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236 results on '"Nambiar, Dhanya"'

1. Corrigendum

Author

Beach, Callum, MacLean, David, Majorova, Dominika, Melemenidis, Stavros, Nambiar, Dhanya K., Kim, Ryan K., Valbuena, Gabriel N., Guglietta, Silvia, Krieg, Carsten, Darvish-Damavandi, Mahnaz, Suwa, Tatsuya, Easton, Alistair, Hillson, Lily V.S., McCulloch, Ashley K., McMahon, Ross K., Pennel, Kathryn, Edwards, Joanne, O'Cathail, Sean M., Roxburgh, Campbell S., Domingo, Enric, Moon, Eui Jung, Jiang, Dadi, Jiang, Yanyan, Zhang, Qingyang, Koong, Albert C., Woodruff, Trent M., Graves, Edward E., Maughan, Tim, Buczacki, Simon J.A., Stucki, Manuel, Le, Quynh-Thu, Leedham, Simon J., Giaccia, Amato J., and Olcina, Monica M.

Abstract

Original citation: J Clin Invest. 2023;133(23):e168277. https://doi.org/10.n72/JCI168277. During the preparation of this manuscript, the dose for PMX205 used for in vitro experiments was stated incorrectly in the legend for Figure [...]

Published
2024
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3. Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell phenotype

Author

Viswanathan, Vignesh, Cao, Hongbin, Saiki, Julie, Jiang, Dadi, Mattingly, Aaron, Nambiar, Dhanya, Bloomstein, Joshua, Li, Yang, Jiang, Sizun, Chamoli, Manish, Sirjani, Davud, Kaplan, Michael, Holsinger, F Christopher, Liang, Rachel, Von Eyben, Rie, Jiang, Haowen, Guan, Li, Lagory, Edward, Feng, Zhiping, Nolan, Garry, Ye, Jiangbin, Denko, Nicholas, Knox, Sarah, Rosen, Daria-Mochly, and Le, Quynh-Thu

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Stem Cell Research, Genetics, Stem Cell Research - Nonembryonic - Non-Human, Regenerative Medicine, Dental/Oral and Craniofacial Disease, Cancer, Digestive Diseases
Abstract

Adult salivary stem/progenitor cells (SSPC) have an intrinsic property to self-renew in order to maintain tissue architecture and homeostasis. Adult salivary glands have been documented to harbor SSPC, which have been shown to play a vital role in the regeneration of the glandular structures postradiation damage. We have previously demonstrated that activation of aldehyde dehydrogenase 3A1 (ALDH3A1) after radiation reduced aldehyde accumulation in SSPC, leading to less apoptosis and improved salivary function. We subsequently found that sustained pharmacological ALDH3A1 activation is critical to enhance regeneration of murine submandibular gland after radiation damage. Further investigation shows that ALDH3A1 function is crucial for SSPC self-renewal and survival even in the absence of radiation stress. Salivary glands from Aldh3a1 -/- mice have fewer acinar structures than wildtype mice. ALDH3A1 deletion or pharmacological inhibition in SSPC leads to a decrease in mitochondrial DNA copy number, lower expression of mitochondrial specific genes and proteins, structural abnormalities, lower membrane potential, and reduced cellular respiration. Loss or inhibition of ALDH3A1 also elevates ROS levels, depletes glutathione pool, and accumulates ALDH3A1 substrate 4-hydroxynonenal (4-HNE, a lipid peroxidation product), leading to decreased survival of murine SSPC that can be rescued by treatment with 4-HNE specific carbonyl scavengers. Our data indicate that ALDH3A1 activity protects mitochondrial function and is important for the regeneration activity of SSPC. This knowledge will help to guide our translational strategy of applying ALDH3A1 activators in the clinic to prevent radiation-related hyposalivation in head and neck cancer patients.

Published
2022

5. Improving radiotherapy in immunosuppressive microenvironments by targeting complement receptor C5aR1

Author

Beach, Callum, MacLean, David, Majorova, Dominika, Melemenidis, Stavros, Nambiar, Dhanya K., Kim, Ryan K., Valbuena, Gabriel N., Guglietta, Silvia, Krieg, Carsten, Darvish-Damavandi, Mahnaz, Suwa, Tatsuya, Easton, Alistair, Hillson, Lily V.S., McCulloch, Ashley K., McMahon, Ross K., Pennel, Kathryn, Edwards, Joanne, O'Cathail, Sean M., Roxburgh, Campbell S., Domingo, Enric, Moon, Eui Jung, Jiang, Dadi, Jiang, Yanyan, Zhang, Qingyang, Koong, Albert C., Woodruff, Trent M., Graves, Edward E., Maughan, Tim, Buczacki, Simon J.A., Stucki, Manuel, Le, Quynh-Thu, Leedham, Simon J., Giaccia, Amato J., and Olcina, Monica M.

