Polyploidy in human malignancy. Hypopentaploid chromosome pattern in malignant reticulosis with secondary sideroachrestic anemia

Bauke, J; Schöffling, Κ.

doi:10.1002/1097-0142(196809)22:3<686::aid-cncr2820220327>3.0.co;2-w

Cited by 25 publications

(3 citation statements)

References 25 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 1858, Virchow reported large nuclei and nucleoli in cancer cells[ 30 ] and in 1968, Bauke and Schöffling provided the first clinical evidence on the correlation between cancer growth and PGCCs. [ 31 ] Since then, despite opposite opinions,[ 32 ] PGCCs have been considered a source of chemo/radio therapy resistance. [ 6 8 33 ] PGCCs and their offspring cells have been also shown to possess stem cell characteristics.…”

Section: Discussionmentioning

confidence: 99%

Cisplatin-resistant ovarian cancer cells reveal a polyploid phenotype with remarkable activation of nuclear processes

2023

View full text Add to dashboard Cite

Background: Tumor recurrence as one of the main causes of cancer death is a big barrier to cancer complete treatment. Various studies denote the possible role of therapeutics in tumor relapse. Cisplatin as one of the generally used chemotherapy agents is supposed to be the source of therapy resistance through formation of polyploid giant cancer cells (PGCCs). Nevertheless, the mechanisms by which PGCCs promote tumor relapse are not fully understood. Materials and Methods: In this study, we performed experimental and bioinformatic investigations to recognize the mechanisms related to cisplatin resistance. A2780 and SCOV-3 cell lines were treated with cisplatin for 72 hours and were evaluated for their morphology by fluorescent microscopy and DNA content analysis. Furthermore, a microarray dataset of cisplatin-resistant ovarian cancer cells was re-analyzed to determine the significantly altered genes and signaling pathways. Results: Although cisplatin led to death of considerable fraction of cells in both cell lines, a significant number of survived cells became polyploid. On the other hand, our high throughput analysis determined significant change in expression of 1930 genes which mainly related to gene regulatory mechanisms and nuclear processes. Besides, mTOR, hypoxia, Hippo, and 14-3-3 signaling pathways previously shown to have role in PGCCs were determined. Conclusion: Taken together, results of this study demonstrated some key biological mechanisms related to cisplatin-resistant polyploid cancer cells.

show abstract

Section: Discussionmentioning

confidence: 99%

Cisplatin-resistant ovarian cancer cells reveal a polyploid phenotype with remarkable activation of nuclear processes

2023

View full text Add to dashboard Cite

show abstract

“…For decades, cancer researchers have tried to recognize the source of this resistance and nd effective ways to combat cancer. In 1858, Virchow reported large nuclei and nucleoli in cancer cells [30] and in 1968, Bauke & Schö ing provided the rst clinical evidence on the correlation between cancer growth and polyploid giant cancer cells [31]. Since then, despite opposite opinions [32], PGCCs have been considered a source of chemo/radio therapy resistance [6,8,33].…”

Section: Discussionmentioning

confidence: 99%

Cisplatin resistant ovarian cancer cells reveal a polyploid phenotype with remarkable activation of nuclear processes

Adibi

Moein

Gheisari

2021

Preprint

View full text Add to dashboard Cite

Background Tumor recurrence as a main cause of cancer death is a big barrier in cancer complete treatment. Various studies denote for the possible role of therapeutics in tumor relapse. Cisplatin as one of the generally-used chemotherapy agents is supposed to be the source of therapy-resistance through formation of polyploid giant cancer cells (PGCCs). Nevertheless, the mechanisms by which PGCCs promote tumor relapse are not fully understood.Methods In this study we performed experimental and bioinformatic investigations to recognize the mechanisms related to cisplatin resistance. A2780 and SCOV-3 cell lines were treated with cisplatin for 72 hours and were evaluated for their morphology by fluorescent microscopy and DNA content analysis. Furthermore, a microarray dataset of cisplatin-resistant ovarian cancer cells was reanalyzed to determine the significantly altered genes and signaling pathways.Result Although cisplatin led to death of considerable fraction of cells in both cell lines, a significant number of survived cells became polyploid. On the other hand, our high throughput analysis determined significant change in expression of 1930 genes which mainly related to gene regulatory mechanisms and nuclear processes. Besides, mTOR, hypoxia, Hippo and 14-3-3 signaling pathways previously shown to have role in PGCCs were determined.Conclusion Taken together, results of this study demonstrated some key biological mechanisms related to cisplatin-resistant polyploid cancer cells.

show abstract

“…Resistance to anticancer treatments remains a significant problem in medicine and society due to the high morbidity of cancer patients. In 1968, the first clinical report on the association of polyploidy with the progression of malignancy appeared [ 1 ]. The chronological landmarks in the field of cancer polyploidy from Virchow and Boveri in the 19th century until now have recently been excellently reviewed [ 2 ].…”

Section: Introductionmentioning

confidence: 99%

Role of the Circadian Clock “Death-Loop” in the DNA Damage Response Underpinning Cancer Treatment Resistance

Vainshelbaum

Salmiņa

Gerashchenko

et al. 2022

Cells

View full text Add to dashboard Cite

Here, we review the role of the circadian clock (CC) in the resistance of cancer cells to genotoxic treatments in relation to whole-genome duplication (WGD) and telomere-length regulation. The CC drives the normal cell cycle, tissue differentiation, and reciprocally regulates telomere elongation. However, it is deregulated in embryonic stem cells (ESCs), the early embryo, and cancer. Here, we review the DNA damage response of cancer cells and a similar impact on the cell cycle to that found in ESCs—overcoming G1/S, adapting DNA damage checkpoints, tolerating DNA damage, coupling telomere erosion to accelerated cell senescence, and favouring transition by mitotic slippage into the ploidy cycle (reversible polyploidy). Polyploidy decelerates the CC. We report an intriguing positive correlation between cancer WGD and the deregulation of the CC assessed by bioinformatics on 11 primary cancer datasets (rho = 0.83; p < 0.01). As previously shown, the cancer cells undergoing mitotic slippage cast off telomere fragments with TERT, restore the telomeres by ALT-recombination, and return their depolyploidised offspring to telomerase-dependent regulation. By reversing this polyploidy and the CC “death loop”, the mitotic cycle and Hayflick limit count are thus again renewed. Our review and proposed mechanism support a life-cycle concept of cancer and highlight the perspective of cancer treatment by differentiation.

show abstract

Polyploidy in human malignancy. Hypopentaploid chromosome pattern in malignant reticulosis with secondary sideroachrestic anemia

Cited by 25 publications

References 25 publications

Cisplatin-resistant ovarian cancer cells reveal a polyploid phenotype with remarkable activation of nuclear processes

Cisplatin-resistant ovarian cancer cells reveal a polyploid phenotype with remarkable activation of nuclear processes

Cisplatin resistant ovarian cancer cells reveal a polyploid phenotype with remarkable activation of nuclear processes

Role of the Circadian Clock “Death-Loop” in the DNA Damage Response Underpinning Cancer Treatment Resistance

Contact Info

Product

Resources

About