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41 results on '"Ju, Yawen"'

7. 666 Safety, efficacy, and biomarker results of SRK-181, a latent TGFβ1 inhibitor, in anti-PD-1 resistant metastatic ccRCC patients

Author

Yap, Timothy, primary, Vaishampayan, Ulka N, additional, Kilari, Deepak, additional, Sweis, Randy, additional, Barve, Minal, additional, Gainor, Justin, additional, Tarhini, Ahmad A, additional, Karim, Raghad, additional, Sher, Amna, additional, Park, David, additional, Babu, Sunil, additional, McKay, Rana, additional, Ju, Yawen, additional, Liu, Lan, additional, Henry, Susan, additional, and Gan, Lu, additional

Published
2023
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8. 726 Establishing proof of mechanism in patients: preliminary biomarker data of SRK-181 (a latent TGFβ1 inhibitor) from DRAGON Study

Author

Henry, Susan, primary, DeWall, Stephen, additional, Vaishampayan, Ulka N, additional, Sher, Amna, additional, Tarhini, Ahmad A, additional, Kilari, Deepak, additional, Sweis, Randy, additional, Yap, Timothy, additional, Gainor, Justin, additional, Barve, Minal, additional, Clark, John, additional, Liu, Lan, additional, McCune, Asia, additional, Ju, Yawen, additional, Qatanani, Mo, additional, and Gan, Lu, additional

Published
2023
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13. 780 SRK-181, a latent TGFβ1 inhibitor: safety, efficacy, and biomarker results from the dose escalation portion of a phase I trial (DRAGON trial) in patients with advanced solid tumors

Author

Yap, Timothy, primary, Gainor, Justin, additional, McKean, Meredith, additional, Johnson, Melissa, additional, Bockorny, Bruno, additional, Barve, Minal, additional, Sweis, Randy, additional, Vaishampayan, Ulka, additional, Tarhini, Ahmad, additional, Kilari, Deepak, additional, Ju, Yawen, additional, Lee-Hoeflich, Si-Tuen, additional, DeWall, Stephen, additional, Liu, Lan, additional, Shah, Nisha, additional, Kennedy, Ann Marie, additional, and Gan, Lu, additional

Published
2022
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16. 532 First-in-human phase 1 trial of SRK-181: a latent TGFβ1 inhibitor, alone or in combination with anti-PD-(L)1 treatment in patients with advanced solid tumors (DRAGON trial)

Author

Yap, Timothy, primary, Barve, Minal, additional, Gainor, Justin, additional, Bockorny, Bruno, additional, Ju, Yawen, additional, Cote, Shaun, additional, Bilic, Sanela, additional, Liu, Lan, additional, Chyung, Yung, additional, Legler, Michelle, additional, Gan, Lu, additional, and McKean, Meredith, additional

Published
2021
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17. First-in-human phase 1 trial (DRAGON) of SRK-181, a potential first-in-class selective latent TGFβ1 inhibitor, alone or in combination with anti-PD-(L)1 treatment in patients with advanced solid tumors.

Author

Yap, Timothy A., primary, Barve, Minal A., additional, Gainor, Justin F., additional, Weekes, Colin D., additional, Bockorny, Bruno, additional, Ju, Yawen, additional, Faucette, Ryan, additional, Bilic, Sanela, additional, Lee-Hoeflich, Si Tuen, additional, Song, Guochen, additional, Chyung, Yung, additional, Legler, Michelle, additional, Gan, Lu, additional, and Bendell, Johanna C., additional

Published
2021
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20. Once weekly selinexor, carfilzomib, and dexamethasone (SKd) in patients with relapsed/refractory multiple myeloma (MM).