Subjects
Thermo Fisher Scientific Inc., Scientific equipment and supplies industry, Gene expression, T cells, Tumors, Genes, Cancer -- Diagnosis, Colorectal cancer, Ethylenediaminetetraacetic acid, B cells, Radiotherapy, Health care industry, Wellcome Trust
Abstract

An immunosuppressive microenvironment causes poor tumor T cell infiltration and is associated with reduced patient overall survival in colorectal cancer. How to improve treatment responses in these tumors is still a challenge. Using an integrated screening approach to identify cancer-specific vulnerabilities, we identified complement receptor C5aR1 as a druggable target, which when inhibited improved radiotherapy, even in tumors displaying immunosuppressive features and poor [CD8.sup.+] T cell infiltration. While C5aR1 is well-known for its role in the immune compartment, we found that C5aR1 is also robustly expressed on malignant epithelial cells, highlighting potential tumor cell-specific functions. C5aR1 targeting resulted in increased NF-[kappa]B-dependent apoptosis specifically in tumors and not normal tissues, indicating that, in malignant cells, C5aR1 primarily regulated cell fate. Collectively, these data revealed that increased complement gene expression is part of the stress response mounted by irradiated tumors and that targeting C5aR1 could improve radiotherapy, even in tumors displaying immunosuppressive features., Introduction The composition of the tumor microenvironment (TME) affects treatment responses in cancer (1-3). Immunosuppressive TME features, which act as a barrier to extensive [CD8.sup.+] T cell infiltration typically characterize [...]

Published
2023
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6. A case for the study of native extracellular vesicles.

Author

Nambiar, Dhanya, Quynh-Thu Le, and Pucci, Ferdinando

Subjects
B cell lymphoma, EXTRACELLULAR vesicles, CELL communication, EARLY detection of cancer, CANCER prevention
Abstract

Threemain areas of research revolve around extracellular vesicles (EVs): their use as early detection diagnostics for cancer prevention, engineering of EVs or other enveloped viral-like particles for therapeutic purposes and to understand how EVs impact biological processes. When investigating the biology of EVs, it is important to consider strategies able to track and alter EVs directly in vivo, as theyare releasedby donor cells. This can be achieved by suitable engineering of EV donor cells, either before implantation or directly in vivo. Here, wemake a case for the study of native EVs, that is, EVs released by cells living within a tissue. Novel genetic approaches to detect intercellular communications mediated by native EVs and profile recipient cells are discussed. The use of Rab35 dominant negative mutant is proposed for functional in vivo studies on the roles of native EVs. Ultimately, investigations on native EVs will tremendously advance our understanding of EV biology and open novel opportunities for therapy and prevention. [ABSTRACT FROM AUTHOR]

Published
2024
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7. Aldehyde dehydrogenase 3A1 activation prevents radiation-induced xerostomia by protecting salivary stem cells from toxic aldehydes

Author

Saiki, Julie P, Cao, Hongbin, Van Wassenhove, Lauren D, Viswanathan, Vignesh, Bloomstein, Joshua, Nambiar, Dhanya K, Mattingly, Aaron J, Jiang, Dadi, Chen, Che-Hong, Stevens, Matthew C, Simmons, Amanda L, Park, Hyun Shin, von Eyben, Rie, Kool, Eric T, Sirjani, Davud, Knox, Sarah M, Le, Quynh Thu, and Mochly-Rosen, Daria

Subjects
Ecological Applications, Biomedical and Clinical Sciences, Environmental Sciences, Regenerative Medicine, Digestive Diseases, Stem Cell Research, Cancer, Dental/Oral and Craniofacial Disease, Aldehyde Dehydrogenase, Aldehydes, Animals, Apoptosis, Cyclohexenes, Female, Head and Neck Neoplasms, Limonene, Medicine, Chinese Traditional, Mice, Mice, Inbred C57BL, Protective Agents, Radiotherapy, Salivary Glands, Stem Cells, Submandibular Gland, Terpenes, Xerostomia, ALDH3A1, aldehyde dehydrogenase, radiation, dry mouth, xerostomia
Abstract

