One of the key challenges to improved testing of new experimental therapeutics in renal cell carcinoma (RCC) is the development of models that faithfully recapitulate early- and late-stage metastatic disease progression. Typical tumor implantation models utilize ectopic or orthotopic primary tumor implantation, but few include systemic spontaneous metastatic disease that mimics the clinical setting. This protocol describes the key steps to develop RCC disease progression stages similar to patients. First, it uses a highly metastatic mouse tumor cell line in a syngeneic model to show orthotopic tumor cell implantation. Methods include superficial and internal implantation into the sub-capsular space with cells combined with matrigel to prevent leakage and early spread. Next it describes the procedures for excision of tumor-bearing kidney (nephrectomy), with critical pre- and post- surgical mouse care. Finally, it outlines the steps necessary to monitor and assess micro-and macro-metastatic disease progression, including bioluminescent imaging as well provides a detailed visual necropsy guide to score systemic disease distribution. The goal of this protocol description is to facilitate the widespread use of clinically relevant metastatic RCC models to improve the predictive value of future therapeutic testing.
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http://dx.doi.org/10.3791/51485 | DOI Listing |
Retina
January 2025
Department of Ophthalmology, Amsterdam UMC, Amsterdam, The Netherlands.
Purpose: To evaluate the presence and progression of maculopathy in patients with sickle cell disease (SCD) using Optical Coherence Tomography (OCT) and OCT-Angiography (OCTA), and to identify clinical/laboratory risk factors for progression during follow-up.
Methods: Complete ophthalmic examination, including fundoscopy and macular SD-OCT/OCTA scans, was performed in consecutive SCD-patients (HbSS/HbSβ0/HbSβ+/HbSC genotype) during baseline and follow-up visits. SCR stage was based on fundoscopy instead of the Goldberg classification, since fluorescein angiography was not routinely used.
Inflamm Bowel Dis
January 2025
Department of Genetics and Genomics, Icahn School of Medicine at Mount Sinai, 1 Gustave L. Levy Pl, Box 1498, New York, NY 10029, USA.
Background: Clonal hematopoiesis of indeterminate potential (CHIP) is the presence of somatic mutations in myeloid and lymphoid malignancy genes in the blood cells of individuals without a hematologic malignancy. Inflammation is hypothesized to be a key mediator in the progression of CHIP to hematologic malignancy and patients with CHIP have a high prevalence of inflammatory diseases. This study aimed to identify the prevalence and characteristics of CHIP in patients with inflammatory bowel disease (IBD).
View Article and Find Full Text PDFPLoS One
January 2025
Department of Microbiology, Faculty of Science, Kasetsart University, Bangkok, Thailand.
The "a" determinant, a highly conformational region within the hepatitis B virus large surface protein (LHBs), is crucial for antibody neutralization and diagnostic assays. Mutations in this area can lead to conformational changes, resulting in vaccination failure, diagnostic evasion, and disease progression. The "a" determinant of LHBs contains a conserved N-linked glycosylation site at N320, but the mechanisms of glycosylation in LHBs remain unclear.
View Article and Find Full Text PDFPLoS One
January 2025
Nephrological Department, Herlev Hospital, University of Copenhagen, Copenhagen, Denmark.
Secondary hyperparathyroidism (sHPT) is a significant clinical complication of CKD leading to bone abnormalities and cardiovascular disease. Current treatment based on activating the parathyroid calcium-sensing receptor (CaSR) using calcimimetics such as Cinacalcet, aims to decrease plasma PTH levels and inhibit the progression of parathyroid hyperplasia. In the present study, we found significant diurnal rhythmicity of Casr, encoding the Cinacalcet drug target in hyperplastic parathyroid glands (p = 0.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Background: Systemic diseases are often associated with endothelial cell (EC) dysfunction. A key function of ECs is to maintain the barrier between the blood and the interstitial space. The integrity of the endothelial cell barrier is maintained by VE-Cadherin homophilic interactions between adjacent cells.
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