Author

Gasparetto, Cristina, primary, Lipe, Brea, additional, Tuchman, Sascha, additional, Callander, Natalie Scott, additional, Lentzsch, Suzanne, additional, Baljevic, Muhamed, additional, Rossi, Adriana C., additional, Bahlis, Nizar J., additional, White, Darell, additional, Chen, Christine, additional, Sutherland, Heather J, additional, Kotb, Rami, additional, LeBlanc, Richard, additional, Sebag, Michael, additional, Venner, Christopher P, additional, Bensinger, William, additional, Sheehan, Heidi, additional, Ju, Yawen, additional, Kai, Kazuharu, additional, and Schiller, Gary J., additional

Published
2020
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26. Abstract 736: Pyridinobenzodiazepines (PDDs): A new class of sequence-selective DNA mono-alkylating ADC payloads with low hydrophobicity

Author

Veillard, Nicolas, primary, Andriollo, Paolo, additional, Mantaj, Julia, additional, Fox, Keith R., additional, Rahman, K Miraz, additional, Procopiou, George, additional, Cascio, Francesco, additional, Corcoran, David B., additional, Pysz, Ilona, additional, Cooper, Patricia A., additional, Shnyder, Steven D., additional, Ju, Yawen, additional, Tan, Edwin, additional, Schopperle, William M., additional, Jackson, Paul J., additional, and Thurston, David E., additional

Published
2018
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29. Lymphatic endothelial cells efferent to inflamed joints produce iNOS and inhibit lymphatic vessel contraction and drainage in TNF-induced arthritis in mice

Author

Liang, Qianqian, primary, Ju, Yawen, additional, Chen, Yan, additional, Wang, Wensheng, additional, Li, Jinlong, additional, Zhang, Li, additional, Xu, Hao, additional, Wood, Ronald W., additional, Schwarz, Edward. M., additional, Boyce, Brendan F., additional, Wang, Yongjun, additional, and Xing, Lianping, additional

Published
2016
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30. Efficacy of B cell Depletion Therapy on Joint Flare is Associated with Increased Lymphatic Flow

Author

Li, Jie, Ju, Yawen, Bouta, Echoe M., Xing, Lianping, Wood, Ronald W., Kuzin, Igor, Bottaro, Andrea, Ritchlin, Christopher T., and Schwarz, Edward M.

Subjects
B-Lymphocytes, CD11b Antigen, Synovitis, Knee Joint, Mice, Transgenic, Flow Cytometry, Immunohistochemistry, Magnetic Resonance Imaging, Article, Lymphocyte Depletion, Arthritis, Rheumatoid, Mice, Treatment Outcome, Microscopy, Fluorescence, Animals, Lymph Nodes, Lymphatic Vessels
Abstract

B cell depletion therapy ameliorates rheumatoid arthritis by mechanisms that are incompletely understood. Arthritis flare in tumor necrosis factor (TNF)-transgenic mice is associated with efferent lymph node (LN) "collapse," triggered by B cell translocation into lymphatic spaces and decreased lymphatic drainage. The aim of this study was to examine whether the efficacy of B cell depletion therapy is associated with restoration of lymphatic drainage due to removal of obstructing nodal B cells.We used contrast-enhanced magnetic resonance imaging, indocyanine green near-infrared imaging, and intravital immunofluorescence imaging to longitudinally assess synovitis, lymphatic flow, and cell migration in lymphatic vessels in TNF-transgenic mice. We conducted tests to determine whether the efficacy of B cell depletion therapy is associated with restoration of lymphatic draining and cell egress from arthritic joints.Unlike active lymphatics to normal and prearthritic knees, afferent lymphatic vessels to collapsed LNs in inflamed knees do not pulse. Intravital immunofluorescence imaging demonstrated that CD11b+ monocyte/macrophages in lymphatic vessels afferent to expanding LNs travel at high velocity (mean±SD 186±37 μm/second), while these cells are stationary in lymphatic vessels afferent to collapsed popliteal LNs. B cell depletion therapy for arthritis flares in TNF-transgenic mice significantly decreased knee synovium volume (by 50% from the baseline level) and significantly increased lymphatic clearance compared with placebo (P0.05). This increased lymphatic drainage restored macrophage egress from inflamed joints without recovery of the lymphatic pulse.These results support a novel mechanism in which B cell depletion therapy for joint arthritis flares lessens inflammation by increasing lymphatic drainage and subsequent migration of cells and cytokines from the synovial space.