Xerostomia (dry mouth) is the most common side effect of radiation therapy in patients with head and neck cancer and causes difficulty speaking and swallowing. Since aldehyde dehydrogenase 3A1 (ALDH3A1) is highly expressed in mouse salivary stem/progenitor cells (SSPCs), we sought to determine the role of ALDH3A1 in SSPCs using genetic loss-of-function and pharmacologic gain-of-function studies. Using DarkZone dye to measure intracellular aldehydes, we observed higher aldehyde accumulation in irradiated Aldh3a1-/- adult murine salisphere cells and in situ in whole murine embryonic salivary glands enriched in SSPCs compared with wild-type glands. To identify a safe ALDH3A1 activator for potential clinical testing, we screened a traditional Chinese medicine library and isolated d-limonene, commonly used as a food-flavoring agent, as a single constituent activator. ALDH3A1 activation by d-limonene significantly reduced aldehyde accumulation in SSPCs and whole embryonic glands, increased sphere-forming ability, decreased apoptosis, and improved submandibular gland structure and function in vivo after radiation. A phase 0 study in patients with salivary gland tumors showed effective delivery of d-limonene into human salivary glands following daily oral dosing. Given its safety and bioavailability, d-limonene may be a good clinical candidate for mitigating xerostomia in patients with head and neck cancer receiving radiation therapy.

Published
2018

11. Novel Aza-podophyllotoxin derivative induces oxidative phosphorylation and cell death via AMPK activation in triple-negative breast cancer

Author

Tailor, Dhanir, Going, Catherine C., Resendez, Angel, Kumar, Vineet, Nambiar, Dhanya K., Li, Yang, Dheeraj, Arpit, LaGory, Edward Lewis, Ghoochani, Ali, Birk, Alisha M., Stoyanova, Tanya, Ye, Jiangbin, Giaccia, Amato J., Le, Quynh-Thu, Singh, Rana P., Sledge, George W., Pitteri, Sharon J., and Malhotra, Sanjay V.

Published
2021
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12. Supplementary Figure 6 from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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13. Supplementary Figure 1 from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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14. Supplementary Figure 5 from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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15. Supplementary Figure 3 from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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16. Data from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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17. Supplementary Figure 4 from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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18. Supplementary Figure 2 from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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19. Supplementary Figure Legends from Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, Cao, Hongbin, primary, Zhang, Weiruo, primary, Guan, Li, primary, Chamoli, Manish, primary, Holmes, Brittany, primary, Kong, Christina, primary, Hildebrand, Rachel, primary, Koong, Amanda Jeanette, primary, von Eyben, Rie, primary, Plevritis, Sylvia, primary, Li, Lingyin, primary, Giaccia, Amato, primary, Engleman, Edgar, primary, and Le, Quynh Thu, primary

Published
2023
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20. Galectin-1-driven T cell exclusion in the tumor endothelium promotes immunotherapy resistance

Author

Nambiar, Dhanya K., Aguilera, Todd, Cao, Hongbin, Kwok, Shirley, Kong, Christina, Bloomstein, Joshua, Wang, Zemin, Rangan, Vangipuram S., Jiang, Dadi, von Eyben, Rie, Liang, Rachel, Agarwal, Sonya, Colevas, A. Dimitrios, Korman, Alan, Allen, Clint T., Uppaluri, Ravindra, Koong, Albert C., Giaccia, Amato, and Le, Quynh Thu

Subjects
Thermo Fisher Scientific Inc., R and D Systems, Cancer -- Drug therapy -- Analysis, Endothelium -- Analysis, Immunotherapy -- Analysis, Software industry -- Analysis, Scientific equipment industry -- Analysis, T cells -- Analysis, Death, Radiotherapy, Head and neck cancer, Tumors, Health care industry, Stanford University. School of Medicine
Abstract

Immune checkpoint inhibitors (ICIs), although promising, have variable benefit in head and neck cancer (HNC). We noted that tumor galectin-1 (Gal1) levels were inversely correlated with treatment response and survival in patients with HNC who were treated with ICIs. Using multiple HNC mouse models, we show that tumor-secreted Gal1 mediates immune evasion by preventing T cell migration into the tumor. Mechanistically, Gal1 reprograms the tumor endothelium to upregulate cell-surface programmed death ligand 1 (PD-L1) and galectin-9. Using genetic and pharmacological approaches, we show that Gal1 blockade increases intratumoral T cell infiltration, leading to a better response to anti-PD1 therapy with or without radiotherapy. Our study reveals the function of Gal1 in transforming the tumor endothelium into an immune-suppressive barrier and that its inhibition synergizes with ICIs., Introduction Immunosuppression is an accepted hallmark of tumor progression, and targeting immune-suppressive pathways has led to enhanced patient survival in multiple cancers, including head and neck cancer (HNC) (1, 2). [...]

