Xiao-Fan Wang

Conference Adv Sci (Weinh) · April 2024 Patient-Derived Organoids (PDO) and Xenografts (PDX) are the current gold standards for patient-derived models of cancer (PDMC). Nevertheless, how patient tumor cells evolve in these models and the impact on drug response remains unclear. Herein, the trans ... Full text Link to item Cite

CHARACTERIZATION OF SENESCENT HEPATOCYTE IDENTIFIED NOVEL SENOLYTICS FOR NAFLD TREATMENT

Conference HEPATOLOGY · October 2023 Link to item Cite

Targeting YAP-mediated HSC death susceptibility and senescence for treatment of liver fibrosis.

Conference Hepatology · June 1, 2023 BACKGROUND AND AIMS: Liver fibrosis results from the accumulation of myofibroblasts (MFs) derived from quiescent HSCs, and yes-associated protein (YAP) controls this state transition. Although fibrosis is also influenced by HSC death and senescence, whethe ... Full text Open Access Link to item Cite

Abstract 3536: Roles of miR-215 and regulatory mechanisms for its biogenesis in response to hypoxia in glioblastoma stem cells

Conference Cancer Research · October 1, 2014 AbstractGlioblastoma (GBM) is the most common and aggressive primary brain tumor in adults, which is highly resistant to conventional therapies. In GBM, glioblastoma stem cells (GSCs) are critical for the tu ... Full text Cite

Smad3 Loss is Associated with Aortic Dilation and Spontaneous Aortic Rupture in Lean and in Obese Diabetic Db/db Mice

Conference CIRCULATION · November 20, 2012 Link to item Cite

The histone deacetylase inhibitor trichostatin a decreases lymphangiogenesis by inducing apoptosis and cell cycle arrest via p21-dependent pathways

Conference BMC Bioinformatics · September 11, 2012 Background: The formation of new lymphatic vessels provides an additional route for tumour cells to metastasize. Therefore, inhibiting lymphangiogenesis represents an interesting target in cancer therapy. First evidence suggests that histone deacetylase in ... Full text Cite

TGF-beta/Smad3 Activation in the Diabetic Mouse Heart Induces Fibrotic Cardiac Remodeling and Diastolic Dysfunction While Protecting From Excessive Matrix Degradation and Preventing the Development of Systolic Dysfunction

Conference CIRCULATION · November 22, 2011 Link to item Cite

Smad3-/- Fibroblasts Are Hyperproliferative Cells With Impaired Migratory Capacity, Reduced Contractile Activity and Diminished Synthetic Function: Implications for Cardiac Repair and Remodeling

Conference CIRCULATION · November 3, 2009 Link to item Cite

PP2A-dependent dephosphorylation of replication protein A (RPA) is required for the removal of DNA breaks induced by replication stress

Conference CANCER RESEARCH · May 1, 2009 Link to item Cite

Xiao-Fan Wang

Scholarly Works - Conferences

Chromatin Remodeling in Patient-Derived Colorectal Cancer Models.

CHARACTERIZATION OF SENESCENT HEPATOCYTE IDENTIFIED NOVEL SENOLYTICS FOR NAFLD TREATMENT

Targeting YAP-mediated HSC death susceptibility and senescence for treatment of liver fibrosis.

Abstract 3536: Roles of miR-215 and regulatory mechanisms for its biogenesis in response to hypoxia in glioblastoma stem cells

Smad3 Loss is Associated with Aortic Dilation and Spontaneous Aortic Rupture in Lean and in Obese Diabetic Db/db Mice

The histone deacetylase inhibitor trichostatin a decreases lymphangiogenesis by inducing apoptosis and cell cycle arrest via p21-dependent pathways

TGF-beta/Smad3 Activation in the Diabetic Mouse Heart Induces Fibrotic Cardiac Remodeling and Diastolic Dysfunction While Protecting From Excessive Matrix Degradation and Preventing the Development of Systolic Dysfunction

Smad3-/- Fibroblasts Are Hyperproliferative Cells With Impaired Migratory Capacity, Reduced Contractile Activity and Diminished Synthetic Function: Implications for Cardiac Repair and Remodeling

PP2A-dependent dephosphorylation of replication protein A (RPA) is required for the removal of DNA breaks induced by replication stress

The Smad3 Pathway Critically Regulates Myofibroblast Proliferation And Synthetic Activity In Healing Myocardial Infarcts

Smad3 signaling critically regulates infarct healing

Disruption of the Smad3 signaling pathway attenuates post-infarction remodeling

Cytoplasmic tyrosine kinase c-Abl is required for bFGF but not VEGF-induced tumor angiogenesis