protein. Spinocerebellar ataxia type1 is one such disease, caused by expansion of a polyglutamine tract in the novel protein ataxin-1. To faithfully model SCA1 in the mouse, we generated knock-in mice carrying 154 CAG repeats in the mouse Sca1 locus. These mice reproduced many aspects of the human disease. Despite ubiquitous expression of the mutant protein, they developed slowly progressive selective neurodegeneration , which is most distinct in Purkinje cells and spinal cord. Alterations in gene expression have been proposed to be involved in the pathogenesis of polyglutamine disease including SCA1, but the changes of gene expression in an authentic disease model have not been characterized. We believe that knowledge of these genes will give insight into the pathophysiology of SCA1 and may ultimately be relevant to the treatment of SCA1. We will determine gene expression patterns in the cerebellum and forebrain at three different time points. We propose that the genes whose expression is affected by mutant ataxin-1 expression are effectors for neuronal dysfunction and neuronal degeneration in the knock-in mice. We also hypothesize the difference in the expression levels of these genes accounts for selective vulnerability of neurons. We will examine three time points: 4 weeks, 11 weeks, and 20 weeks of age. We have shown that the mice developed motor incoordination as revealed by rotating rod test as early as 5 weeks of age but it was not until 10 weeks that they start showing clear neurological phenotype such as clasping. At each point, we will compare the pattern between the mutant and wild-type littermate. Animals will be prepared and sacrificed by a standard procedure. Cerebellum and spinal cord are the most affected areas whereas forebrain shows less neurodegeneration. Tissue will be rapidly dissected from cerebellum and forebrain, frozen in liquid nitrogen, and stored at ?80 C until analysis. Tissues will be sent to the centers (as opposed to RNA). We will be providing 9 tissue samples from three litters for each time point to mitigate any expression differences resulting from subtle differences of procedure or environment where the mice grow. Keywords: time-course

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Immunological Variables Associated to ICI Toxicity in Cancer Patients

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