Published
2019
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22. Galectin-1 Mediates Chronic STING Activation in Tumors to Promote Metastasis through MDSC Recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh, additional, Cao, Hongbin, additional, Zhang, Weiruo, additional, Guan, Li, additional, Chamoli, Manish, additional, Holmes, Brittany, additional, Kong, Christina, additional, Hildebrand, Rachel, additional, Koong, Amanda Jeanette, additional, von Eyben, Rie, additional, Plevritis, Sylvia, additional, Li, Lingyin, additional, Giaccia, Amato, additional, Engleman, Edgar, additional, and Le, Quynh Thu, additional

Published
2023
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24. Supplementary Figures S1-S7 from The Combination of Radiotherapy and Complement C3a Inhibition Potentiates Natural Killer cell Functions Against Pancreatic Cancer

Author

Sodji, Quaovi H., primary, Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, von Eyben, Rie, primary, Colburg, Deana, primary, Binkley, Michael S., primary, Li, Caiyun G., primary, Olcina, Monica M., primary, Chang, Daniel T., primary, Le, Quynh-Thu, primary, and Giaccia, Amato J., primary

Published
2023
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25. Supplementary Table S1 from The Combination of Radiotherapy and Complement C3a Inhibition Potentiates Natural Killer cell Functions Against Pancreatic Cancer

Author

Sodji, Quaovi H., primary, Nambiar, Dhanya K., primary, Viswanathan, Vignesh, primary, von Eyben, Rie, primary, Colburg, Deana, primary, Binkley, Michael S., primary, Li, Caiyun G., primary, Olcina, Monica M., primary, Chang, Daniel T., primary, Le, Quynh-Thu, primary, and Giaccia, Amato J., primary

Published
2023
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27. Abstract 66: Galectin-1 mediated chronic tumoral-STING activation promotes metastasisthrough MDSC recruitment

Author

Nambiar, Dhanya K., primary, Viswanathan, Vignesh Vignesh, additional, Cao, Hongbin, additional, Zhang, Weiruo, additional, Guan, Li, additional, Chamoli, Manish, additional, Holmes, Brittany, additional, Kong, Christina, additional, Hildebrand, Rachel, additional, Koong, Amanda, additional, Eyben, Rie, additional, Giaccia, Amato, additional, Li, Lingyin, additional, Engleman, Edgar, additional, and Le, Quynh Thu, additional

Published
2023
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35. Supplemental Figure 4 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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36. Supplemental Figure 2 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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37. Supplemental Figure 1 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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38. Supplemental Figure 3 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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39. Supplemental Figure 5 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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40. Supplemental Figure 6 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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41. Supplemental Figure 7 from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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42. Supplemental Tables from NFE2L2 Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., primary, Cao, Hongbin, primary, Viswanathan, Vignesh, primary, Kwok, Shirley, primary, Hui, Angela B., primary, Hou, Yuan, primary, Hildebrand, Rachel, primary, von Eyben, Rie, primary, Holmes, Brittany J., primary, Zhao, Junfei, primary, Kong, Christina S., primary, Wamsley, Nathan, primary, Zhang, Weiruo, primary, Major, Michael B., primary, Seol, Seung W., primary, Sunwoo, John B., primary, Hayes, D. Neil, primary, Diehn, Maximilian, primary, and Le, Quynh-Thu, primary

Published
2023
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43. NFE2L2Mutations Enhance Radioresistance in Head and Neck Cancer by Modulating Intratumoral Myeloid Cells

Author

Guan, Li, primary, Nambiar, Dhanya K., additional, Cao, Hongbin, additional, Viswanathan, Vignesh, additional, Kwok, Shirley, additional, Hui, Angela B., additional, Hou, Yuan, additional, Hildebrand, Rachel, additional, von Eyben, Rie, additional, Holmes, Brittany J., additional, Zhao, Junfei, additional, Kong, Christina S., additional, Wamsley, Nathan, additional, Zhang, Weiruo, additional, Major, Michael B., additional, Seol, Seung W., additional, Sunwoo, John B., additional, Hayes, D. Neil, additional, Diehn, Maximilian, additional, and Le, Quynh-Thu, additional

Published
2023
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44. Innate immune receptor C5aR1 regulates cancer cell fate and can be targeted to improve radiotherapy in tumours with immunosuppressive microenvironments

Author

Beach, Callum, primary, MacLean, David, additional, Majorova, Dominika, additional, Melemenidis, Stavros, additional, Nambiar, Dhanya K., additional, Kim, Ryan K., additional, Valbuena, Gabriel N, additional, Guglietta, Silvia, additional, Krieg, Carsten, additional, Darvish, Damavandi Mahnaz, additional, Suwa, Tatsuya, additional, Easton, Alistair, additional, Domingo, Enric, additional, Moon, Eui Jung, additional, Jiang, Dadi, additional, Jiang, Yanyan, additional, Koong, Albert C, additional, Woodruff, Trent M., additional, Graves, Edward E., additional, Maughan, Tim, additional, Buczacki, Simon J. A., additional, Stucki, Manuel, additional, Le, Quynh-Thu, additional, Leedham, Simon J., additional, Giaccia, Amato J., additional, and Olcina, Monica M, additional

Published
2023
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