Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mutagenesis sensitizes murine models of triple negative breast cancer to immunotherapy

ABSTRACT: Mutagenesis sensitizes murine models of triple negative breast cancer to immunotherapy

PROVIDER: PRJNA561596 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10069035_1.fastq.gz	Fastqsanger.gz
	SRR10069035_2.fastq.gz	Fastqsanger.gz
	SRR10069036_1.fastq.gz	Fastqsanger.gz
	SRR10069036_2.fastq.gz	Fastqsanger.gz
	SRR10069037_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 32

Similar Datasets

Mutagenesis sensitizes murine models of triple negative breast cancer to immunotherapy

Project description:This study identifies mechanisms of response to immune checkpoint inhibition in mouse models of triple negative breast cancer.

2019-11-13 | GSE136206 | GEO

Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy

Project description:Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy

| PRJNA1368989 | ENA

Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy

Project description:Despite the widespread adoption of chemo-immunotherapy in triple-negative breast cancer (TNBC), how cytotoxic chemotherapy engages antitumor immunity remains poorly defined. Here, we identify cytosolic single-stranded DNA (ssDNA) accumulation as the mechanistic bridge linking genotoxic stress to immune activation. By integrating in vivo TREX1-deficiency transcriptional signatures, we show that ssDNA-driven immunostimulatory programs—rather than TREX1 expression—robustly predict clinical response to chemo-immunotherapy across independent TNBC cohorts. Through a chemotherapeutic screen, we identify LP-184, an acylfulvene-derived alkylating agent in clinical development, as a potent pharmacologic inducer of cytosolic ssDNA and type I interferon signaling. LP-184 enhances antigen presentation, reduces M2-like tumor-suppressive macrophages, and promotes CD8⁺ T-cell priming, thereby synergizing with anti-PD-1 therapy in vivo. These findings redefine the interface between DNA damage and immune activation, establishing ssDNA-driven immune programs as both a predictive biomarker and a therapeutic axis for next-generation chemo-immunotherapy design.

2026-06-20 | GSE311343 | GEO

Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy [scRNA-seq]

Project description:Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy [scRNA-seq]

| PRJNA1369543 | ENA

Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy [RNA-Seq]

Project description:Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy [RNA-Seq]

| PRJNA1391488 | ENA

Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy [RNA-Seq]

2026-06-20 | GSE314549 | GEO

Chemotherapeutic Induction of Single-Stranded DNA Accumulation Sensitizes Triple-Negative Breast Cancer to Immunotherapy [scRNA-seq]

2026-06-20 | GSE311488 | GEO

Murine models for triple-negative breast cancer with differential responsiveness to immunotherapy

Project description:Breast cancer is the most common cancer diagnosis in women. Clinical studies with triple-negative breast cancer (TNBC) are encouraging for immunotherapy combined with chemotherapy (aPD-1 with paclitaxel and/or carboplatin). However, additional clinical advances may be pursued more rapidly with assistance from preclinical TNBC models including syngeneic mammary tumor cell lines. Here, we report two mammary tumor cell lines that exhibit differential responsiveness to immunotherapy in vivo. Spontaneous mammary tumors from C57BL/6J MMTV-Cre Trp53fl/+ animals were passaged serially in cell culture and in vivo in the mammary fat pad of fully wildtype animals. The resulting lines, MM001i and MM008i, lost Trp53 and formed 1000 mm3 tumors in the mammary fat pad within 21-28 days. Despite originating from the same genetic background, these lines exhibit differential responses to immunotherapy. For aPD-1 therapy, MM001i is poorly responsive and MM008i is strongly responsive with near-complete tumor regression. In comparison, both MM001i and MM008i respond rapidly to aCTLA-4 therapy. Both models express unique tumor antigens as evidenced by immunity to subsequent engraftments. Primary MM008i tumors exhibit greater T cell infiltration, and CD8-positive T lymphocytes are required for aPD-1 responses. These TNBC models are promising for further mechanistic studies and testing future single and combinatorial therapies.

2026-01-30 | GSE305800 | GEO

Blocking Fra-1 sensitizes triple-negative breast cancer to olaparib

Project description:Blocking Fra-1 sensitizes triple-negative breast cancer to olaparib

| PRJNA629373 | ENA

Murine models for triple-negative breast cancer with differential responsiveness to immunotherapy [scRNA-Seq]

2026-01-30 | GSE305842 | GEO