All Publications

  • TeleHelp Ukraine: A distributed international telemedicine response to the ongoing war. Journal of global health Narayan, A., Petryk, M., Savchuk, S., Villarino, K., Lopez, I., Morgun, E., Bakirova, A., Kamets, B., Le Tran, Q., Komzyuk, S., Kharbas, V., Asch, S., Pickering, A. 2024; 14: 04158

    Abstract

    Humanitarian crises frequently garner solidarity and robust volunteer recruitment among health care communities. However, a common obstacle is matching providers to those in need across geographic and other barriers. We examined the application of a decentralised governance strategy in establishing an emergency telemedicine response, TeleHelp Ukraine (THU).Using a case study approach, we explored how global networking and technological advancements empower organisations to generate, access, disseminate, and utilise knowledge for sustainable health care delivery.Preliminary results suggest that a non-profit, decentralised model strengthened by robust team dynamics may optimise the distribution of clinical workload and scheduling procedures. Institutional and cultural diversity among health care providers and volunteers fosters the mobilisation of knowledge resources, synergistic collaboration, and tailored care standards that align with both provider and patient expectations. By integrating these diverse, distributed networks, a synergistic effect is achieved, combining effective learning mechanisms with intellectual capital.Our study provides insights into the structure, implementation strategies, dissemination methodologies, and initial results of THU's operation. These findings may inform future emergency telemedicine responses in humanitarian scenarios, thereby reinforcing the practical implementation of health as a human right.

    View details for DOI 10.7189/jogh.14.04158

    View details for PubMedID 39451063

  • Oral cavity cancer in young, non-smoking, and non-drinking patients: a contemporary review. Critical reviews in oncology/hematology Tran, Q., Maddineni, S., Arnaud, E. H., Divi, V., Megwalu, U., Topf, M. C., Sunwoo, J. B. 2023: 104112

    Abstract

    Oral squamous cell carcinoma (OSCC) in non-smoking and non-drinking (NSND) individuals appears to be distinct from the traditional head and neck squamous cell carcinoma (HNSCC). The incidence of this subset is increasing, as are the number of studies examining its characteristics. NSND OSCC individuals tend to be younger (<45 years) compared to traditional HNSCC patients. The proportion of females in the NSND OSCC cohort is also higher. The tongue is the predominantly affected subsite. Studies have revealed several gene mutations and unique epigenomic profiles but no definitive genetic etiology. Transcriptomic analysis has not found any causative viral agents. Other proposed etiologies include chronic dental trauma, microbiome abnormalities, marijuana consumption, and genetic disorders. There are international efforts to determine the relative prognostic outcome of this unique cohort, but no consensus has been reached. Here, we review the incidence, demographics, subsite, possible etiologies, prognosis, and therapy implications of the NSND OSCC cohort.

    View details for DOI 10.1016/j.critrevonc.2023.104112

    View details for PubMedID 37633348

  • Targeting KRAS4A splicing through the RBM39/DCAF15 pathway inhibits cancer stem cells NATURE COMMUNICATIONS Chen, W., To, M. D., Westcott, P. K., Delrosario, R., Kim, I., Philips, M., Tran, Q., Bollam, S. R., Goodarzi, H., Bayani, N., Mirzoeva, O., Balmain, A. 2021; 12 (1): 4288

    Abstract

    The commonly mutated human KRAS oncogene encodes two distinct KRAS4A and KRAS4B proteins generated by differential splicing. We demonstrate here that coordinated regulation of both isoforms through control of splicing is essential for development of Kras mutant tumors. The minor KRAS4A isoform is enriched in cancer stem-like cells, where it responds to hypoxia, while the major KRAS4B is induced by ER stress. KRAS4A splicing is controlled by the DCAF15/RBM39 pathway, and deletion of KRAS4A or pharmacological inhibition of RBM39 using Indisulam leads to inhibition of cancer stem cells. Our data identify existing clinical drugs that target KRAS4A splicing, and suggest that levels of the minor KRAS4A isoform in human tumors can be a biomarker of sensitivity to some existing cancer therapeutics.

    View details for DOI 10.1038/s41467-021-24498-7

    View details for Web of Science ID 000675656600022

    View details for PubMedID 34257283

    View details for PubMedCentralID PMC8277813

  • Humanized Mouse Models for the Advancement of Innate Lymphoid Cell-Based Cancer Immunotherapies. Frontiers in immunology Horowitz, N. B., Mohammad, I., Moreno-Nieves, U. Y., Koliesnik, I., Tran, Q., Sunwoo, J. B. 2021; 12: 648580

    Abstract

    Innate lymphoid cells (ILCs) are a branch of the immune system that consists of diverse circulating and tissue-resident cells, which carry out functions including homeostasis and antitumor immunity. The development and behavior of human natural killer (NK) cells and other ILCs in the context of cancer is still incompletely understood. Since NK cells and Group 1 and 2 ILCs are known to be important for mediating antitumor immune responses, a clearer understanding of these processes is critical for improving cancer treatments and understanding tumor immunology as a whole. Unfortunately, there are some major differences in ILC differentiation and effector function pathways between humans and mice. To this end, mice bearing patient-derived xenografts or human cell line-derived tumors alongside human genes or human immune cells represent an excellent tool for studying these pathways in vivo. Recent advancements in humanized mice enable unparalleled insights into complex tumor-ILC interactions. In this review, we discuss ILC behavior in the context of cancer, the humanized mouse models that are most commonly employed in cancer research and their optimization for studying ILCs, current approaches to manipulating human ILCs for antitumor activity, and the relative utility of various mouse models for the development and assessment of these ILC-related immunotherapies.

    View details for DOI 10.3389/fimmu.2021.648580

    View details for PubMedID 33968039

  • DGAT1-Dependent Lipid Droplet Biogenesis Protects Mitochondrial Function during Starvation-Induced Autophagy. Developmental cell Nguyen, T. B., Louie, S. M., Daniele, J. R., Tran, Q., Dillin, A., Zoncu, R., Nomura, D. K., Olzmann, J. A. 2017; 42 (1): 9-21.e5

    Abstract

    Lipid droplets (LDs) provide an "on-demand" source of fatty acids (FAs) that can be mobilized in response to fluctuations in nutrient abundance. Surprisingly, the amount of LDs increases during prolonged periods of nutrient deprivation. Why cells store FAs in LDs during an energy crisis is unknown. Our data demonstrate that mTORC1-regulated autophagy is necessary and sufficient for starvation-induced LD biogenesis. The ER-resident diacylglycerol acyltransferase 1 (DGAT1) selectively channels autophagy-liberated FAs into new, clustered LDs that are in close proximity to mitochondria and are lipolytically degraded. However, LDs are not required for FA delivery to mitochondria but instead function to prevent acylcarnitine accumulation and lipotoxic dysregulation of mitochondria. Our data support a model in which LDs provide a lipid buffering system that sequesters FAs released during the autophagic degradation of membranous organelles, reducing lipotoxicity. These findings reveal an unrecognized aspect of the cellular adaptive response to starvation, mediated by LDs.

    View details for DOI 10.1016/j.devcel.2017.06.003

    View details for PubMedID 28697336

    View details for PubMedCentralID PMC5553613