Published
2013

32. Elucidating the Role of Lymphatics in the Pathogenesis of Chronic Inflammatory-Erosive Arthritis

Author

Ju, Yawen, Schwarz, Edward M., Ju, Yawen, and Schwarz, Edward M.

Abstract

Thesis (Ph.D.)--University of Rochester. School of Medicine & Dentistry. Dept. of Pathology and Laboratory Medicine, 2014., Rheumatoid arthritis (RA) is a chronic inflammatory joint disease in which patients often suffer from arthritic flare. Using longitudinal contrast-enhanced (CE)-MRI to study knee arthritis in tumor necrosis factor-transgenic (TNF-Tg) mice, we observed that the popliteal lymph nodes (PLN) firstly “expand” in size and contrast enhancement, and then suddenly “collapse” during arthritic flare. Since CE-MRI is too costly for phenotyping and longitudinal analyses of PLN, our aim was to develop ultrasound (US) methods that could replace MRI. In our initial study, we demonstrated a significant correlation between PLN volumes determined by US vs. MRI. However, since PLN collapse is more closely associated with lymphatic draining function than volume, we evaluated CE-US methods to distinguish changes in lymphatic transport, which was shown as a biomarker of arthritic flare. Unfortunately, delivery of the contrast agent prior to US significantly impairs lymphatic function, making it unsuitable for phenotyping PLNs. Thus, we went on to develop power Doppler (PD) US methods to phenotype PLN with greater accuracy and cost effectiveness vs. CE-MRI. Another important prior observation we made is that arthritic flare is associated with the loss of lymphatic pulse. From other models of inflammation, lymphatic pulse is known to be controlled by endothelial nitric oxide synthase (eNOS), and inhibited by inducible NOS (iNOS) expressed in Gr-1+ cells. To test the hypothesis that eNOS/iNOS dysregulation is responsible for the loss of lymphatic pulse during arthritic flare in TNF-Tg mice, we performed IHC and in vivo pharmacological intervention studies with selective and non-selective iNOS inhibitors. The IHC results demonstrated that large numbers of iNOS expressing Gr-1+ cells exist in collapsed PLN. By evaluating the lymphatics with NIR-ICG imaging, we observed that the specific iNOS inhibitor L-NIL increased lymphatic pulse and afferent lymphatic drainage in TNF-Tg mice. Additionally

Published
2014

35. Increased numbers of CD23+CD21hi Bin-like B cells in human reactive and rheumatoid arthritis lymph nodes.

Author

Kuzin, Igor I., Kates, Stephen L., Ju, Yawen, Zhang, Longze, Rahimi, Homaira, Wojciechowski, Wojciech, Bernstein, Steven H., Burack, Richard, Schwarz, Edward M., and Bottaro, Andrea

Abstract

A unique population of CD23+ CD21high B cells in inflamed nodes (Bin) has been shown to accumulate in lymph nodes (LNs) draining inflamed joints of TNF-transgenic (TNF-tg) mice. Bin cells contribute to arthritis flare in mice by distorting node architecture and hampering lymphatic flow, but their existence in human inflamed LNs has not yet been described. Here, we report the characterization of resident B-cell populations in fresh popliteal lymph nodes (PLNs) from patients with severe lower limb diseases (non-RA) and rheumatoid arthritis (RA) patients, and from banked, cryopreserved reactive and normal human LN single cell suspension samples. Bin-like B cells were shown to be significantly increased in reactive LNs, and strikingly elevated (>30% of total) in RA samples. Histopathology and immunofluorescence analyses were consistent with B follicular hyperplasia and histological alterations in RA vs. non-RA PLNs. This is the first description of Bin-like B cells in human inflamed LNs. Consistent with published mouse data, this population appears to be associated with inflammatory arthritis and distortion of LN architecture. Further analyses are necessary to assess the role of CD23+CD21hi Bin-like B cells in RA pathogenesis and arthritic flare. [ABSTRACT FROM AUTHOR]

Published
2016
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40. Regulation of human osteoclast development by dendritic cell-specific transmembrane protein (DC-STAMP).

