A5050993162- Cancer Immunotherapy and Biomarkers
- Ferroptosis and cancer prognosis
- RNA modifications and cancer
- Immune cells in cancer
- Immunotherapy and Immune Responses
- Adenosine and Purinergic Signaling
- Nanoplatforms for cancer theranostics
- Cell Image Analysis Techniques
- Galectins and Cancer Biology
- Neurological Disease Mechanisms and Treatments
- Cancer-related molecular mechanisms research
- Epigenetics and DNA Methylation
- Single-cell and spatial transcriptomics
- Barrier Structure and Function Studies
McGill University
2023-2024
The tumor-immune microenvironment (TIME) is a critical determinant of therapeutic response. However, the mechanisms regulating its modulation are not fully understood. HER2Δ16, an oncogenic splice variant HER2, has been implicated in breast cancer and other tumor types as driver tumorigenesis metastasis. Nevertheless, underlying HER2Δ16-mediated oncogenicity remain poorly Here, we show that HER2∆16 expression exclusive to clinically HER2+ subtype associates with poor clinical outcome cancer....
Abstract Triple-negative breast cancer (TNBC) accounts for 15% of cancers and is the most aggressive subtype lacking precision oncology therapeutic strategies. Standard-of-care predominantly chemotherapy in neoadjuvant setting (NACT). Despite good responses, ∼40% TNBC patients develop resistance present residual disease at surgery. Overcoming implementing better options critical. Our objectives are to targeting opportunities drug tolerant persister (DTP) cells which underlie disease. Using...
e21517 Background: Up to 60% of metastatic melanoma patients develop brain metastases, and 5% leptomeningeal disease (LD), which presents with the worst prognosis any metastasis (MBM) infiltration pattern. Median survival duration for MBM is ~12 months, however LD it can be < 10 weeks. The spatial immune landscape without remains poorly understood. Methods: To spatially characterize tumor microenvironment (TME) MBM, we performed CyTOF Imaging Mass Cytometry (CyTOF-IMC) on a highly...
<div>Abstract<p>The tumor immune microenvironment (TIME) is a critical determinant of therapeutic response. However, the mechanisms regulating its modulation are not fully understood. HER216, an oncogenic splice variant human epidermal growth factor receptor (HER2), has been implicated in breast cancer and other types as driver tumorigenesis metastasis. Nevertheless, underlying HER2Δ16-mediated oncogenicity remain poorly Here, we show that HER2∆16 expression exclusive to...
<p>Legends for Supp. Figures S1-20</p>
<p>Legends for Supp. Figures S1-20</p>
<p>Supp. Figures S1-20</p>
<p>Supp. Figures S1-20</p>
<div>Abstract<p>The tumor–immune microenvironment (TIME) is a critical determinant of therapeutic response. However, the mechanisms regulating its modulation are not fully understood. HER2Δ16, an oncogenic splice variant HER2, has been implicated in breast cancer and other tumor types as driver tumorigenesis metastasis. Nevertheless, underlying HER2Δ16-mediated oncogenicity remain poorly Here, we show that HER2∆16 expression exclusive to clinically HER2<sup>+</sup>...
<p>Supp. Figures S1-20</p>
<p>Legends for Supp. Figures S1-20</p>
<div>Abstract<p>The tumor–immune microenvironment (TIME) is a critical determinant of therapeutic response. However, the mechanisms regulating its modulation are not fully understood. HER2Δ16, an oncogenic splice variant HER2, has been implicated in breast cancer and other tumor types as driver tumorigenesis metastasis. Nevertheless, underlying HER2Δ16-mediated oncogenicity remain poorly Here, we show that HER2∆16 expression exclusive to clinically HER2<sup>+</sup>...
<p>Legends for Supp. Figures S1-20</p>
<p>Supp. Figures S1-20</p>
<p>Legends for Supp. Figures S1-20</p>
<div>Abstract<p>The tumor–immune microenvironment (TIME) is a critical determinant of therapeutic response. However, the mechanisms regulating its modulation are not fully understood. HER2Δ16, an oncogenic splice variant HER2, has been implicated in breast cancer and other tumor types as driver tumorigenesis metastasis. Nevertheless, underlying HER2Δ16-mediated oncogenicity remain poorly Here, we show that HER2∆16 expression exclusive to clinically HER2<sup>+</sup>...
<p>Supp. Figures S1-20</p>
<p>Legends for Supp. Figures S1-20</p>
<p>Supp. Figures S1-20</p>