Human Dihydropyrimidine Dehydrogenase ELISA , DPYD
- Known as:
- Human Dihydropyrimidine Dehydrogenase Enzyme-linked immunosorbent assay test , DPYD
- Catalog number:
- E01D0256
- Product Quantity:
- 96 Tests/kit
- Category:
- -
- Supplier:
- BGene
- Gene target:
- Human Dihydropyrimidine Dehydrogenase ELISA DPYD
Related genes to: Human Dihydropyrimidine Dehydrogenase ELISA , DPYD
- Gene:
- DPYD NIH gene
- Name:
- dihydropyrimidine dehydrogenase
- Previous symbol:
- -
- Synonyms:
- DPD
- Chromosome:
- 1p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-07
- Date modifiied:
- 2019-04-23
Related products to: Human Dihydropyrimidine Dehydrogenase ELISA , DPYD
Related articles to: Human Dihydropyrimidine Dehydrogenase ELISA , DPYD
- Fluoropyrimidines, including 5-fluorouracil and capecitabine, are widely used antimetabolite agents and remain central to the treatment of several solid tumors, particularly gastrointestinal malignancies. However, they are a well-established cause of chemotherapy-related cardiotoxicity. Although coronary vasospasm is the best recognized manifestation, fluoropyrimidine cardiotoxicity encompasses a broad clinical spectrum, ranging from chest pain and arrhythmias to acute heart failure, and, rarely, fulminant cardiogenic shock. This review discusses severe fluoropyrimidine-associated cardiotoxicity through the illustrative presentation of a young woman without prior cardiovascular disease who developed acute biventricular dysfunction and cardiogenic shock shortly after first exposure to FOLFIRINOX, requiring temporary mechanical circulatory support. Administration of uridine triacetate within the recommended therapeutic window was associated with rapid recovery of ventricular function. Cardiac magnetic resonance imaging demonstrated diffuse myocardial edema without late gadolinium enhancement, consistent with reversible toxic-inflammatory myocardial injury. Expanded genomic analysis identified DPYD and TYMS variants not detected by standard pretreatment pharmacogenetic screening. We herein examine the pathophysiological mechanisms of fluoropyrimidine cardiotoxicity, the rationale for uridine triacetate in severe presentations, and the potential role of expanded pharmacogenomic profiling within a precision cardio-oncology framework. - Source: PubMed
Publication date: 2026/07/06
Filomia SimoneDel Buono Marco GiuseppeSaponara GianluigiAurigemma CristinaMarano RiccardoMoliterno EleonoraTortora GiampaoloMinucci AngeloSalvatore LisaSoave Paolo MaurizioBurzotta FrancescoSanna Tommaso - The management of resectable stage II/III colon cancer (CC) has long relied on clinicopathological features and fluoropyrimidine-based adjuvant chemotherapy. However, this approach fails to capture the profound biological heterogeneity of the disease, often leading to overtreatment or undertreatment. A new generation of biomarkers now allows a shift toward precision oncology, refining prognosis and predicting therapeutic response. This systematic review critically appraises the evidence for biomarker-guided adjuvant therapy. - Source: PubMed
Publication date: 2026/07/05
Ismaili Nabil - Colorectal cancer is a common yet survivable malignancy, partly due to the addition of chemoradiation to treatment regimens. Many patients suffer treatment-related side effects such as pain, diarrhea, and myelosuppression, and increasing tolerance of treatment has the potential to improve outcomes. BMX-001, a superoxide dismutase mimetic, is currently in clinical trials as a selective radioprotector for anal and rectal cancer; however, the mechanism by which BMX-001 exerts selective radioprotection of healthy tissue over cancer tissue, particularly when administered at physiologically achievable doses, is not well understood. BMX-001 was given before and during chemoradiation and did not interfere with chemoradiation-induced cancer cell killing in mouse models. , BMX-001 still induced cancer cell killing in the presence of exogenous catalase, suggesting that BMX-001's anti-tumor activity is not solely reliant on hydrogen peroxide production. BMX-001 exerted robust acute radioprotection in radiation mouse models five and nine days post-radiation. To assess whether BMX-001's protection is contingent on Nrf2 expression, we evaluated the effect of BMX-001 on 5-FU treated mouse bone marrow, where Nrf2 is crucial to maintaining hematopoietic stem cell niches. Interestingly, BMX-001 could still exert some chemoprotection in mice without functional Nrf2. To assess whether BMX-001 had any functional effects on protein oxidation status, we performed mass spectrometry analysis to evaluate sulfenylated proteins in bone marrow treated with 5-FU in wildtype mice and mice without Nrf2. We found that BMX-001 given before 5-FU treatment resulted in the sulfenylation of CRTC2 and CBP, two proteins involved in CREB signaling and known to enhance Nrf2 activity. We also found that BMX-001 with 5-FU treatment enhanced DPYD sulfenylation, a protein known to detoxify 5-FU, and ALDH7A1 sulfenylation, a protein known to detoxify aldehydes. Together, these results suggest that BMX-001 can protect against oxidative stress in normal tissue via Nrf2 dependent and independent mechanisms. - Source: PubMed
Publication date: 2026/03/12
Myers Molly SKosmacek Elizabeth ALiew Chia SinChatterjee ArpitaWojtkiewicz MelindaRoy PoojaHyde R KatherineDhawan PunitaSpasojevic IvanWang ShuoHewitt Kyle JFurdui Cristina MGundry Rebekah LRiethoven Jean-Jack MLin ChiOberley-Deegan Rebecca E - DPYD genotyping before capecitabine therapy represents a clinically actionable pharmacogenomic strategy to reduce avoidable fluoropyrimidine-related toxicity in metastatic breast cancer. Commenting on the cost-effectiveness analysis by Chiddarwar, Blaes and Kuntz, this correspondence supports the authors' findings while extending the discussion from economic value to implementation readiness. We propose that DPYD testing should be evaluated through a globally transferable framework incorporating ancestry-aware variant coverage, rapid turnaround pathways, genotype-linked dose decision support, budget-impact assessment and real-world toxicity surveillance. Such an approach may help translate cost-effective pharmacogenomics into equitable, operationally feasible breast cancer care across diverse health systems. - Source: PubMed
Publication date: 2026/06/26
Jayaswal Rajesh PrasadRana Anuj KumarBadyal Rama Kumari - We examined the distribution of clinically-relevant DPYD polymorphisms in Yanomami and Munduruku individuals, from Indigenous reservation areas in the Brazilian Amazon. The estimated proportion of Native ancestry exceeded 90% in all participants. - Source: PubMed
Publication date: 2026/06/23
Suarez-Kurtz GuilhermeBasta Paulo CPerini Jamila Alessandra