Aplastic anemia is a rare hematological disorder characterized by suppressed hematopoiesis and pancytopenia. Although several drugs have been associated with aplastic anemia, its occurrence in response to Osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), is extremely rare. We present a case report of a 63-year-old patient with locally advanced non-small cell lung cancer (NSCLC) who developed aplastic anemia following adjuvant treatment with Osimertinib. Extensive investigations ruled out infectious etiology, and the absence of bone marrow involvement or other identifiable causes suggested a drug-induced etiology, specifically Osimertinib. This case report emphasizes the importance of recognizing this adverse event and considering it as a potential complication of Osimertinib therapy. Vigilant monitoring and prompt management are essential for optimizing patient outcomes. Further studies are needed to better understand the risk factors, underlying mechanisms, and management strategies for Osimertinib-induced aplastic anemia in the adjuvant settings.
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http://dx.doi.org/10.3389/fonc.2024.1275275 | DOI Listing |
Discov Med
December 2024
Department of Biological Hematology, Tours University Hospital, 37000 Tours, France.
Aldehyde dehydrogenases (ALDHs) constitute a group of enzymes that catalyze the oxidation of aldehydes to carboxylic acids. The human ALDH superfamily, including 19 different isoenzymes (ALDH1A1, ALDH1A2, ALDH1A3, AHDH1B1, ALDH1L1, ALDH1L2, ALDH2, ALDH3A1, ALDH3A2, ALDH3B1, ALDH3B2, ALDH4A1, ALDH5A1, ALDH6A1, ALDH7A1, ALDH8A1, ALDH9A1, ALDHA16A1, ALDH18A1), displays different key physiological and toxicological functions, with specific tissue expression and substrate specificity. Several studies have established that ALDH are interesting markers for the identification and quantification of human hematopoietic stem cells and cancer stem cells, notably leukemic stem cells.
View Article and Find Full Text PDFNeurol Sci
December 2024
The Division of Neurology at Nemours, Mayo Clinic, Jacksonville, FL, 32207, USA.
Introduction: The effect of felbamate (FBM) on genetic generalized epilepsy (GGE) remains largely unknown. The utilization of FBM has been limited due to its potential risk of aplastic anemia and hepatic failure. This study aimed to comprehensively evaluate the efficacy and safety of FBM in the treatment of drug-resistant GGE.
View Article and Find Full Text PDFInt J Gen Med
December 2024
Institute of Hematology, School of Medicine, Jinan University, Guangzhou, People's Republic of China.
Purpose: Aplastic anemia (AA) is a bone marrow failure syndrome with an unclear pathogenesis. Abnormal T cell immunity is one of the mechanisms involved in AA, and CD3ζ is an important signaling molecule for T cell activation. Single-nucleotide polymorphisms (SNPs) in CD3ζ 3'-untranslated region (3'-UTR) were associated with some immune-related disease occurrence and affect CD3ζ protein level.
View Article and Find Full Text PDFBlood Res
December 2024
Division of Hematology-Oncology, Hanyang University Seoul Hospital, Seoul, Republic of Korea.
Purpose: This study investigated the occurrence of subsequent malignancies (SM) in adult patients with severe aplastic anemia (SAA) after allogeneic hematopoietic stem cell transplantation (allo-HSCT) to address the lack of large-scale, long-term data on this complication.
Methods: A retrospective cohort analysis of 376 adult patients with SAA who underwent allo-HSCT between 2002 and 2021 at a single center was conducted. The incidence, risk factors, and survival impact of SM were also examined.
FEBS Lett
December 2024
Department of Genetics, Research Institute of Environmental Medicine (RIeM), Nagoya University, Furo-cho, Chikusa-ku, Nagoya, 464-8601, Japan.
The transcription-coupled repair (TCR) pathway resolves transcription-blocking DNA lesions to maintain cellular function and prevent transcriptional arrest. Stalled RNA polymerase II (RNAPII) triggers repair mechanisms, including RNAPII ubiquitination, which recruit UVSSA and TFIIH. Defects in TCR-associated genes cause disorders like Cockayne syndrome, UV-sensitive syndrome, xeroderma pigmentosum, and recently defined AMeDS.
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