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Dynamics of genomic and immune responses during primary immunotherapy resistance in mismatch repair deficient tumors

ABSTRACT: Dynamics of genomic and immune responses during primary immunotherapy resistance in mismatch repair deficient tumors

PROVIDER: PRJNA671439 | ENA |

REPOSITORIES: ENA

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Dynamics of genomic and immune responses during primary immunotherapy resistance in mismatch repair deficient tumors

Project description:Dynamics of genomic and immune responses during primary immunotherapy resistance in mismatch repair deficient tumors

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Tislelizumab for the Treatment of Recurrent Mismatch Repair Deficient Endometrial Cancer

Project description:This clinical trial evaluates the effect of tislelizumab in treating patients with mismatch repair deficient endometrial cancer that has come back (recurrent). Deoxyribonucleic acid (DNA) mismatch repair (MMR) is a system for recognizing and repairing DNA errors and damage. Mismatch repair deficient tumors (dMMR) may have difficulty repairing DNA mutations during replication that may affect tumor’s response to therapy. Immunotherapy with monoclonal antibodies, such as tislelizumab, may help the body’s immune system attack the cancer, and may interfere with the ability of tumor cells to grow and spread. Giving tislelizumab may help treat patients with mismatch repair deficient endometrial cancer.

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Dynamics of genomic and immune responses during primary immunotherapy resistance in mismatch repair-deficient tumors.

Project description:Mismatch repair-deficient (dMMR) cancers generate a substantial number of immunogenic neoantigens, rendering them sensitive to immunotherapy. Yet, there is considerable variability in responses, and roughly one-half of dMMR cancers are refractory to immunotherapy. Here we study a patient with dMMR lung cancer refractory to immunotherapy. The tumor exhibited typical dMMR molecular features, including exceptionally high frameshift insertions and deletions (indels). Despite the treatment inducing abundant intratumoral T-cell infiltrates, it failed to elicit tumor regression, pointing to the T cells lacking cytotoxic activity. A post-treatment tumor demonstrated compound heterozygous frameshift deletions located upstream of the kinase domain in the gene encoding JAK1 protein, down-regulation of JAK1 and mediators of its signal transduction, and total loss of JAK1 phosphorylation. Importantly, one of the JAK1 mutations, despite not being detected in the pretreatment tumor, was found at low variant allele frequency in the pretreatment circulating tumor DNA, suggesting clonal selection of the mutation. To our knowledge, this report provides the most detailed look yet at defective JAK1 signaling in the context of dMMR and immunotherapy resistance. Together with observations of JAK1 frameshift indels being enriched in dMMR compared with MMR-proficient tumors, our findings demonstrate the critical function of JAK1 in immunological surveillance of dMMR cancer.

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Novel Mechanisms of Antibiotic Resistance in Mismatch Repair-Deficient Pseudomonas aeruginosa hypermutators

Project description:Using in vitro directed evolution, we show that mismatch repair-deficient Pseudomonas aeruginosa can engage novel resistance mechanisms to ceftazidime-avibactam.

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Project description:We used Affymetrix microarrays to determine the cisplatin-induced gene expression changes in E. coli deficient in dam and mismatch repair (dam, dam mutS, and mutS mutant strains). E. coli deficient in dam are hypersensitive to cisplatin. However introducing an additional mutation in mismatch repair (i.e., a mutation in mutS or mutL) abrogates this sensitivity and essentially restores wildtype levels of resistance. Keywords: Drug-induced expression

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Project description:Transcriptomic evaluation of mismatch repair defects

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Project description:Rhesus Macaque Model of Mismatch Repair-Deficient Colorectal Cancer

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