Author

Chiu, Ya-Hui, Mensah, Kofi A, Schwarz, Edward M, Ju, Yawen, Takahata, Masahiko, Feng, Changyong, McMahon, Loralee A, Hicks, David G, Panepento, Ben, Keng, Peter C, and Ritchlin, Christopher T

Abstract

Osteoclasts (OC) are bone-resorbing, multinucleated cells that are generated via fusion of OC precursors (OCP). The frequency of OCP is elevated in patients with erosive inflammatory arthritis and metabolic bone diseases. Although many cytokines and cell surface receptors are known to participate in osteoclastogenesis, the molecular mechanisms underlying the regulation of this cellular transformation are poorly understood. Herein, we focused our studies on the dendritic cell- specific tr ans membrane protein (DC-STAMP), a seven-pass transmembrane receptor-like protein known to be essential for cell-to-cell fusion during osteoclastogenesis. We identified an immunoreceptor tyrosine-based inhibitory motif (ITIM) in the cytoplasmic tail of DC-STAMP, and developed an anti-DC-STAMP monoclonal antibody 1A2 that detected DC-STAMP expression on human tumor giant cells, blocked OC formation in vitro, and distinguished four patterns of human PBMC with a positive correlation to OC potential. In freshly isolated monocytes, DC-STAMPhigh cells produced a higher number of OC in culture than DC-STAMPlow cells and the surface expression of DC-STAMP gradually declined during osteoclastogenesis. Importantly, we showed that DC-STAMP is phosphorylated on its tyrosine residues and physically interacts with SHP-1 and CD16, an SH2-domain-containing tyrosine phosphatase and an ITAM-associated protein, respectively. Taken together, these data show that DC-STAMP is a potential OCP biomarker in inflammatory arthritis. Moreover, in addition to its effect on cell fusion, DC-STAMP dynamically regulates cell signaling during osteoclastogenesis. © 2012 American Society for Bone and Mineral Research [ABSTRACT FROM AUTHOR]

Published
2012
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41. Increased numbers of CD23(+) CD21(hi) Bin-like B cells in human reactive and rheumatoid arthritis lymph nodes.

Author

Kuzin II, Kates SL, Ju Y, Zhang L, Rahimi H, Wojciechowski W, Bernstein SH, Burack R, Schwarz EM, and Bottaro A

Subjects
Animals, Arthritis, Rheumatoid pathology, Biomarkers, Humans, Immunophenotyping, Lymph Nodes pathology, Lymphocyte Count, Mice, Mice, Transgenic, Arthritis, Rheumatoid immunology, Arthritis, Rheumatoid metabolism, B-Lymphocyte Subsets immunology, B-Lymphocyte Subsets metabolism, Lymph Nodes immunology, Lymph Nodes metabolism, Receptors, Complement 3d metabolism, Receptors, IgE metabolism
Abstract

A unique population of CD23(+) CD21(high) B cells in inflamed nodes (Bin) has been shown to accumulate in lymph nodes (LNs) draining inflamed joints of TNF-transgenic (TNF-tg) mice. Bin cells contribute to arthritis flare in mice by distorting node architecture and hampering lymphatic flow, but their existence in human inflamed LNs has not yet been described. Here, we report the characterization of resident B-cell populations in fresh popliteal lymph nodes (PLNs) from patients with severe lower limb diseases (non-RA) and rheumatoid arthritis (RA) patients, and from banked, cryopreserved reactive and normal human LN single cell suspension samples. Bin-like B cells were shown to be significantly increased in reactive LNs, and strikingly elevated (>30% of total) in RA samples. Histopathology and immunofluorescence analyses were consistent with B follicular hyperplasia and histological alterations in RA vs. non-RA PLNs. This is the first description of Bin-like B cells in human inflamed LNs. Consistent with published mouse data, this population appears to be associated with inflammatory arthritis and distortion of LN architecture. Further analyses are necessary to assess the role of CD23(+) CD21(hi) Bin-like B cells in RA pathogenesis and arthritic flare., (© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)

Published
2016
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