A5065774987- Cancer Immunotherapy and Biomarkers
- Immunotherapy and Immune Responses
- CAR-T cell therapy research
- Immune Cell Function and Interaction
- Pancreatic and Hepatic Oncology Research
- Phagocytosis and Immune Regulation
- Bacterial biofilms and quorum sensing
- Cancer Genomics and Diagnostics
- Photoreceptor and optogenetics research
- T-cell and B-cell Immunology
- vaccines and immunoinformatics approaches
- Ferroptosis and cancer prognosis
- Nanoparticles: synthesis and applications
- Immune cells in cancer
Massachusetts Institute of Technology
2022-2025
Koch Institute for Integrative Cancer Research At MIT
2021-2023
Allen Institute
2021-2023
IIT@MIT
2021
Abstract Tumor cell–intrinsic signaling pathways can drastically affect the tumor immune microenvironment, promoting progression and resistance to immunotherapy by excluding immune-cell populations from tumor. Several have been reported modulate myeloid-cell T-cell infiltration creating “cold” tumors. However, clinical evidence suggests that cytotoxic T cells core also mediates evasion. Here, we find SOX2 in non-small cell lung cancer induces exclusion of promotes checkpoint blockade...
<div>Abstract<p>Tumor cell–intrinsic signaling pathways can drastically affect the tumor immune microenvironment, promoting progression and resistance to immunotherapy by excluding cell populations from tumor. Several have been reported modulate myeloid-cell T-cell infiltration, creating “cold” tumors. However, clinical evidence suggests that cytotoxic T cells core also mediates evasion. In this study, we find SOX2 in non–small lung cancer induces exclusion of promotes checkpoint...
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Abstract Tumor-intrinsic signaling pathways can drastically affect the tumor immune microenvironment (TME), promoting progression and resistance to immunotherapy by excluding cell populations from tumor. Several tumor-cell intrinsic have been reported myeloid infiltration downstream T infiltration. Clinical evidence suggests that exclusion of cytotoxic cells core likewise mediates resistance. Here, we find cell-intrinsic SOX2 expression induces promotes checkpoint blockade therapy. CD8 + was...
Abstract Pancreatic ductal Adenocarcinoma (PDAC) is an aggressive malignancy complicated by poor early diagnosis and a lack of response to traditional treatments. It characterized desmoplastic stroma, infiltration activation T cells, low mutational burden. The genetic landscape PDAC defined activating KRAS mutations (~90%) p53 alterations (~70%), but the molecular switches perturbed these aberrations remain unclear. missense mutations, unlike resulting in loss p53, are considered acquire...
Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer without effective treatments. It characterized by activating KRAS mutations and p53 alterations. However, how these dysregulate cancer-cell-intrinsic gene programs to influence the immune landscape of tumor microenvironment (TME) remains poorly understood. Here, we show that
<h3>Background</h3> Conventional dendritic cells (cDC) are critical mediators of protective anti-tumor CD8<sup>+</sup> T-cell responses.<sup>1</sup> Batf3-driven DC1 the predominant cDC subset driving immunity due to their specialized ability cross-present antigens for activation.<sup>2–4</sup> However, contribution other tumor-infiltrating DC subsets such as CD11b<sup>+</sup> DC2 remains poorly characterized. Recent studies suggest that under inflammation, can exist in various functional...
Abstract The small size of nanoparticles is both an advantage and a problem. Their high surface-area-to-volume ratio enables novel medical, industrial, commercial applications. However, their also allows them to evade conventional filtration during water treatment, posing health risks humans, plants, aquatic life. This project aims remove wastewater treatment using genetically modified Escherichia coli in two ways: 1) binding citrate-capped with the membrane protein Proteorhodopsin, 2)...
<h3>Background</h3> Although failure to respond checkpoint blockade immunotherapies is frequently associated with a lack of T-cell infiltration into the tumor, clinical data suggests that in patients lung cancer, T-cell-inflamed tumors can also be resistant therapy.<sup>1</sup> Work by us identified immunotherapy resistance cancer driven cancer-specific CD8<sup>+</sup> dysfunction, characterized reduced cytolytic capacity and established during priming mediastinal lymph nodes...
<h3>Background</h3> Checkpoint blockade therapy (CBT) can effectively treat lung tumors; however, only 30% of cancer patients respond to CBT [1]. Clinical data showed that with low T cell infiltration in the tumor microenvironment (TME) poorly [2]. Gaining insight into molecular and immunological mechanism impact entry CD8 cells TME will enable development innovative therapeutic approaches be used combination individuals cancer. Using a gene signature, we segregated NSCLC cell-infiltrated...