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1,115 results on '"Wang, Eric"'

1. Systematic evaluation of AML-associated antigens identifies anti-U5 SNRNP200 therapeutic antibodies for the treatment of acute myeloid leukemia

Author

Knorr, Katherine, Rahman, Jahan, Erickson, Caroline, Wang, Eric, Monetti, Mara, Li, Zhuoning, Ortiz-Pacheco, Juliana, Jones, Andrew, Lu, Sydney X., Stanley, Robert F., Baez, Maria, Fox, Nina, Castro, Cynthia, Marino, Alessandra E., Jiang, Caroline, Penson, Alex, Hogg, Simon J., Mi, Xiaoli, Nakajima, Hideaki, Kunimoto, Hiroyoshi, Nishimura, Koutarou, Inoue, Daichi, Greenbaum, Benjamin, Knorr, David, Ravetch, Jeffrey, and Abdel-Wahab, Omar

Published
2023
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8. GPATCH8 modulates mutant SF3B1 mis-splicing and pathogenicity in hematologic malignancies

Author

Benbarche, Salima, Pineda, Jose Mario Bello, Galvis, Laura Baquero, Biswas, Jeetayu, Liu, Bo, Wang, Eric, Zhang, Qian, Hogg, Simon J., Lyttle, Kadeen, Dahi, Ariana, Lewis, Alexander M., Sarchi, Martina, Rahman, Jahan, Fox, Nina, Ai, Yuxi, Mehta, Sanjoy, Garippa, Ralph, Ortiz-Pacheco, Juliana, Li, Zhuoning, Monetti, Mara, Stanley, Robert F., Doulatov, Sergei, Bradley, Robert K., and Abdel-Wahab, Omar

Published
2024
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18. PSGL-1 attenuates early TCR signaling to suppress CD8+ T cell progenitor differentiation and elicit terminal CD8+ T cell exhaustion

Author

Hope, Jennifer L., Otero, Dennis C., Bae, Eun-Ah, Stairiker, Christopher J., Palete, Ashley B., Faso, Hannah A., Lin, Michelle, Henriquez, Monique L., Roy, Sreeja, Seo, Hyungseok, Lei, Xue, Wang, Eric S., Chow, Savio, Tinoco, Roberto, Daniels, Gregory A., Yip, Kevin, Campos, Alexandre Rosa, Yin, Jun, Adams, Peter D., Rao, Anjana, and Bradley, Linda M.

Published
2023
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19. NUDT21 limits CD19 levels through alternative mRNA polyadenylation in B cell acute lymphoblastic leukemia

Author

Witkowski, Matthew T., Lee, Soobeom, Wang, Eric, Lee, Anna K., Talbot, Alexis, Ma, Chao, Tsopoulidis, Nikolaos, Brumbaugh, Justin, Zhao, Yaqi, Roberts, Kathryn G., Hogg, Simon J., Nomikou, Sofia, Ghebrechristos, Yohana E., Thandapani, Palaniraja, Mullighan, Charles G., Hochedlinger, Konrad, Chen, Weiqiang, Abdel-Wahab, Omar, Eyquem, Justin, and Aifantis, Iannis

Published
2022
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29. SMARCA4 biology in alveolar rhabdomyosarcoma

Author

Bharathy, Narendra, Cleary, Megan M., Kim, Jin-Ah, Nagamori, Kiyo, Crawford, Kenneth A., Wang, Eric, Saha, Debarya, Settelmeyer, Teagan P., Purohit, Reshma, Skopelitis, Damianos, Chang, Kenneth, Doran, Jessica A., Kirschbaum, C. Ward, Bharathy, Suriya, Crews, Davis W., Randolph, Matthew E., Karnezis, Anthony N., Hudson-Price, Lisa, Dhawan, Jyotsna, Michalek, Joel E., Ciulli, Alessio, Vakoc, Christopher R., and Keller, Charles

Published
2022
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43. Real-world drug utilization and treatment patterns in patients with tenosynovial giant cell tumors in the USA.

Author

Dharmani, Charles, Fofah, Oluwatosin, Wang, Eric, Salas, Maribel, Wooddell, Margaret, Tu, Nora, Tse, Jenny, Near, Aimee, and Tinoco, Gabriel

