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Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Nanostring]

ABSTRACT: Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Nanostring]

PROVIDER: PRJNA749276 | ENA |

REPOSITORIES: ENA

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Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Nanostring]

Project description:To find metastatic recurrence biomarkers of triple negative breast cancer (TNBC) treated by neoadjuvant chemotherapy and anti-EGFR antibodies (NAT), we evaluated tumor genomic, transcriptomic and immune features, using MSK-IMPACT assay, gene arrays, Nanostring technology and TIL assessment on H&E. Six patients experienced a rapid fatal recurrence (RR) and other 6 had later non-fatal recurrences (LR). Before NAT, RR had low expression of 6 MHC class I and 13 MHC class II genes but were enriched in upregulated genes involved in the cell cycle-related pathways. Their TIL number before NAT in RR was very low (<5%) and did not increase after treatment. In post-NAT residual tumors, RR cases showed high expression of SOX2 and CXCR4. Our results indicate that high expression of cell cycle genes, combined with cold immunological phenotype, may predict strong TNBC resistance to NAT and rapid progression after it. This biomarker combination is worth validation in larger studies.

2021-07-26 | GSE180717 | GEO

Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Agilent]

2021-07-28 | GSE180775 | GEO

Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Agilent]

Project description:Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy combined with anti-EGFR antibodies [Agilent]

| PRJNA749501 | ENA

Neoadjuvant sintilimab plus chemotherapy in early-stage EGFR-mutant NSCLC: phase 2 trial interim results (NEOTIDE/CTONG2104)

Project description:We launched an investigator-initiated, Simon’s two-stage design trial of neoadjuvant sintilimab combined with carboplatin and nab-paclitaxel (nab-PC) in early-stage EGFR-mutant NSCLC (Clinicaltrial.gov number NCT05244213). Here we report the first interim results of stage 1 cohort which met the overall primary endpoint in advance, and multi-omics profiling of neoadjuvant immunotherapy combination in early-stage EGFR-mutant patients. We performed in-depth single-cell RNA/TCR sequencing (scRNA/TCR-seq) of cells derived from 11 resected tumors as well as 34 tumors from real-world cohort which were all confirmed wild-type lung adenocarcinoma (LUAD) or adeno-squamous carcinoma (ASC) and received neoadjuvant immunochemotherapy as control. By associating the tumor microenvironment (TME) and with responses, we uncovered heterogeneous mechanisms of primary resistance, providing insights into further strategic developments of combination regimens to improve the clinical outcome of EGFR-mutant NSCLC patients.

2024-05-17 | GSE241934 | GEO

Response and recurrence correlates in patients treated with neoadjuvant anti-PD-1 therapy for resectable oral-cavity squamous cell carcinoma

Project description:Neoadjuvant PD-1 blockade may be efficacious in patients with high-risk, resectable oral-cavity, head-and-neck cancer. To explore correlates of response patterns to neoadjuvant nivolumab treatment and post-surgical recurrences, we analyzed longitudinal tumor and blood samples in a cohort of 12 patients displaying 33% responsiveness. Pretreatment tumor-based detection of FLT4 mutations and PTEN signature enrichment favors response, and high tumor mutational burden improves recurrence-free survival. In contrast, preexisting and/or acquired mutations (in CDKN2A, YAP1, JAK2) correlate with innate resistance and/or tumor recurrence. Immunologically, tumor response after therapy entails T-cell receptor repertoire diversification in peripheral blood and intratumoral expansion of preexisting T-cell clones. A high ratio of regulatory to Th17 T cells in pretreatment blood predicts innate resistance, low cytolytic T-cell signature in pretreatment tumor, and low T-cell receptor repertoire diversity in pretreatment blood. Our study provides a molecular framework to advance neoadjuvant anti-PD-1 therapy for patients with resectable head-and-neck cancer.

2021-09-30 | GSE179730 | GEO

Recurrence biomarkers of triple negative breast cancer treated with neoadjuvant chemotherapy and anti-EGFR antibodies.

