Purine nucleoside phosphorylase (PNP) deficiency is an autosomal recessive metabolic disorder characterized by severe combined immunodeficiency and by complex neurologic symptomatology including ataxia, developmental delay, and spasticity. Herein we report severe marrow dysplasia in a patient with PNP deficiency. Drug-related marrow dysfunction was unlikely, and marrow virological studies were negative. A preleukemic myelodysplastic syndrome was also unlikely due to normal marrow CD34+ cells, colony growth in clonogenic assay of marrow mononuclear cells, apoptosis rate, and Fas expression on marrow nucleated cells, as well as morphologic improvement of the marrow dysplasia after normal red blood cell transfusion. The patient's marrow stroma showed hypersensitivity to irradiation and undetectable PNP enzyme activity similar to peripheral lymphocytes. This is the first report of PNP deficiency associated with increased lymphocyte and marrow stromal sensitivity to irradiation. We conclude that marrows from patients with PNP deficiency might have hypersensitivity to irradiation and can develop dysplastic morphology, caused either directly or indirectly by the inherited enzymatic defect.
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http://dx.doi.org/10.1203/01.PDR.0000111286.23110.F8 | DOI Listing |
Cureus
December 2024
Pediatric Neurology, Armed Forces Hospital Southern Region, Khamis Mushayt, SAU.
Purine nucleoside phosphorylase (PNP) deficiency is one of the very rare types of immune deficiency disorders inherited in an autosomal recessive (AR) manner. PNP deficiency is a progressive immune disorder that can range from severe combined immunodeficiency (SCID) to combined immunodeficiency and is associated with recurrent infections, neurological manifestations, and sometimes autoimmune disorders. In our case, we describe the case of a female patient, two years and six months old, with recurrent infections, severe neutropenia, failure to thrive, and a history of a deceased sister with the same condition.
View Article and Find Full Text PDFHematology
December 2025
Department of Hematology & Oncology, Children's Hospital of Soochow University, Suzhou, People's Republic of China.
Purpose: We report the case of a 6-year-old boy who presented with muscular hypertonia, impaired growth, and recurrent infections, who was diagnosed with purine nucleoside phosphorylase (PNP) deficiency with two novel mutations in the gene. He underwent a hematopoietic stem cell transplantation (HSCT) from an unrelated donor, and we observed the clinical outcome.
Methods: We retrospectively analyzed the clinical manifestations and outcomes of this patient who underwent HSCT.
J Med Chem
January 2025
Department of Pharmaceutical Engineering, School of Engineering, China Pharmaceutical University, 639 Longmian Avenue, Nanjing 211198, China.
Cancer Med
December 2024
School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai, Shandong, People's Republic of China.
Background: Methylthioadenosine phosphorylase (MTAP) and protein arginine methyltransferase 5 (PRMT5) are considered to be a synthetic lethal pair of targets, due to the fact that deletion of MTAP leads to massive production of methylthioadenosine (MTA) decreasing the activity of PRMT5. In vitro and in vivo experiments have demonstrated that MRTX1719, a small molecule that selectively binds PRMT5/MTA complex, significantly inhibits the proliferation of MTAP-deficient tumors and has a weak toxic effect on normal cells. However, it has been reported that MTAP-deleted tumors did not significantly accumulate MTA in vivo due to metabolism of MTA by MTAP-expressing stroma, which might lead to a diminished anti-cancer effect of MRTX1719.
View Article and Find Full Text PDFLung Cancer
November 2024
Institute of Medical Genetics and Pathology, University Hospital Basel, Basel, Schönbeinstrasse 40, CH-4031 Basel, Switzerland. Electronic address:
S-methyl-5'-thioadenosine phosphorylase (MTAP) deficiency is an emerging biomarker in non-small cell lung cancer (NSCLC) and beyond. The MTAP gene is located in the chromosomal region 9p21.3, which shows one of the most common homozygous deletions across all human cancers (9p21 loss).
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