Abstract

Aim: Real-world treatment patterns in tenosynovial giant cell tumor (TGCT) patients remain unknown. Pexidartinib is the only US FDA-approved treatment for TGCT associated with severe morbidity or functional limitations and not amenable to improvement with surgery. Objective: To characterize drug utilization and treatment patterns in TGCT patients. Methods: In a retrospective observational study using IQVIA's linked prescription and medical claims databases (2018–2021), TGCT patients were stratified by their earliest systemic therapy claim (pexidartinib [N = 82] or non-FDA-approved systemic therapy [N = 263]). Results: TGCT patients treated with pexidartinib versus non-FDA-approved systemic therapies were predominantly female (61 vs 50.6%) and their median age was 47 and 54 years, respectively. Pexidartinib-treated patients had the highest 12-month probability of remaining on treatment (54%); 34.1% of pexidartinib users had dose reduction after their first claim. Conclusion: This study provides new insights into the unmet need, utilization and treatment patterns of systemic therapies for the treatment of TGCT patients. Plain language summary Treatment patterns in patients with tenosynovial giant cell tumors in the USA This database study is the first investigation of how drugs are used to treat patients with tenosynovial giant cell tumor (TGCT) in the real world. We researched adult TGCT patients from IQVIA's prescription and medical claims databases who started treatment with pexidartinib (N = 82) or other non-US FDA-approved systemic therapies (N = 263). The patients included in this analysis were mostly women (61.0 and 50.6%) and their median age was 47 and 54 years for pexidartinib and other non-FDA-approved systemic therapies, respectively. The patients treated with pexidartinib were most likely to remain on treatment (54.0%) at the end of the first year. Most patients (79.3%) started pexidartinib treatment at a total daily dose of 800 mg/day, as per the product label. Only 34.1% of patients had reduced medication dose during follow-up. Of note, this study found that TGCT patients were treated with other systemic therapies which remain unproven to be safe and effective in medical studies of TGCT. Given the unmet need, and with pexidartinib being the only approved systemic treatment in USA, there is an opportunity for the larger population of adult TGCT patients to benefit from its use. Further research is needed to identify barriers for access to pexidartinib and treatment of TGCT patients. Summary points Tenosynovial giant cell tumor (TGCT) is a rare, locally aggressive neoplasm affecting the synovial membrane lining joints, bursae and tendon sheaths. Pexidartinib is currently the only systemic treatment approved by the US FDA for the treatment of adult patients with symptomatic TGCT associated with severe morbidity or functional limitations and not amenable to improvement with surgery. Other systemic therapies have been investigated in clinical studies of TGCT patients, none of them have been approved by the FDA for the treatment of TGCT specifically. Using a real-world claims database, this study characterized TGCT patients newly treated with pexidartinib or other unapproved systemic treatments and described their treatment patterns, including treatment duration and dosing. In this study, we found that although the median duration of pexidartinib treatment was not reached, patients on pexidartinib had the highest 12-month probability of remaining on treatment. Dose reductions after the first medication claim were commonly observed in the pexidartinib cohort (34.1%) and some patients (9.8%) had evidence of dose increase. Dose levels of the non-FDA-approved systemic therapies were consistent with the recommended dosages for other indications, as per their label, none of which were TGCT. As expected, 63.6–82.9% of TGCT patients treated with non-FDA-approved systemic therapies discontinued treatment at 12 months. This study provided novel insights into how systemic therapies for TGCT are used in real-world clinical practice, where surgery has been the standard of care. Given the large unmet need for the treatment of TGCT patients, and as pexidartinib is the only regulatory-approved systemic treatment, there is opportunity for its wider use in this patient population. [ABSTRACT FROM AUTHOR]

Published
2024
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44. Myospreader improves gene editing in skeletal muscle by myonuclear propagation.

Author

Poukalov, Kiril K., Valero, M. Carmen, Muscato, Derek R., Adams, Leanne M., Heejae Chun, Young il Lee, Andrade, Nadja S., Zeier, Zane, Sweeney, H. Lee, and Wang, Eric T.

Subjects
GENOME editing, SKELETAL muscle, GENE therapy, DUCHENNE muscular dystrophy, CRISPRS
Abstract

Successful CRISPR/Cas9-based gene editing in skeletal muscle is dependent on efficient propagation of Cas9 to all myonuclei in the myofiber. However, nuclear-targeted gene therapy cargos are strongly restricted to their myonuclear domain of origin. By screening nuclear localization signals and nuclear export signals, we identify "Myospreader," a combination of short peptide sequences that promotes myonuclear propagation. Appending Myospreader to Cas9 enhances protein stability and myonuclear propagation in myoblasts and myofibers. AAV-delivered Myospreader dCas9 better inhibits transcription of toxic RNA in a myotonic dystrophy mouse model. Furthermore, Myospreader Cas9 achieves higher rates of gene editing in CRISPR reporter and Duchenne muscular dystrophy mouse models. Myospreader reveals design principles relevant to all nuclear-targeted gene therapies and highlights the importance of the spatial dimension in therapeutic development. [ABSTRACT FROM AUTHOR]

Published
2024
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45. Alpha-Melanocyte-Stimulating Hormone Maintains Retinal Homeostasis after Ischemia/Reperfusion.

Author

Ng, Tat Fong, Cho, Jenna Y., Zhao, John L., Gardiner, John R., Wang, Eric S., Leung, Elman, Xu, Ziqian, Fineman, Samantha L., Lituchy, Melinda, Lo, Amy C., and Taylor, Andrew W.

Subjects
MELANOCORTIN receptors, RETINAL ganglion cells, REPERFUSION, RETINAL degeneration, CELL anatomy, ISCHEMIA
Abstract

Augmenting the natural melanocortin pathway in mouse eyes with uveitis or diabetes protects the retinas from degeneration. The retinal cells are protected from oxidative and apoptotic signals of death. Therefore, we investigated the effects of a therapeutic application of the melanocortin alpha-melanocyte-stimulating hormone (α-MSH) on an ischemia and reperfusion (I/R) model of retinal degenerative disease. Eyes were subjected to an I/R procedure and were treated with α-MSH. Retinal sections were histopathologically scored. Also, the retinal sections were immunostained for viable ganglion cells, activated Muller cells, microglial cells, and apoptosis. The I/R caused retinal deformation and ganglion cell loss that was significantly reduced in I/R eyes treated with α-MSH. While α-MSH treatment marginally reduced the number of GFAP-positive Muller cells, it significantly suppressed the density of Iba1-positive microglial cells in the I/R retinas. Within one hour after I/R, there was apoptosis in the ganglion cell layer, and by 48 h, there was apoptosis in all layers of the neuroretina. The α-MSH treatment significantly reduced and delayed the onset of apoptosis in the retinas of I/R eyes. The results demonstrate that therapeutically augmenting the melanocortin pathways preserves retinal structure and cell survival in eyes with progressive neuroretinal degenerative disease. [ABSTRACT FROM AUTHOR]

Published
2024
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