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Yi He

Researcher at University of Texas MD Anderson Cancer Center

Publications -  5
Citations -  200

Yi He is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Internal medicine & Stromal cell. The author has an hindex of 3, co-authored 3 publications receiving 174 citations.

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The selective hypoxia inducible factor-1 inhibitor PX-478 provides in vivo radiosensitization through tumor stromal effects.

TL;DR: It is shown that PX-478 prevents postradiation HIF-1 signaling and abrogates downstream stromal adaptation in C6 and HN5 reporter xenografts as measured by serial ultrasound, vascular magnetic resonance imaging, and hypoxia response element–specific micro–positron emission tomography imaging.
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Radiosensitization and Stromal Imaging Response Correlates for the HIF-1 Inhibitor PX-478 Given with or without Chemotherapy in Pancreatic Cancer

TL;DR: PX-478 is a mechanistically appealing and potentially clinically relevant enhancer of pancreatic cancer radiosensitivity, inhibiting tumor and stromal HIF-1 proangiogenic signaling and reducing the innate radiation resistance of hypoxic tumor cells.
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HIF-1–Dependent Stromal Adaptation to Ischemia Mediates In Vivo Tumor Radiation Resistance

TL;DR: The results illustrate that tumor radioresistance is mediated by a capacity to compensate for stromal vascular disruption through HIF-1–dependent proangiogenic signaling and that clinically relevant vascular imaging techniques can spatially define mechanisms associated with tumor irradiation.
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Multifunctional co-transport carriers based on cyclodextrin assembly for cancer synergistic therapy

TL;DR: An overview of latest progress in the field of cyclodextrin-based multifunctional co-delivery systems for cancer synergistic therapy is provided.
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Breast metastatic tumors in lung can be substituted by lung-derived malignant cells transformed by alternative splicing H19 lncRNA

TL;DR: In this article , the authors modified the classical MMTV-PyMT breast carcinoma model to trace the fate of mammary-derived carcinoma cells, and they showed that within the lung, when the metastatic breast cancer cells are conditionally depleted, transformed lung epithelial cells generate new metastases.