Clonal hematopoiesis of indeterminate potential is rare in pediatric patients undergoing autologous stem cell transplantation

被引:0
作者
Kartal-Kaess, Mutlu [1 ,2 ]
Karow, Axel [1 ,2 ,3 ]
Bacher, Ulrike [2 ,4 ]
Pabst, Thomas [2 ,5 ]
Joncourt, Raphael [2 ,4 ]
Zweier, Christiane [6 ]
Kuehni, Claudia E. [1 ,7 ]
Porret, Naomi Azur [2 ,4 ]
Roessler, Jochen [1 ,2 ]
机构
[1] Univ Bern, Univ Hosp, Dept Pediat, Inselspital,Div Pediat Hematol & Oncol, Bern, Switzerland
[2] Univ Bern, Dept Biomed Res, Freiburgstr 1, CH-3010 Bern, Switzerland
[3] Friedrich Alexander Univ Erlangen Nurnberg FAU, Dept Pediat & Adolescent Med, Erlangen, Germany
[4] Univ Bern, Bern Univ Hosp, Dept Hematol, Cent Hematol Lab, Bern, Switzerland
[5] Univ Bern, Bern Univ Hosp, Inselspital, Dept Med Oncol, Bern, Bern, Switzerland
[6] Univ Bern, Bern Univ Hosp, Inselspital, Dept Human Genet, Bern, Switzerland
[7] Univ Bern, Inst Social & Prevent Med, Childhood Canc Res Grp, Bern, Switzerland
关键词
Autologous stem cell transplantation; cancer; CHIP; pediatric; JOINT-CONSENSUS-RECOMMENDATION; MYELOID NEOPLASMS; SEQUENCE VARIANTS; MUTATIONS; TP53; RISK; ASSOCIATION; GUIDELINES; STANDARDS; PATTERNS;
D O I
10.1080/08880018.2024.2362885
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Clonal hematopoiesis of indeterminate potential (CHIP) describes recurrent somatic gene mutations in the blood of healthy individuals, associated with higher risk for hematological malignancies and higher all-cause mortality by cardiovascular disease. CHIP increases with age and is more common in adult patients after chemotherapy or radiation for cancer. Furthermore, in some adult patients undergoing autologous stem cell transplantation (ASCT) or thereafter, CHIP has been identified. In children and adolescents, it remains unclear how cellular stressors such as cytotoxic therapy influence the incidence and expansion of CHIP. We conducted a retrospective study on 33 pediatric patients mostly with solid tumors undergoing ASCT for presence of CHIP. We analyzed CD34+ selected peripheral blood stem cell grafts after several cycles of chemotherapy, prior to cell infusion, by next-generation sequencing including 18 "CHIP-genes". Apart from a somatic variant in TP53 in one patient no other variants indicative of CHIP were identified. As a CHIP-unrelated finding, germline variants in CHEK2 and in ATM were identified in two and four patients, respectively. In conclusion, we could not detect "typical" CHIP variants in our cohort of pediatric cancer patients undergoing ASCT. However, more studies with larger patient numbers are necessary to assess if chemotherapy in the pediatric setting contributes to an increased CHIP incidence and at what time point.
引用
收藏
页码:530 / 539
页数:10
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