Chromosome aberrations are frequently found in B-cell chronic lymphocytic leukaemia (B-CLL), and specific chromosome aberrations identify poor prognostic subgroups. Almost all the aberrations identified in B-CLL involve loci where genes with a role in the regulation of centrosome duplication have been mapped. Centrosome aberrations have been described as a possible cause of numerical chromosome abnormalities in both solid and haematological tumours. However, little is known about the possible role of centrosome aberrations in B-CLL. To investigate whether centrosome aberrations do occur in B-CLL and correlate with cytogenetically defined prognostic subgroups, we examined a set of 64 B-CLL samples by immunofluorescent staining. B-CLL cases differed significantly from controls in the mean frequency of cells with centrosome aberrations, while no difference was found between subgroups with or without specific chromosome aberrations. Our results indicated that although centrosome aberrations were a common feature in B-CLL, they did not represent a reliable prognostic marker.
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http://dx.doi.org/10.1002/hon.838 | DOI Listing |
Microcephaly affects 1 in 2,500 babies per year. Primary microcephaly results from aberrant neurogenesis leading to a small brain at birth. This is due to altered patterns of proliferation and/or early differentiation of neurons.
View Article and Find Full Text PDFEur J Med Chem
January 2025
Department of Respiratory and Critical Care Medicine, Targeted Tracer Research and Development Laboratory, Institute of Respiratory Healthand, Department of Frontiers Science Center for Disease-related Molecular Network, Core Facilities, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China. Electronic address:
NEK2, a serine/threonine protein kinase, is integral to mitotic events such as centrosome duplication and separation, microtubule stabilization, spindle assembly checkpoint, and kinetochore attachment. However, NEK2 overexpression leads to centrosome amplification and chromosomal instability, which are significantly associated with various malignancies, including liver, breast, and non-small cell lung cancer. This overexpression could facilitate tumor development and confer resistance to therapy by promoting aberrant cell division and centrosome amplification.
View Article and Find Full Text PDFCytoskeleton (Hoboken)
January 2025
Department of Life Sciences, University of Siena, Siena, Italy.
We analysed here the dynamic of the kinesin-like Pavarotti (Pav) during male gametogenesis of wild-type and Sas4 mutant flies. Pav localizes to the equatorial region and the inner central spindle of late anaphase wild-type spermatogonia and displays a strong concentration at the midbody during late telophase. At metaphase of the first meiotic division, Pav shows widespread localization on the equatorial region of the spermatocytes.
View Article and Find Full Text PDFCurr Oncol
December 2024
Department of Tumor Pathology, Hamamatsu University School of Medicine, Hamamatsu 431-3192, Japan.
STIL is a regulatory protein essential for centriole biogenesis, and its dysregulation has been implicated in various diseases, including malignancies. However, its role in non-small-cell lung carcinoma (NSCLC) remains unclear. In this study, we examined STIL expression and its potential association with chromosomal numerical abnormalities (CNAs) in NSCLC using The Cancer Genome Atlas (TCGA) dataset, immunohistochemical analysis, and in vitro experiments with NSCLC cell lines designed to overexpress STIL.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
December 2024
Department of Infectious Diseases and Pathobiology, Institute of Animal Pathology, Vetsuisse Faculty, University of Bern, 3012 Bern, Switzerland.
Taxanes are frequently used anticancer drugs known to kill tumor cells by inducing mitotic aberrations and segregation defects. A defining feature of specific cancers, notably triple-negative breast cancer (TNBC) and particularly those deficient in BRCA1, is chromosomal instability (CIN). Here, we focused on understanding the mechanisms of docetaxel-induced cytotoxicity, especially in the context of BRCA1-deficient TNBC.
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