Mitotic Checkpoint Genes, hsMAD2 and BubR1, in Oesophageal Squamous Cancer Cells and their Association with 5-fluorouracil and Cisplatin-based Radiochemotherapy

Tanaka, Keisuke; Mohri, Yasuhiko; Ohi, Masaki; Yokoe, Takeshi; Koike, Yuhki; Morimoto, Yuhki; Miki, Chikao; Tonouchi, Hitoshi; Kusunoki, Masato

doi:10.1016/j.clon.2008.06.010

Cited by 27 publications

(25 citation statements)

References 24 publications

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“…Assessment of BUBR1 expression may influence the choice of adequate treatment, also in consideration of the recently demonstrated association between the levels of the spindle checkpoint proteins, including BUBR1, and sensitivity to certain anticancer drugs. 23,[38][39][40] …”

Section: Discussionmentioning

confidence: 99%

“…On the contrary, such studies that have investigated BUBR1 at the expression level have achieved more interesting albeit controversial results. BUBR1 was found to be upregulated in carcinomas of the lung, 16 colon, 12,17 stomach, 18,19 breast, 15,20 bladder, 21 kidney, 22 esophagus, 23 thyroid, 24 ovary, 25 salivary duct, 26 and liver. 27 In a number of these studies, overexpression of BUBR1 has been related not only to genomic complexity, 22 chromosomal instability, 15,20,21 DNA aneuploidy, 18,21 p53 expression, 27 and high cell proliferation, 17,19,21,27 but also to a more advanced pathologic stage, 21,25,27 a higher histologic grade, 21,22,25,27 presence of metastases, 18 and to a poor prognosis.…”

mentioning

confidence: 98%

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BUBR1 expression in oral squamous cell carcinoma and its relationship to tumor stage and survival

et al. 2010

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

BUBR1 expression in oral squamous cell carcinoma and its relationship to tumor stage and survival

et al. 2010

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“…For example, Mad2 is overexpressed and associated with poorer prognosis and/or advanced tumor grade in certain lines of lymphoma, 10 osteosarcoma, 72 soft tissue sarcoma, 73 testicular germ cell tumor, 74 neuroblastoma, 75 retinoblastoma, 75 and cancers of the bladder, 75 colon, 76 esophagus, 77 liver, 78 lung, 79 and stomach. 80 SAC involvement in tumorigenesis, however, is very complex and context-dependent.…”

Section: Surviving With Surplus: Managing Supernumerary Centrosomes Bmentioning

confidence: 99%

Let's huddle to prevent a muddle: centrosome declustering as an attractive anticancer strategy

2012

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Nearly a century ago, cell biologists postulated that the chromosomal aberrations blighting cancer cells might be caused by a mysterious organelle-the centrosome-that had only just been discovered. For years, however, this enigmatic structure was neglected in oncologic investigations and has only recently reemerged as a key suspect in tumorigenesis. A majority of cancer cells, unlike healthy cells, possess an amplified centrosome complement, which they manage to coalesce neatly at two spindle poles during mitosis. This clustering mechanism permits the cell to form a pseudo-bipolar mitotic spindle for segregation of sister chromatids. On rare occasions this mechanism fails, resulting in declustered centrosomes and the assembly of a multipolar spindle. Spindle multipolarity consigns the cell to an almost certain fate of mitotic arrest or death. The catastrophic nature of multipolarity has attracted efforts to develop drugs that can induce declustering in cancer cells. Such chemotherapeutics would theoretically spare healthy cells, whose normal centrosome complement should preclude multipolar spindle formation. In search of the 'Holy Grail' of nontoxic, cancer cell-selective, and superiorly efficacious chemotherapy, research is underway to elucidate the underpinnings of centrosome clustering mechanisms. Here, we detail the progress made towards that end, highlighting seminal work and suggesting directions for future research, aimed at demystifying this riddling cellular tactic and exploiting it for chemotherapeutic purposes. We also propose a model to highlight the integral role of microtubule dynamicity and the delicate balance of forces on which cancer cells rely for effective centrosome clustering. Finally, we provide insights regarding how perturbation of this balance may pave an inroad for inducing lethal centrosome dispersal and death selectively in cancer cells.

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“…5) are higher than the reported 50% inhibiting concentrations (IC 50 ) of 5-FU on esophageal squamous cell carcinoma (ESCC) cell lines (TE1, TE2), about 130 mg/mL. 31 This suggests that with a proper dosing, the stents will perform effective treatment of esophagus cancer in clinical therapy.…”

Section: Concentrations Of 5-fu In Serum Liver and Esophageal Tissuesmentioning

confidence: 69%

In Vivo Evaluation of 5-Fluorouracil-Containing Self-Expandable Nitinol Stent in Rabbits: Efficiency in Long-Term Local Drug Delivery

Guo

Wang

Zhang

et al. 2010

Journal of Pharmaceutical Sciences

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Mitotic Checkpoint Genes, hsMAD2 and BubR1, in Oesophageal Squamous Cancer Cells and their Association with 5-fluorouracil and Cisplatin-based Radiochemotherapy

Cited by 27 publications

References 24 publications

BUBR1 expression in oral squamous cell carcinoma and its relationship to tumor stage and survival

BUBR1 expression in oral squamous cell carcinoma and its relationship to tumor stage and survival

Let's huddle to prevent a muddle: centrosome declustering as an attractive anticancer strategy

In Vivo Evaluation of 5-Fluorouracil-Containing Self-Expandable Nitinol Stent in Rabbits: Efficiency in Long-Term Local Drug Delivery

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