A5024073568- Neurofibromatosis and Schwannoma Cases
- Musculoskeletal synovial abnormalities and treatments
- Nerve Injury and Rehabilitation
- Nerve injury and regeneration
- Surface Treatment and Residual Stress
- Sarcoma Diagnosis and Treatment
- Bone Tumor Diagnosis and Treatments
- Neuroblastoma Research and Treatments
- Testicular diseases and treatments
- Reconstructive Surgery and Microvascular Techniques
- Cancer-related molecular mechanisms research
- Cytokine Signaling Pathways and Interactions
- Cancer-related gene regulation
- Peripheral Artery Disease Management
- Cell Adhesion Molecules Research
- Kruppel-like factors research
- Angiogenesis and VEGF in Cancer
- Tumors and Oncological Cases
- Soft tissue tumor case studies
Washington University in St. Louis
2021-2025
Abstract Purpose: Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with limited treatment options and poor survival rates. About half of MPNST cases associated the neurofibromatosis type 1 (NF1) cancer predisposition syndrome. Overexpression TYK2 occurs in majority MPNST, implicating as a therapeutic target. Experimental Design: The effects pharmacologic inhibition on cell proliferation were examined using IncuCyte live assays vitro, downstream actions analyzed...
The rising demand for autologous breast reconstruction presents challenges patients with primary hypercoagulability disorders due to their elevated thrombotic risks. In this article, we reviewed 13 who underwent 23 free flap reconstructions from 1998 2023 various anticoagulation regimens. Results showed a loss rate of 4%, additional intraoperative and postoperative potentially reducing complications. data concludes that in hypercoagulable is reliable careful management.
Sutureless anastomotic devices present several advantages over traditional suture anastomosis, including expanded global access to microvascular surgery, shorter operation and ischemic times, reduced costs. However, their adaptation for arterial use remains a challenge. This review aims provide comprehensive overview of sutureless approaches that are either FDA-approved or under investigation. These include extraluminal couplers, intraluminal devices, methods assisted by lasers vacuums, with...
Abstract Background Malignant peripheral nerve sheath tumors (MPNST) are aggressive soft tissue sarcomas that often develop in patients with neurofibromatosis type 1 (NF1). To address the critical need for novel therapeutics MPNST, we aimed to establish an ex vivo 3D platform accurately captured genomic diversity of MPNST and could be utilized a medium-throughput manner drug screening studies validated using patient-derived xenografts (PDX). Methods Genomic analysis was performed on all...
We show that loss of chr3q is associated with worse outcomes in fusion-negative (FN)-RMS compared fusion-positive (FP)-RMS, suggesting this chromosomal abnormality could be a prognostic marker for (FN) RMS.
Abstract OBJECTIVES Malignant peripheral nerve sheath tumors (MPNST) are highly aggressive sarcomas with limited treatment options and poor survival rates, necessitating the development of novel therapeutics. Approximately 25-50% MPNST harbor loss enzyme methylthioadenosine phosphorylase (MTAP) due to a passenger deletion driven by proximal tumor suppressor gene, CDKN2A. PRMT5 was identified as selective dependence in MTAP-deleted cells accumulation substrate (MTA), which is itself an...
Abstract OBJECTIVES Malignant peripheral nerve sheath tumors (MPNST) are aggressive soft tissue sarcomas that frequently arise from benign plexiform neurofibromas (PN). Approximately half of MPNST associated with Neurofibromatosis type 1 (NF1). Despite partial elucidation the molecular mechanisms underlying MPNST, diagnosis remains challenging, and prognosis is poor. Previously, we found cells have elevated βIII-spectrin, a cytoskeletal protein involved in cell morphology regulation...
<div>AbstractPurpose:<p>Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with limited treatment options and poor survival rates. About half of MPNST cases associated the neurofibromatosis type 1 (NF1) cancer predisposition syndrome. Overexpression TYK2 occurs in majority MPNST, implicating as a therapeutic target.</p>Experimental Design:<p>The effects pharmacologic inhibition on cell proliferation were examined using IncuCyte live assays...
<div>AbstractPurpose:<p>Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with limited treatment options and poor survival rates. About half of MPNST cases associated the neurofibromatosis type 1 (NF1) cancer predisposition syndrome. Overexpression TYK2 occurs in majority MPNST, implicating as a therapeutic target.</p>Experimental Design:<p>The effects pharmacologic inhibition on cell proliferation were examined using IncuCyte live assays...
<div>AbstractPurpose:<p>Malignant peripheral nerve sheath tumors (MPNST) are aggressive sarcomas with limited treatment options and poor survival rates. About half of MPNST cases associated the neurofibromatosis type 1 (NF1) cancer predisposition syndrome. Overexpression TYK2 occurs in majority MPNST, implicating as a therapeutic target.</p>Experimental Design:<p>The effects pharmacologic inhibition on cell proliferation were examined using IncuCyte live assays...
<p>Supplementary Table S3</p>
<p>Supplementary Table S2</p>
<p>Supplementary Table S1</p>
<p>Supplemental Fig.S7. The TYK2 inhibitor, WU-76, reduces activation of STAT3 while stimulating ERK1/2 in MPNST cells.</p>
<p>Supplemental Fig.S8. Inhibitors of TYK2 (deucravacitinib) and MEK (mirdametinib) act synergistically to reduce proliferation increase apoptosis in JH-2-002 MPNST cells.</p>
<p>Supplemental Fig.S8. Inhibitors of TYK2 (deucravacitinib) and MEK (mirdametinib) act synergistically to reduce proliferation increase apoptosis in JH-2-002 MPNST cells.</p>
<p>Supplemental Fig.S3. Genetic knockout of TYK2 blocks the effects inhibitors on proliferation in JW23.3 cells.</p>
<p>Supplemental Fig.S1. Inhibition of TYK2 induces apoptosis in MPNST cell-lines</p>
<p>Supplemental Fig.S7. The TYK2 inhibitor, WU-76, reduces activation of STAT3 while stimulating ERK1/2 in MPNST cells.</p>
<p>Supplementary Table S3</p>
<p>Supplemental Fig.S9. Synergy of TYK2 and MEK inhibitors in MPNST-724 cells.</p>