Chronic myeloid leukemia is characterized by a single genetic abnormality resulting in a fusion gene whose mRNA product is easily detected and quantified by reverse-transcriptase polymerase chain reaction analysis. Measuring residual disease was originally introduced to identify patients relapsing after allogeneic stem cell transplantation but rapidly adopted to quantify responses to tyrosine kinase inhibitors. Real-time quantitative polymerase chain reaction is now an essential tool for the management of patients and is used to influence treatment decisions. In this review we track this development including the international collaboration to standardize results, discuss the integration of molecular monitoring with other factors that affect patients' management, and describe emerging technology. Four case histories describe varying scenarios in which the accurate measurement of residual disease identified patients at risk of disease progression and allowed appropriate investigations and timely clinical intervention.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9713565 | PMC |
http://dx.doi.org/10.3324/haematol.2022.281493 | DOI Listing |
Blood
January 2025
Department I of Internal Medicine and German CLL Study Group; Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf (CIO ABCD); University of Cologne, Faculty of Medicine and University Hos, Cologne, Germany.
The phase 2 CLL2-BZAG trial tested a measurable residual disease (MRD)-guided combination treatment of zanubrutinib, venetoclax and obinutuzumab after an optional bendamustine debulking in patients with relapsed/refractory CLL. In total, 42 patients were enrolled and two patients with ≤2 induction cycles were excluded from the analysis population per protocol. Patients had a median of one prior therapy (range 1-5), 18 patients (45%) had already received a BTK inhibitor (BTKi), seven patients (17.
View Article and Find Full Text PDFInvest Ophthalmol Vis Sci
January 2025
State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou, China.
Purpose: The purpose of this study was to investigate the contribution and natural progression of ABCA4 deep intronic variants (DIVs) among a Chinese Stargardt disease (STGD) cohort.
Methods: For unsolved STGD probands, DIVs in ABCA4 were detected by next-generation sequencing, and splicing effects were evaluated by in silico tools and validated through minigene experiments. Comprehensive ocular examinations, especially fundus changes, were carried out and analyzed.
Eur J Nucl Med Mol Imaging
January 2025
Nuclear Medicine and Clinical Molecular Imaging, University Hospital Tuebingen, Otfried-Mueller-Str. 14, 72076, Tuebingen, Germany.
Purpose: Somatostatin receptor (SSTR)-PET is crucial for effective treatment stratification of neuroendocrine neoplasms (NENs). In highly proliferating or poorly differentiated NENs, dual-tracer approaches using additional [F]FDG PET can effectively identify SSTR-negative disease, usually requiring separate imaging sessions. We evaluated the feasibility of a one-day dual-tracer imaging protocol with a low activity [F]FDG PET followed by an SSTR-PET using the recently introduced [F]SiFAlin-TATE tracer in a long axial field-of-view (LAFOV) PET/CT scanner and its implications in patient management.
View Article and Find Full Text PDFBiomater Res
January 2025
Department of Ultrasound, Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, Guangdong Province 519000, China.
Insufficient radio-frequency ablation (IRFA) of hepatocellular carcinoma accelerates the recurrence of residual tumor, leading to a poor prognosis. Neutrophils (NEs), as the initial leukocytes to infiltrate the IRFA-associated inflammatory area, were utilized as drug carriers due to their inherent chemotactic properties for targeted delivery of chemotherapy drugs to the inflammatory site where residual tumor persists post-IRFA. Previous research has highlighted that the immunosuppressive cytokines in the tumor microenvironment could promote the transition of NEs into a protumorigenic phenotype.
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