Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “polyploid cancer cell”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

8 recordsLinked to original sources
PubMed2026

RHAMM drives formation of polyploid cancer cells and confers resistance to ER-targeted therapy in breast cancer.

Endocrine resistance in ER+ breast cancer remains a major clinical challenge. Here, we identify RHAMM as a key driver of resistance by orchestrating polyploid cancer cell (PCC) formation. Single-cell transcriptomics uncovered a G2/M-enriched, RHAMM+ subpopulation in endocrine-resistant tumors. Mechanistically, RHAMM binds Septin9/10 to promote aberrant cytoskeleton polymerization, activating YAP independent of Hippo signaling, which induces cytokinesis failure and facilitates PCC generation. Concurrently, RHAMM destabilizes p21 mRNA, enabling cell cycle progression despite genomic instability. The RHAMM-p21 axis serves as a bypass mechanism supporting polyploidization. Upon endocrine treatment, RHAMM is transcriptionally up-regulated by Slug. Clinically, RHAMMhigh signatures are enriched in metastatic and recurrent ER+ tumors and correlate with poor prognosis, highlighting its therapeutic relevance. Importantly, targeting RHAMM or YAP abrogates PCC formation and restores fulvestrant sensitivity. These findings reveal RHAMM-mediated polyploidization as an adaptive mechanism underlying endocrine resistance, suggesting the therapeutic potential of targeting the RHAMM-YAP axis.

Humans↗
PubMed1976

"Non-condensed" and "condensed" chromain in transitional cell carcinoma of the human urinary bladder.

The area and content of "non-condensed" and "condensed" chromatin in smeared Feulgen-stained malignant urothelial cells were determined by means of scanning-cytophotometry. The results were compared with those from similar measurements of benign human transitional epithelial cells. There was no difference between the relative area and content of "non-condensed" and "condensed" chromatin in cancer nuclei and normal urothelial nuclei as far as nuclei of the same size and ploidy class were considered. Within the same ploidy class the relative area and content of "non-condensed" chromatin increased with increasing nuclear size. As increased nuclear size within the same ploidy class is typical for most cancer cells, cancer specimens therefore contained relatively more "non-condensed" chromatin than normal urothelium. Analogously the relative values of "condensed" chromatin decreased in cancer specimens. Only in high-polyploid cancer cells, which occurred more frequently in undifferentiated tumours, a slight decrease of the relative area and content of "non-condensed" chromatin was observed as compared with well differentiated diploid tumour cells. It was in polyploid tumours that the absolute area and content of "condensed" chromatin was increased as compared with diploid normal urothelium. This means that the changes in "non-condensed" and "condensed" chromatin were primarily dependent on nuclear size and total chromatin content and were not found to be a characteristic of cancer nuclei as compared with control nuclei of the same size and ploidy. These findings differ from the results of biochemical analyses of heterochromatin both in cells during carcinogenesis and also in cancer cells, but are in agreement with qualitative and quantitative morphological studies of smeared cancer nuclei.

Carcinoma, Transitional Cell↗
PubMed2025

Unscheduled polyploidy synergizes with oncogenic mutations to enhance genome instability and tumorigenesis.

Polyploid Giant Cancer Cells (PGCCs) occur across multiple cancer types and are associated with therapy resistance, genome instability, disease progression, and metastasis. PGCCs can grow through endocycles, a variant cell cycle of alternating Growth (G) and DNA Synthesis (S) phases without cell division. Unlike programmed endocycles that occur during normal tissue development, PGCCs switch from mitotic cycles to unscheduled endocycles in response to stress. PGCCs can subsequently return to error-prone divisions which generate aneuploid daughter cells that contribute to disease progression. However, the regulation of PGCC cell cycles and contributions to cancer are still being defined. Filling this knowledge gap will lead to the development of improved cancer therapies. In this study, we used a molecular-genetic system in the model organism Drosophila melanogaster to examine how oncogenes interact with unscheduled endocycles in vivo. We found that several oncogenes promote bypass of an endocycle arrest, resulting in increased polyploid cell size and DNA content. The extent of this increased growth was dependent on the type of oncogenic mutation. When these polyploid cells returned to division, RasG12V promoted continued divisions of polyploid daughter cells with elevated genome instability. RasG12V expression during transient endocycles and subsequent divisions also induced expression of a matrix metalloprotease and a Wnt pathway ligand. Importantly, RasG12V with transient endocycles enhanced the growth of large, neoplastic tumors. These findings indicate that oncogenic mutations can synergize with transient, unscheduled endocycles to promote tumorigenesis with important broader implications for cancer prognosis and therapies.

Animals↗
PubMed1978

Cytogenetic diagnosis of cancer: abnormalities of chromosomes and polyploid levels in the bone marrow of patients with small cell anaplastic carcinoma of the lung.

