Here we describe the second case of primary microcephaly caused by a novel homozygous splice-site variant at the NCAPD2 gene. The proband was born with microcephaly, and developed intellectual disability. Whole exome sequencing identified a canonical splice-site variant, c.3477+2T>C, at the NCAPD2 gene. Sanger sequencing showed that the proband and her sibling, a symptomatic fetus, carried a homozygous c.3477+2T>C variant, while the unaffected parents were heterozygous and her younger brother had wild-type alleles. To date, only one case of primary microcephaly with a homozygous splice-site pathogenic variant at the NCAPD2 gene has been reported. Our study of two siblings provides additional evidence that NCAPD2 is a causative gene of primary microcephaly. This finding adds new knowledge in the etiology of microcephaly and contributes to more accurate counseling of affected families.
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http://dx.doi.org/10.1111/cge.13559 | DOI Listing |
Inflamm Bowel Dis
September 2024
First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China.
Oncol Res
September 2024
Department of Respiratory and Critical Care Medicine, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
Objectives: The pro-oncogenic effects of NCAPD2 have been extensively studied across various tumor types; however, its precise role within the context of lung adenocarcinoma (LUAD) remains elusive. This study aims to elucidate the biological functions of NCAPD2 in LUAD and unravel the underlying mechanistic pathways.
Methods: Utilizing bioinformatics methodologies, we explored the differential expression of NCAPD2 between normal and tumor samples, along with its correlations with clinical-pathological characteristics, survival prognosis, and immune infiltration.
Int J Mol Med
October 2024
Department of Laboratory Medicine and Department of Pathology, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei 442000, P.R. China.
Non‑SMC condensin I complex subunit D2 () is a newly identified oncogene; however, the specific biological function and molecular mechanism of NCAPD2 in liver cancer progression remain unknown. In the present study, the aberrant expression of in liver cancer was investigated using public tumor databases, including TNMplot, The Cancer Genome Atlas and the International Cancer Genome Consortium based on bioinformatics analyses, and it was validated using a clinical cohort. It was revealed that NCAPD2 was significantly upregulated in liver cancer tissues compared with in control liver tissues, and served as an independent prognostic factor and predicted poor prognosis in liver cancer.
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March 2024
Department of Stomatology, The Affiliated Hospital of Inner Mongolia Medical University, Inner Mongolia, China.
Oral squamous cell carcinoma (OSCC) is the most common type of oral cancer, with a poor prognosis, yet the underlying mechanism needs further exploration. Non-SMC condensin I complex subunit D2 (NCAPD2) is a widely expressed protein in OSCC, but its role in tumor development is unclear. This study aimed to explore NCAPD2 expression and its biological function in OSCC.
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