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Journal Articles

Therapeutic Targeting of the Inflammasome to Mitigate Murine Sclerodermatous Chronic Graft Versus Host Disease

Shanid Mohiyuddin, Vasantharaja Raguraman, Nashwan Jabbour, Melissa Kesler, Jayakrishna Ambati, Senthilnathan Palaniyandi, Gerhard C Hildebrandt

Blood (2024) 144 (Supplement 1): 3394.

https://doi.org/10.1182/blood-2024-206103

Published: 2024

Journal Articles

Stabilization of HIF-1α By the Prolyl Hydroxylase Inhibitor Roxadustat Reduces Gastrointestinal Graft-Versus-Host Disease

Vasantharaja Raguraman, Shanid Mohiyuddin, Catherine Benge, Linnea Banker, Tyler Plank, Richard D Hammer, Senthilnathan Palaniyandi, Gerhard C Hildebrandt

Blood (2024) 144 (Supplement 1): 262.

https://doi.org/10.1182/blood-2024-204027

Published: 2024

Journal Articles

Dimethyl Oxalyl Glycine a Prolyl Hydroxylase Inhibitor Decreases Early Gastrointestinal Gvhd Via Two Independent Pathways of Apoptosis after Allogeneic Hematopoietic Cell Transplantation

Reena Kumari, PhD, Senthilnathan Palaniyandi, PhD, Ethan Strattan, BS, Sabarinath Venniyil Radhakrishnan, MBBS, MD, Gerhard Carl Hildebrandt, MD

Blood (2018) 132 (Supplement 1): 3317.

https://doi.org/10.1182/blood-2018-99-116245

Published: 2018

Journal Articles

TNFAIP8 (TIPE) Deficiency Exacerbates Acute Graft Versus-Host Disease in Murine Model

Reena Kumari, PhD, Senthilnathan Palaniyandi, PhD, Ethan Strattan, BS, Katharina Kohler, Nashwan Jabbour, Joanna Dalland, MD, Melissa Kesler, MD, Gerhard Carl Hildebrandt, MD

Blood (2017) 130 (Supplement 1): 3169.

https://doi.org/10.1182/blood.V130.Suppl_1.3169.3169

Published: 2017

Journal Articles

The Prolyl Hydroxylase Inhibitor Dimethyl Oxalyl Glycine Decreases the Severity of Acute Lung Injury After Allogeneic Hematopoietic Cell Transplantation.

Sabarinath Venniyil Radhakrishnan, MD, Senthilnathan Palaniyandi, PhD, Fridrik Karlsson, PhD, Elisabeth Huber, MD, Gerhard Hildebrandt, MD

Blood (2012) 120 (21): 3006.

https://doi.org/10.1182/blood.V120.21.3006.3006

Published: 2012

Journal Articles

Enhanced activation of STAT pathways and overexpression of survivin confer resistance to FLT3 inhibitors and could be therapeutic targets in AML

Jianbiao Zhou, Chonglei Bi, Jasinghe V. Janakakumara, Shaw-Cheng Liu, Wee-Joo Chng, Kian-Ghee Tay, Lai-Fong Poon, Zhigang Xie, Senthilnathan Palaniyandi, Hanry Yu, Keith B. Glaser, Daniel H. Albert, Steven K. Davidsen, Chien-Shing Chen

Blood (2009) 113 (17): 4052–4062.

https://doi.org/10.1182/blood-2008-05-156422

Published: 2009

Includes: Supplemental data

NARROW

Therapeutic Targeting of the Inflammasome to Mitigate Murine Sclerodermatous Chronic Graft Versus Host Disease

Stabilization of HIF-1α By the Prolyl Hydroxylase Inhibitor Roxadustat Reduces Gastrointestinal Graft-Versus-Host Disease

Dimethyl Oxalyl Glycine a Prolyl Hydroxylase Inhibitor Decreases Early Gastrointestinal Gvhd Via Two Independent Pathways of Apoptosis after Allogeneic Hematopoietic Cell Transplantation

TNFAIP8 (TIPE) Deficiency Exacerbates Acute Graft Versus-Host Disease in Murine Model

The Prolyl Hydroxylase Inhibitor Dimethyl Oxalyl Glycine Decreases the Severity of Acute Lung Injury After Allogeneic Hematopoietic Cell Transplantation.

Enhanced activation of STAT pathways and overexpression of survivin confer resistance to FLT3 inhibitors and could be therapeutic targets in AML

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ASH Publications

American Society of Hematology

Therapeutic Targeting of the Inflammasome to Mitigate Murine Sclerodermatous Chronic Graft Versus Host Disease

Stabilization of HIF-1α By the Prolyl Hydroxylase Inhibitor Roxadustat Reduces Gastrointestinal Graft-Versus-Host Disease

Dimethyl Oxalyl Glycine a Prolyl Hydroxylase Inhibitor Decreases Early Gastrointestinal Gvhd Via Two Independent Pathways of Apoptosis after Allogeneic Hematopoietic Cell Transplantation

TNFAIP8 (TIPE) Deficiency Exacerbates Acute Graft Versus-Host Disease in Murine Model

The Prolyl Hydroxylase Inhibitor Dimethyl Oxalyl Glycine Decreases the Severity of Acute Lung Injury After Allogeneic Hematopoietic Cell Transplantation.

Enhanced activation of STAT pathways and overexpression of survivin confer resistance to FLT3 inhibitors and could be therapeutic targets in AML

Email alerts

ASH Publications

American Society of Hematology

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