The chromosomes of metastatic cells and polyploid levels in the bone marrow of 26 patients with small cell anaplastic carcinoma were studied by direct bone marrow preparation and trypsin-Giemsa banding. Eighteen of these patients had received no tumor therapy and 8 had had chemotherapy and/or radiation therapy; 18 patients, including 5 who had received therapy, had karyotypic abnormalities with or without elevation of the polyploid level. Modal numbers and chromosome abnormalities were highly variable in treated and untreated patients. Modes ranged from hypodiploid to polyploid, but polyploid modes were the most frequently observed abnormal modes. Polyploid modes were not seen, however, in post-therapy patients with the exception of one who had received radiation therapy to the mediastinum for only 4 days prior to withdrawal of the specimen for chromosome analysis. Ten patients had elevated polyploid levels that ranged from 4.24 to 44.8% and always occurred in conjunction with karyotypic abnormalities. Both aneusomy (abnormal number) of normal chromosomes and structural aberrations (markers) occurred frequently. Some markers were consistent within an individual, but other variable aberrations were also typically present. Very few markers were common to 2 or more patients. The no. 1 chromosome participated in marker formation in 14 of the 18 patients with karyotypic abnormalities. Of the 26 patients, 5 were negative for metastasis to the marrow by pathologic examination but positive by cytogenetic diagnosis, whereas none were positive by pathologic examination and negative by cytogenetic diagnosis; this demonstrated that cytogenetics may be used as a rapid adjunct diagnostic procedure for the detection of metastasis in the marrow.

Bone Marrow↗
PubMed1977

[DNA content in dysplasias and early invasive forms of cervical cancer].

Cytological preparations of normal cervical epithelium and in different forms of the epithelial dysplasia and in early cervical cancer were studied in 8 healthy females and in 35 patients. To determine the content of DNA in these cells a fluorescent variant of the Feulgen reaction was employed, using the national drug rivanol as fluorochromium in the Shiff reagent. The amount of DNA in cell nuclei of the normal epithelium and in moderate dysplasia is shown to correspond to diploid, while in marked dysplasia the content of DNA varies from di-to tetraploid values. But there are some cases when in marked dysplasia the DNA content in cells is diploid, i. e. it is characteristic of moderate dysplasia, or considerably exceeds tetraploid level, and it is in such cases that histological assays reveal early forms of cancer. Invasive cancer is charcterized by a sharp increase in the DNA content in most cells and by a considerable number of polyploid cells. Fluorescence-microscopy may serve as a valuable diagnostic adjunct to recognize early forms of cervical cancer and be used clinically.

Carcinoma, Squamous Cell↗
PubMed1977

[Cytophotometric method of determination of DNA content of neoplastic cells].

The content of DNA was investigated by the method of pulsed cytophotometry in cells of the following neoplasms: pulmonary cancer, benign lesions and cancer of the stomach, melanomas of the skin, malignant lymphomas and metastases of cancer into the lymphatic node. In the normal tissues and benign tumours the number of proliferating cells (DNA value of 3p, 4p) was not significant--from 2.0 to 5.0%. Polyploid cells were absent. In tumours the number of cells varied broadly--proliferating cells from 5.0 to 27,0%, polyploid cells from 9.0 to 40.0%. The use of the method of pulsed cytophotometry in prophylactic examinations is not effective, since in many cases changes could be detected only in single cells not identifiable on DNA-cytograms. Investigation of DNA content by the method of pulsed cytophotometry in a great number of tumour cells makes it possible to determine more accurately the character of the tumoral process, the level of differentiation of the tumoral tissue.

Cell Nucleus↗
PubMedDate not supplied

A behavior of Y chromatin in cancer cells of males.

Y-chromatin or Y-body which is present in interphase nuclei in over 78 per cent of somatic male cells varied in frequency and multiplication in malignant tumors. The variation is characteristic of each tumor and kept fairly constant in cultured cell lines unless modulation occurs during continuous subcultures. The variation was due to chromosomal abnormality, aneuploidization or polyploidization, but in part appears to be related to abnormality of intercalary quinacrine binding to chromosomes.

Adenocarcinoma↗
PubMed1977

Chromosomes and causation of human cancer and leukemia. XXII. Karyotypic changes in malignant melanoma.

Detailed karyotypic analysis with G- and C-banding has been performed on cells of four malignant melanomas. The modal number in two cases was in the hypodiploid range, the chromosome numbers varying from 39 to 43. These two tumors had 5 to 13 marker chromosomes. The other two tumors were in the polyploid range, with modal numbers of 63 to 157 chromosomes. The cells had a minimum of 11 and a maximum of 40 marker chromosomes. Chromosome no. 1 was more frequently involved in aberrations than any other chromosome. The most common breakpoints on this chromosome were 1q21, 1q25 and 1q32. Frequent breakpoints were also noticed in the centromeric region in various chromosomes. In chromosome no. 1, however, the centromeric area does not seem to be involved. The more common breakpoints on the various chromosomes were 1q21, 1q25, 1q32, 5p13, 9q13, 11q23, 12q13. No common markers were noticed among these four cases of melanoma, but are noticed in unrelated tumors.

Aged↗