SMC1A (phospho-Ser957) Antibody
- Known as:
- SMC1A (phosphorilated-Ser957) Antibody
- Catalog number:
- abx000162
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- SMC1A (phospho-Ser957) Antibody
Related genes to: SMC1A (phospho-Ser957) Antibody
- Gene:
- SMC1A NIH gene
- Name:
- structural maintenance of chromosomes 1A
- Previous symbol:
- SMC1L1
- Synonyms:
- DXS423E, KIAA0178, SB1.8, Smcb
- Chromosome:
- Xp11.22
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-11
- Date modifiied:
- 2019-04-23
Related products to: SMC1A (phospho-Ser957) Antibody
Related articles to: SMC1A (phospho-Ser957) Antibody
- [This corrects the article on p. 852 in vol. 13, PMID: 37034215.]. - Source: PubMed
Publication date: 2026/07/15
Luan NaWang JiaojiaoSheng BiaoZhou QinYe XunZhu XiaolingSun JianguoTang ZheWang Jianwei - Lineage switch (LS), defined as a change in leukemic lineage during the disease course, is a rare but clinically significant event in acute leukemia and is typically associated with poor prognosis. Although LS has been increasingly reported following targeted immunotherapies, the clonal mechanisms underlying this phenomenon remain incompletely understood, particularly in cases without KMT2A rearrangement. We report a case of LS from B-precursor acute lymphoblastic leukemia (BCP-ALL) to acute myeloid leukemia (AML) following treatment with the CD22-targeted antibody-drug conjugate inotuzumab ozogamicin. To elucidate the clonal architecture underlying LS, targeted next-generation sequencing was performed on bone marrow samples obtained at multiple time points throughout the disease course. Genomic analysis demonstrated that the lymphoid and myeloid disease phases shared ancestral genetic alterations but displayed distinct mutational profiles. At the time of LS, TP53 and SMC1A mutations newly emerged, whereas only a subset of mutations detected at ALL relapse was retained. These findings suggest that the AML phase most likely resulted from the selective expansion of a genetically distinct subclone derived from a common progenitor, rather than the direct transdifferentiation of the dominant ALL clone, consistent with immunotherapy-driven clonal selection. Longitudinal genomic profiling revealed stepwise clonal evolution during disease progression, supporting a model of immunotherapy-driven clonal selection leading to LS. This case provides molecular evidence suggesting that immune-targeted therapy can promote expansion of minor pre-existing subclones with alternative lineage potential within a common progenitor even in non-KMT2A-rearranged leukemia. Our findings highlight the importance of comprehensive genomic monitoring during immunotherapy to identify therapy-resistant subclones and better understand mechanisms of lineage plasticity in acute leukemia. - Source: PubMed
Publication date: 2026/07/29
Kondo KaoriSadato DaichiNajima YuhoItabashi ToshikazuUeda TakahiroHirama ChizukoShimabukuro MasashiJinguji AtushiShingai NaokiToya TakashiShimizu HiroakiToubai TomomiHarada HironoriHarada YukaDoki Noriko - To evaluate time to diagnosis in infants with very early-onset genetic epilepsies, identify contributing factors to diagnostic delay, and assess the impact of a definite diagnosis on clinical management. - Source: PubMed
Publication date: 2026/08/10
Pizzuto ChiaraMorabito ValeriaCarapancea EvelinaCilio Maria Roberta
- Source: PubMed
- Source: PubMed