A Human Cell Line From a Pleural Effusion Derived From a Breast Carcinoma
            2

Soule, Herbert D.; Vazguez, J; Long, Anna; Albert, Samuel; Brennan, Michael

doi:10.1093/jnci/51.5.1409

Cited by 2,086 publications

(1,076 citation statements)

References 10 publications

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“…With the exception of melanomias C-32 and C-143, the human tumour lines and methods of establishment and maintenance in culture have been described in previous publications (Weichselbaum et al, 1977a(Weichselbaum et al, , 1980b. In summary, each line was epithelial in morphology, had gone through at least 100 passages in vitro, and continued to proliferate after reaching confluence in a manner not characteristic of normal fibroblasts.…”

Section: Methodsmentioning

confidence: 99%

Cellular repair factors influencing radiocurability of human malignant tumours

Weichselbaum¹,

Schmit²,

Little³

1982

Br J Cancer

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Summary.-We have studied the repair of X-ray-induced, potentially lethal damage (PLD) in 9 human tumour lines derived from tumours of varying radiocurability. Cells derived from 3 tumours considered non-radiocurable (1 osteosarcoma, 2 melanoma) repaired significantly more X-ray PLD than cells from 3 tumours considered radiocurable (2 breast, 1 neuroblastoma). The remaining tumour lines were intermediate in their ability for repair, and included cells from another osteosarcoma, a hypernephroma and a glioblastoma. We conclude that the repair of X-ray PLD may be an important cellular determinant of clinical radiocurability.

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Section: Methodsmentioning

confidence: 99%

Cellular repair factors influencing radiocurability of human malignant tumours

Weichselbaum¹,

Schmit²,

Little³

1982

Br J Cancer

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“…In addition PMA has been suggested to induce differentiation of MCF-7 cells [20][21][22]. Therefore, we examined the effects of these differentiation inducing compounds on PMCA expression in MCF-7 cells [35]. After treating cells with butyrate, phenylbutyrate, valerate (SCFAs) or with PMA, the expression of PMCA isoforms was determined by Western blot analysis.…”

Section: Scfas and Pma Enhanced The Expression Of Pmca4b In Mcf-7 Cellsmentioning

confidence: 99%

Histone deacetylase inhibitor- and PMA-induced upregulation of PMCA4b enhances Ca2+ clearance from MCF-7 breast cancer cells

et al. 2014

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The expression of the plasma membrane Ca 2+ ATPase (PMCA) isoforms is altered in several types of cancer cells suggesting that they are involved in cancer progression. In this study we induced differentiation of MCF-7 breast cancer cells by histone deacetylase inhibitors (HDACis) such as short chain fatty acids (SCFAs) or suberoylanilide hydroxamic acid (SAHA), and by phorbol 12-myristate 13-acetate (PMA) and found strong upregulation of PMCA4b protein expression in response to these treatments. Furthermore, combination of HDACis with PMA augmented cell differentiation and further enhanced PMCA4b expression both at mRNA and protein levels. Immunocytochemical analysis revealed that the upregulated protein was located mostly in the plasma membrane. To examine the functional consequences of elevated PMCA4b expression, the characteristics of intracellular Ca 2+ signals were investigated before and after differentiation inducing treatments, and also in cells overexpressing PMCA4b. The increased PMCA4b expression -either by treatment or overexpression -led to enhanced Ca 2+ clearance from the stimulated cells. We found pronounced PMCA4 protein expression in normal breast tissue samples highlighting the importance of this pump for the maintenance of mammary epithelial Ca 2+ homeostasis. These results suggest that modulation of Ca 2+ signaling by enhanced PMCA4b expression may contribute to normal development of breast epithelium and may be lost in cancer.3

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“…HeLa cells were derived from a cervical carcinoma (Scherer et al, 1953) obtained from Dr Aubee. The T47D-B8 and MCF-7 cell lines descended from human breast carcinomas (Soule et al, 1973;Soto et al, 1986;Ruiz de Almodovar et al, 1994). The MCF-7 subclones BB and Bus were described to differ from MCF-7 parental cells with respect to dsb induction and repair, p53 status, cell cycle and apoptosis Siles et al, 1995).…”

Section: Cell Lines and Culture Conditionsmentioning

confidence: 99%

Radiosensitivity of human tumour cells is correlated with the induction but not with the repair of DNA double-strand breaks

2003

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Nine human tumour cell lines (four mammary, one bladder, two prostate, one cervical, and one squamous cell carcinoma) were studied as to whether cellular radiosensitivity is related to the number of initial or residual double-strand breaks (dsb). Cellular sensitivity was measured by colony assay and dsb by means of constant-and graded-field gel electrophoresis (CFGE and GFGE, respectively). The nine tumour cell lines showed a broad variation in cellular sensitivity (SF2 0.17 -0.63). The number of initial dsb as measured by GFGE ranged between 14 and 27 dsb/Gy/diploid DNA content. In contrast, normal fibroblasts raised from skin biopsies of seven individuals showed only a marginal variation with 18 -20 dsb/Gy/diploid DNA content. For eight of the nine tumour cell lines, there was a significant correlation between the number of initial dsb and the cellular radiosensitivity. The tumour cells showed a broad variation in the amount of dsb measured 24 h after irradiation by CFGE, which, however, was not correlated with the cellular sensitivity. This residual damage was found to be influenced not only by the actual number of residual dsb, but also by apoptosis and cell cycle progression which had impact on CFGE measurements. Some cell line strains were able to proliferate even after exposure to 150 Gy while others were found to degrade their DNA. Our results suggest that for tumour cells, in contrast to normal cells, the variation in sensitivity is mainly determined by differences in the initial number of dsb induced.

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A Human Cell Line From a Pleural Effusion Derived From a Breast Carcinoma 2

Cited by 2,086 publications

References 10 publications

Cellular repair factors influencing radiocurability of human malignant tumours

Cellular repair factors influencing radiocurability of human malignant tumours

Histone deacetylase inhibitor- and PMA-induced upregulation of PMCA4b enhances Ca2+ clearance from MCF-7 breast cancer cells

Radiosensitivity of human tumour cells is correlated with the induction but not with the repair of DNA double-strand breaks

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