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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [TCR-seq]

ABSTRACT: ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [TCR-seq]

PROVIDER: PRJNA1006385 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25665200_1.fastq.gz	Fastqsanger.gz
	SRR25665200_2.fastq.gz	Fastqsanger.gz
	SRR25665201_1.fastq.gz	Fastqsanger.gz
	SRR25665201_2.fastq.gz	Fastqsanger.gz
	SRR25665202_1.fastq.gz	Fastqsanger.gz

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [TCR-seq]

Project description:Unlike many other hematologic malignancies, Richter syndrome (RS), an aggressive B cell lymphoma originating from indolent chronic lymphocytic leukemia, is responsive to PD-1 blockade. To discover the determinants of response, we analyzed single-cell transcriptome data generated from 17 bone marrow samples longitudinally collected from 6 RS patients. Response was associated with intermediate exhausted CD8 effector/effector memory T cells marked by high expression of the transcription factor ZNF683, determined to be evolving from stem-like memory cells and divergent from terminally exhausted cells. This signature overlapped with that of tumor-infiltrating populations from PD-1 responsive solid tumors. ZNF683 was found to directly target key T cell genes (TCF7, LMO2, CD69) and impact pathways of T cell cytotoxicity and activation. Analysis of pre-treatment peripheral blood from 10 independent RS PD-1 treated patients, as well as solid tumor PD-1 treated patients, supported an association of ZNF683high T cells with response.

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [CUT&RUN]

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [RNA-Seq]

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome

Project description:ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [CUT&RUN]

Project description:ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [CUT&RUN]

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [RNA-Seq]

Project description:ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome [RNA-Seq]

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Cancer specific tissue-resident memory T cells expressed ZNF683 up-regulated by autocrine IFN-γin colorectal cancer

Project description:Tissue-resident memory T (Trm) cells express CD103 to be maintained in the local microenvironment and to be strongly involved in local immunity of epithelial tissue. Trm has been associated with cytotoxicity in pathologies of not only virus infection and autoimmune disease but also many cancers. Tumor infiltration by CD103+ Trm cells was associated with patient survival in colorectal cancer. Tumor infiltrating CD103+ Trm cells were comprised predominantly of CD8 T cells expressing cytotoxic activation and immune check-point molecules called exhausted markers. Therefore, we focused on ZNF683 as a marker of cancer-specific Trm. The expression of ZNF683 in Trm was up-regulated by TCR and IFN-γ signaling that was positive feedback by autocrine IFN-γ. These results indicate that IFN-γ and TCR signaling and ZNF683 are involved in the activation of Trm in tumor and would be promising targets for regulation of cancer immunity.

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ZNF683 marks a CD8+ T cell population associated with anti-tumor immunity following anti-PD-1 therapy for Richter syndrome

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Genomic profiling of Richter-syndrome Chronic Lymphocytic Leukemia

Project description:Richter syndrome (RS) occurs in up to 15% of patients with chronic lymphocytic leukemia (CLL). While RS, usually represented by the histologic transformation to a diffuse large B-cell lymphoma (DLBCL), is associated with a very poor outcome, especially when clonally related to the pre-existing CLL, mechanisms leading to RS have not been clarified yet. To better understand the pathogenesis of RS, we analyzed a series of cases including: 59 RS, 28 CLL-phase of RS, 315 CLL and 127 de novo DLBCL. RS demonstrated a genomic complexity intermediate between CLL and DLBCL. Cell cycle deregulation via inactivation of TP53 and of CDKN2A was a main mechanism in the histologic transformation from CLL-phase, being present in approximately half of the cases, and affected the outcome of the RS patients. A second major subgroup was characterized by the presence of trisomy 12 and comprised one third of the cases. While RS shared some of the lesions seen in de novo DLBCL, its genomic profile was clearly separate. The CLL-phase preceding RS had not a generalized increase in genomic complexity when compared with untransformed CLL, but it presented clear differences in the frequency of specific genetic lesions. Genomic profiling of Richter-syndrome Chronic Lymphocytic Leukemia

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