Chemotherapeutic agents that bind tubulin cause mitotic arrest, which may be seen histologically. Such mitotic arrest has been reported to occur in the skin, alimentary canal, lungs, liver, bone marrow, endometrium, breasts, or in ascites following treatment with paclitaxel, vincristine, colchicine, podophyllotoxin, or maytansine. Mitotic arrest as a result of docetaxel, a taxane that binds tubulin, has yet to be reported. Mitotic arrest in the gallbladder has also yet to be reported. We recently encountered a case of dramatic mitotic arrest as a result of docetaxel, involving the gallbladder of a 66-year-old man with metastatic bronchogenic carcinoma. Strikingly abundant bizarre mitoses initially prompted a diagnosis of primary carcinoma. Carcinoma was eventually excluded based on the absence of dysplasia in all cells at interphase and the history of recent administration of docetaxel. This is the first case of mitotic arrest involving docetaxel or the gallbladder. Awareness of this phenomenon is necessary to avoid misdiagnosing carcinoma.
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http://dx.doi.org/10.1177/1066896907304989 | DOI Listing |
Int J Mol Sci
December 2024
Departamento de Biologia, Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto 14040-901, SP, Brazil.
In the flower development study, we identified SCI1 (Stigma/style Cell-cycle Inhibitor 1), a regulator of cell proliferation. SCI1 interacts with NtCDKG;2 ( Cyclin-Dependent Kinase G;2), a homolog of human CDK11, which is responsible for RanGTP-dependent microtubule stabilization, regulating spindle assembly rate. In a Y2H screening of a cDNA library using NtCDKG;2 as bait, a RanBP1 (Ran-Binding Protein 1) was revealed as its interaction partner.
View Article and Find Full Text PDFAm J Dermatopathol
December 2024
Department of Diagnostic Pathology and Cytology, Osaka International Cancer Institute, Osaka, Japan.
Microtubule-stabilizing agents (enfortumab vedotin and brentuximab vedotin) and microtubule-disrupting agents (docetaxel and paclitaxel) are used as anticancer agents but can also induce drug eruptions. Recently, mitotic arrest figures have been reported in various non-neoplastic cells as the histopathologic side effect of these drug eruptions. Therefore, we performed a comparative analysis of drug eruptions associated with these microtubule-targeting agents.
View Article and Find Full Text PDFNat Cell Biol
January 2025
CNRS UMR144 - UMR3664, Institut Curie, Sorbonne Université, PSL Research University, Paris, France.
Errors during cell division lead to aneuploidy, which is associated with genomic instability and cell transformation. In response to aneuploidy, cells activate the tumour suppressor p53 to elicit a surveillance mechanism that halts proliferation and promotes senescence. The molecular sensors that trigger this checkpoint are unclear.
View Article and Find Full Text PDFPharmaceuticals (Basel)
December 2024
Laboratory of Molecular and Cellular Neurogenetics, N.N. Burdenko National Medical Research Center of Neurosurgery, 125047 Moscow, Russia.
Indolo[2,3-]pyrrolo[3,4-]carbazole scaffold is successfully used as an efficient structural motif for the design and development of different antitumor agents. In this study, we investigated the anti-glioblastoma therapeutic potential of glycosylated indolocarbazole analog LCS1269 utilizing in vitro, in vivo, and in silico approaches. Cell viability was estimated by an MTT assay.
View Article and Find Full Text PDFClin Transl Med
January 2025
Department of Urology, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China.
Background: Chromosomal instability (CIN), a hallmark of cancer, is commonly linked to poor prognosis in high-grade prostate cancer (PCa). Paradoxically, excessively high levels of CIN may impair cancer cell viability. Consequently, understanding how tumours adapt to CIN is critical for identifying novel therapeutic targets.
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