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RNA-Seq profiling of pre- and on-treatment tumor samples from breast cancer patients enrolled in the NeoTRIP trial.

ABSTRACT: Triple-negative breast cancer (TNBC) is immunogenic, but only a subset of patients benefits from neoadjuvant immune checkpoint inhibitors (ICIs) combined with chemotherapy. Predictive biomarkers to guide patient selection and treatment adaptation are lacking. In the NeoTRIPaPDL1 (NeoTRIP) Phase III trial, 280 high-risk TNBC patients were randomized to neoadjuvant carboplatin plus nab-paclitaxel (CT, n=142) or the same regimen with atezolizumab (CT/A, n=138). Tumor biopsies were collected at baseline and on the first day of the second cycle (D1C2). Longitudinal transcriptome sequencing and analyses of selected gene signatures were performed, including hallmark, ferroptosis-related, and immune cell type–specific signatures. Treatment-induced gene expression changes and association with pathological complete response were investigated.

ORGANISM(S): Homo sapiens

PROVIDER: GSE319641 | GEO | 2026/05/26

REPOSITORIES: GEO

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			Action	DRS
		Other
	GSE319641_NeoTRIP_baseline_D1C2_TPM_ComBat_all_samples.txt.gz	Txt

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Project description:Purpose:Triple negative breast cancer (TNBC) commonly metastasizes to the brain and predicts poor prognosis with limited therapeutic options. TNBC frequently harbors BRCA mutations translating to platinum sensitivity; platinum response may be augmented by additional suppression of DNA repair mechanisms through poly(ADP-ribose)polymerase (PARP) inhibition. We evaluated brain penetrance and efficacy of Carboplatin +/- the PARP inhibitor ABT888, and investigated gene expression changes in murine intracranial (IC) TNBC models stratified by BRCA and molecular subtype status. Experimental design:Athymic mice were inoculated intra-cerebrally with BRCA-mutant: SUM149 (basal), MDA-MB-436 (claudin-low), or BRCA-wild-type: MDA-MB-468 (basal), MDA-MB-231BR (claudin-low) TNBC cells and treated with PBS control (IP, weekly), Carboplatin (50mg/kg/week, IP), ABT888 (25mg/kg/day, OG), or their combination. DNA-damage (?-H2AX) and apoptosis (cleaved-Caspase-3(cC3)) were assessed via IHC of IC tumors. Gene expression of BRCA-mutant IC tumors was measured. Results: Carboplatin+/-ABT888 significantly improved survival in BRCA-mutant IC models compared to control, but did not improve survival in BRCA-wild-type IC models. Carboplatin+ABT888 revealed a modest survival advantage versus Carboplatin in BRCA-mutant models. ABT888 yielded a marginal survival benefit in the MDA-MB-436 but not in the SUM149 model. BRCA-mutant SUM149 expression of ?-H2AX and cC3 proteins was elevated in all treatment groups compared to Control, while BRCA-wild-type MDA-MB-468 cC3 expression did not increase with treatment. Carboplatin treatment induced common gene expression changes in BRCA-mutant models.Conclusions: Carboplatin+/-ABT888 improves survival in BRCA-mutant IC TNBC models with corresponding DNA damage and gene expression changes. Combination therapy represents a promising treatment strategy for patients with TNBC brain metastases warranting further clinical investigation. reference x sample

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RNA-Seq profiling of pre- and on-treatment tumor samples from breast cancer patients enrolled in the NeoTRIP trial.

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