Iris H I M Hollink
Overview
Explore the profile of Iris H I M Hollink including associated specialties, affiliations and a list of published articles.
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26
Citations
740
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Recent Articles
11.
van Rij M, Hollink I, Terhal P, Kant S, Ruivenkamp C, van Haeringen A, et al.
Am J Med Genet A
. 2018 Apr;
176(5):1212-1215.
PMID: 29681085
The SETD2-related overgrowth syndrome is also called "Luscan-Lumish syndrome" (OMIM 616831) with the clinical characteristics of intellectual disability, speech delay, macrocephaly, facial dysmorphism, and autism spectrum disorders. We report on...
12.
Hollink I, Alfadhel M, Al-Wakeel A, Ababneh F, Pfundt R, de Man S, et al.
J Hum Genet
. 2018 Mar;
63(4):539.
PMID: 29576627
Correction to: Journal of Human Genetics (2016) 61, 229-33 https://doi.org/10.1038/jhg.2015.134 ; published online 26 November 2015.
13.
Dubbink H, Hollink I, Avenca Valente C, Wang W, Liu P, Doukas M, et al.
Pediatr Blood Cancer
. 2018 Feb;
65(6):e26991.
PMID: 29446530
Background: The Wnt/β-catenin pathway plays a central role in the pathogenesis of most hepatoblastomas (HBs), that is, up to 60-80% carry activating CTNNB1 mutations. HBs can however also be the...
14.
Hollink I, van den Ouweland A, Beverloo H, Arentsen-Peters S, Zwaan C, Wagner A
J Med Genet
. 2017 Apr;
54(12):805-808.
PMID: 28432085
Background: Recently a novel syndromic form of overgrowth with intellectual disability and distinct facial features was identified caused by constitutional mutations in the epigenetic regulator DNA-methyltransferase 3A (), referred to...
15.
Hollink I, Alfadhel M, Al-Wakeel A, Ababneh F, Pfundt R, de Man S, et al.
J Hum Genet
. 2015 Nov;
61(3):229-33.
PMID: 26607181
In 2012 Alazami et al. described a novel syndromic cause of primordial dwarfism with distinct facial features and severe intellectual disability. A homozygous frameshift mutation in LARP7, a chaperone of...
16.
Luesink M, Hollink I, van der Velden V, Knops R, Boezeman J, de Haas V, et al.
Blood
. 2012 Jul;
120(10):2064-75.
PMID: 22786876
In acute myeloid leukemia (AML), aberrant expression and mutations of transcription factors have been correlated with disease outcome. In the present study, we performed expression and mutation screening of GATA2,...
17.
Blink M, van den Heuvel-Eibrink M, Aalbers A, Balgobind B, Hollink I, Meijerink J, et al.
Br J Haematol
. 2012 Jul;
158(6):800-3.
PMID: 22775985
No abstract available.
18.
Hollink I, van den Heuvel-Eibrink M, Arentsen-Peters S, Pratcorona M, Abbas S, Kuipers J, et al.
Blood
. 2011 Aug;
118(13):3645-56.
PMID: 21813447
Translocations involving nucleoporin 98kD (NUP98) on chromosome 11p15 occur at relatively low frequency in acute myeloid leukemia (AML) but can be missed with routine karyotyping. In this study, high-resolution genome-wide...
19.
Balgobind B, Hollink I, Arentsen-Peters S, Zimmermann M, Harbott J, Beverloo H, et al.
Haematologica
. 2011 Jul;
96(10):1478-87.
PMID: 21791472
Background: Several studies of pediatric acute myeloid leukemia have described the various type-I or type-II aberrations and their relationship with clinical outcome. However, there has been no recent comprehensive overview...
20.
Hollink I, van den Heuvel-Eibrink M, Arentsen-Peters S, Zimmermann M, Peeters J, Valk P, et al.
Haematologica
. 2010 Dec;
96(3):384-92.
PMID: 21134981
Background: Dysfunctioning of CCAAT/enhancer binding protein α (C/EBPα) in acute myeloid leukemia can be caused, amongst others, by mutations in the encoding gene (CEBPA) and by promoter hypermethylation. CEBPA-mutated acute...