دورية أكاديمية
Evaluating targeted therapies in older patients with TP53 -mutated AML.
| العنوان: | Evaluating targeted therapies in older patients with TP53 -mutated AML. |
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| المؤلفون: | Sabile JMG; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA., Swords R; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.; Division of Hematology & Medical Oncology, Department of Medicine, Oregon Health & Science University, Portland, OR, USA., Tyner JW; Knight Cancer Institute, Oregon Health & Science University, Portland, OR, USA.; Department of Cell, Developmental & Cancer Biology, Oregon Health & Science University, Portland, OR, USA. |
| المصدر: | Leukemia & lymphoma [Leuk Lymphoma] 2024 Apr 22, pp. 1-18. Date of Electronic Publication: 2024 Apr 22. |
| Publication Model: | Ahead of Print |
| نوع المنشور: | Journal Article; Review |
| اللغة: | English |
| بيانات الدورية: | Publisher: Taylor & Francis Country of Publication: United States NLM ID: 9007422 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1029-2403 (Electronic) Linking ISSN: 10268022 NLM ISO Abbreviation: Leuk Lymphoma Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: [Philadelphia, PA] : Taylor & Francis Original Publication: Chur ; New York : London, UK : Harwood Academic Publishers ; Distributed by STBS, 1989- |
| مستخلص: | Mutation of thetumor suppressor gene, TP53 ( tumor protein 53 ), occurs in up to 15% of all patients with acute myeloid leukemia (AML) and is enriched within specific clinical subsets, most notably in older adults, and including secondary AML cases arising from preceding myeloproliferative neoplasm (MPN), myelodysplastic syndrome (MDS), patients exposed to prior DNA-damaging, cytotoxic therapies. In all cases, these tumors have remained difficult to effectively treat with conventional therapeutic regimens. Newer approaches fortreatmentof TP53- mutated AML have shifted to interventions that maymodulate TP53 function, target downstream molecular vulnerabilities, target non-p53 dependent molecular pathways, and/or elicit immunogenic responses. This review will describe the basic biology of TP53 , the clinical and biological patterns of TP53 within myeloid neoplasms with a focus on elderly AML patients and will summarize newer therapeutic strategies and current clinical trials. |
| فهرسة مساهمة: | Keywords: AML; TP53; clinical trial; precision medicine |
| تواريخ الأحداث: | Date Created: 20240422 Latest Revision: 20240422 |
| رمز التحديث: | 20240422 |
| DOI: | 10.1080/10428194.2024.2344057 |
| PMID: | 38646877 |
| قاعدة البيانات: | MEDLINE |
PDF full text from Publisher | تدمد: | 1029-2403 |
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| DOI: | 10.1080/10428194.2024.2344057 |