Project description:To find metastatic recurrence biomarkers of triple-negative breast cancer (TNBC) treated by neoadjuvant chemotherapy and anti-EGFR antibodies (NAT), we evaluated tumor genomic, transcriptomic, and immune features, using MSK-IMPACT assay, gene arrays, Nanostring technology, and TIL assessment on H&E. Six patients experienced a rapid fatal recurrence (RR) and other 6 had later non-fatal recurrences (LR). Before NAT, RR had low expression of 6 MHC class I and 13 MHC class II genes but were enriched in upregulated genes involved in the cell cycle-related pathways. Their TIL number before NAT in RR was very low (<5%) and did not increase after treatment. In post-NAT residual tumors, RR cases showed high expression of SOX2 and CXCR4. Our results indicate that high expression of cell cycle genes, combined with cold immunological phenotype, may predict strong TNBC resistance to NAT and rapid progression after it. This biomarker combination is worth validation in larger studies.

| S-EPMC8448841 | biostudies-literature

EGFR pathway expression persists in recurrent glioblastoma independent of amplification status

Project description:Background: Glioblastoma mortality is driven by tumour progression or recurrence despite administering a therapeutic arsenal consisting of surgical resection, radiation, and alkylating chemotherapy. The genetic changes underlying tumour progression and chemotherapy resistance are poorly understood. Methods: In this work, we sought to define the relationship between EGFR amplification status, EGFR mRNA expression, and EGFR pathway activity. We compared RNA-sequencing data from matched primary and recurrent tumour samples (N = 40 patients, 20 with EGFR amplification). Results: In the setting of glioblastoma recurrence, the EGFR pathway was overexpressed regardless of EGFR amplification status, suggesting a common genomic endpoint in recurrent glioblastoma, although EGFR amplification did associate with higher EGFR mRNA expression. Three of forty patients in the study cohort had EGFR-amplified tumours and received targeted EGFR therapy. Their molecular subtypes and clinical outcomes did not significantly differ from patients who received conventional chemotherapy. Conclusion: Our findings suggest that while the EGFR amplification may confer a unique molecular profile in primary glioblastoma, pathway analysis reveals upregulation of the EGFR pathway in recurrence, regardless of amplification status. As such, the EGFR pathway may be a key mediator of glioblastoma progression.

2023-01-25 | GSE222515 | GEO

Neoadjuvant use of oncolytic herpes virus G47Δ prevents local recurrence after insufficient resection in tongue cancer models

Project description:Mice with orthotopic tongue cancer received neoadjuvant G47Δ therapy. Neoadjuvant G47Δ and resection led to 10/10 survival even with insufficient resection margins.

2023-04-13 | GSE227813 | GEO

Notch3-dependent beta-catenin signaling mediates EGFR TKI drug persistence in EGFR mutant NSCLC

Project description:EGFR tyrosine kinase inhibitors cause dramatic responses in EGFR-mutant lung cancer, but resistance universally develops. The involvement of β-catenin in EGFR TKI resistance has been previously reported however the precise mechanism by which β-catenin activation contributes to EGFR TKI resistance is not clear. Here, we show that EGFR inhibition results in the activation of β-catenin signaling in a Notch3-dependent manner, which facilitates the survival of a subset of cells that we call “adaptive persisters”. We previously reported that EGFR-TKI treatment rapidly activates Notch3, and here describe the physical association of Notch3 with β-catenin, leading to increased stability and activation of β-catenin. We demonstrate that the combination of EGFR-TKI and a β-catenin inhibitor inhibits the development of these adaptive persisters, decreases tumor burden, improves recurrence free survival, and overall survival in xenograft models. These results supports combined EGFR-TKI and β-catenin inhibition in patients with EGFR mutant lung cancer.

2018-08-31 | GSE115864 | GEO

Systemic LRG1 expression in melanoma is associated with disease progression and recurrence

Project description:Treatment of late-stage melanoma patients with immune checkpoint blockade (ICB) is currently one of the most effective standard therapies. The response rates upon neoadjuvant ICB in stage III melanoma are higher as compared to stage IV disease. Given that successful ICB depends on systemic immune response, we hypothesized that systemic immune suppression might be a mechanism responsible for lower response rates in late-stage disease, and also potentially with disease recurrence in early-stage disease.

2024-01-09 | PXD040399 | Pride

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