Amber M. Amparo
A5082407072- Pancreatic and Hepatic Oncology Research
- Advanced Breast Cancer Therapies
- Colorectal Cancer Treatments and Studies
- Neuroendocrine Tumor Research Advances
- Cancer Genomics and Diagnostics
- Biochemical and Molecular Research
- Amino Acid Enzymes and Metabolism
- Cancer Treatment and Pharmacology
- Cancer Research and Treatments
- Cancer, Hypoxia, and Metabolism
- Cancer Mechanisms and Therapy
- ATP Synthase and ATPases Research
- Peptidase Inhibition and Analysis
- Protein Tyrosine Phosphatases
- Chronic Lymphocytic Leukemia Research
- Computational Drug Discovery Methods
- Venous Thromboembolism Diagnosis and Management
- Lung Cancer Research Studies
- Neuroblastoma Research and Treatments
- Vascular Procedures and Complications
- Peripheral Artery Disease Management
- PI3K/AKT/mTOR signaling in cancer
- Protein Kinase Regulation and GTPase Signaling
University of North Carolina at Chapel Hill
2022-2024
University of Cincinnati
2024
University of Cincinnati Medical Center
2024
UNC Lineberger Comprehensive Cancer Center
2023
Mutational loss of CDKN2A (encoding p16INK4A) tumor-suppressor function is a key genetic step that complements activation KRAS in promoting the development and malignant growth pancreatic ductal adenocarcinoma (PDAC). However, pharmacologic restoration p16INK4A with inhibitors CDK4 CDK6 (CDK4/6) has shown limited clinical efficacy PDAC. Here, we found concurrent treatment both CDK4/6 inhibitor (CDK4/6i) an ERK-MAPK (ERKi) synergistically suppresses PDAC cell lines organoids by cooperatively...
Abstract Broad-spectrum RAS inhibition has the potential to benefit roughly a quarter of human patients with cancer whose tumours are driven by mutations 1,2 . RMC-7977 is highly selective inhibitor active GTP-bound forms KRAS, HRAS and NRAS, affinity for both mutant wild-type variants 3 More than 90% cases pancreatic ductal adenocarcinoma (PDAC) activating in KRAS 4 Here we assessed therapeutic comprehensive range PDAC models. We observed broad pronounced anti-tumour activity across models...
Despite significant advancements in the treatment of other cancers, pancreatic ductal adenocarcinoma (PDAC) remains one world’s deadliest cancers. More than 90% PDAC patients harbor a Kirsten rat sarcoma (KRAS) gene mutation. Although clinical potential anti-KRAS therapies has long been realized, all initial efforts to target KRAS were unsuccessful. However, with recent development new generation KRAS-targeting drugs, multiple KRAS-targeted options for have entered trials. In this review, we...
Critical limb ischemia represents the most severe stage of peripheral vascular disease and patients often present with complex, calcified infrapopliteal lesions. Atherectomy is an endovascular treatment modality that can be used to debulk otherwise uncrossable We performed a retrospective, single-center, case report two who presented critical whose complex lesions were treated 1.5 mm Phoenix System after prior failed angioplasty attempts. The successfully debulked each lesion, patient...
<b>Abstract ID 91572</b> <b>Poster Board 244</b> Text</b> Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease that projected to become the 2<sup>nd</sup> leading cause of cancer-related mortality by 2030, surpassing colorectal cancer deaths. Mutational activation <i>KRAS</i> oncogene present in over 90% PDAC cases. For nearly four decades, KRAS small GTPase was deemed undruggable. Due recent breakthroughs, inhibitors targeting KRAS<sup>G12C</sup> mutation are FDA-approved and various...
Abstract KRASQ61 mutations are associated with the worst prognosis among various KRAS mutational subtypes of pancreatic ductal adenocarcinoma (PDAC). RMC-7977 is a RAS(ON) multi-selective noncovalent inhibitor broad spectrum activity against oncogenic RAS mutants and wild-type RAS. The related investigational agent RMC-6236 currently undergoing clinical trials. Binary complexes CypA: bind equipotently to multiple however less potent at inhibiting growth in KRASQ61H-mutant cell lines. In...
<div>Abstract<p>Mutational loss of CDKN2A (encoding p16INK4A) tumor-suppressor function is a key genetic step that complements activation KRAS in promoting the development and malignant growth pancreatic ductal adenocarcinoma (PDAC). However, pharmacologic restoration p16INK4A with inhibitors CDK4 CDK6 (CDK4/6) has shown limited clinical efficacy PDAC. Here, we found concurrent treatment both CDK4/6 inhibitor (CDK4/6i) an ERK–MAPK (ERKi) synergistically suppresses PDAC cell lines...
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<p>Supplementary Data and Materials</p>
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