Growth Inhibition of Laryngeal UM-SCC Cell Lines by Tamoxifen: Comparison With Effects on the MCF-7 Breast Cancer Cell Line

Shapira, Amnon; Virolainen, Erkki; Jameson, John J.; Ossakow, Steven J.; Carey, Thomas E.

doi:10.1001/archotol.1986.03780110027002

Cited by 23 publications

(9 citation statements)

References 21 publications

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“…Tissue from the primary tumor had low levels of ER, but we were unable to show receptor activity in cultured cells. Nevertheless, we found a tamoxifen sensitivity equal to that of the estrogenreceptor-positive MCF-7 cell line (Lippman et al, 1976;Sutherland et al, 1983;Shapira et al, 1986;Grinman et al, 1988a,b). The growth-inhibitory effect of tamoxifen in MCF-7 cultures has been shown to be dose-dependent, and partially reversible by E2 (Lippman et al, 1976; GRBNMAN ET AL.…”

Section: Time (Days)mentioning

confidence: 54%

“…3). The degree of growth retardation observed with the UM-SCV-1A cell line at concentrations of 2, 3.5 and 5 p~ is equivalent to that observed at the same concentrations with the ER-positive breast cancer cell line MCF-7 (Lippman et al, 1976;Sutherland et al, 1983;Shapira et al, 1986;GrCnman et al, 1988~). Growth inhibition of 1B cells was slightly less pronounced than that of 1A cultures at each drug concentration tested, and 1B cells were not maintained in cytostasis by daily feeding with 5 J*.M tamoxifen (Fig.…”

Section: Steroid Hormone Receptorsmentioning

confidence: 71%

“…For example, complete regression of pulmonary metastases from malignant melanoma of the vulva following therapy with tamoxifen has been reported (Amin, 1986), and we reported a case in which there was in vitro sensitivity to tamoxifen of an ER-negative endometrial cell line and subsequently the patient had an objective response to this drug (Grinman et al, 1988~). For these reasons and because of our previous findings of tamoxifen-induced growth inhibition in other squamous carcinoma cell lines (Shapira et al, 1986;Grinman et al, 1988a), we tested the growth-inhibitory effects of tamoxifen on UM-SCV-1A and 1B cells. Tissue from the primary tumor had low levels of ER, but we were unable to show receptor activity in cultured cells.…”

Section: Discussionmentioning

confidence: 99%

“…Cell growth rate and sensitivity to tamoxifen were studied as described by Shapira et al (1986) and GrCnman et al (1988a,b). Tamoxifen citrate was provided by Leiras Pharmaceuticals, Turku, Finland.…”

Section: Growth Rate and Growth Inhibition By Tamoxifenmentioning

confidence: 99%

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Phenotypic characterization, karyotype analysis and in vitro tamoxifen sensitivity of new ER‐negative vulvar carcinoma cell lines, UM‐SCV‐1A and UM‐SCV‐1B

Grénman

Dyke

Worsham

et al. 1990

Intl Journal of Cancer

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Two cell lines (University of Michigan squamous carcinoma of the vulva UM-SCV-1A and UM-SCV-1B) were established from the primary tumor and a malignant pleural effusion of a 62-year-old woman. Both tumor specimens grew vigorously in vitro and could be passaged after only 14 and 10 days in culture, respectively. Both cell lines undergo 3 population doublings in 4 days, reaching saturation densities of 5 x 10(5) cells/cm2, and have been carried through more than 30 in vitro passages. In nude mice the cultured cells initially formed tumors but these regressed 2-3 weeks after inoculation. The regressing mouse tumors consisted of poorly differentiated squamous carcinoma surrounded by an inflammatory lymphoid infiltrate. The UM-SCV-1 cell lines express membrane antigens typically displayed by squamous-cell carcinomas. These include the HLA class-1 light chain beta 2-microglobulin, pemphigus, pemphigoid, and the alpha 6 beta 4 integrin defined by the UM-A9 monoclonal antibody (MAb). In contrast to the A431 vulvar carcinoma, these tumor lines do not have amplified expression of the epidermal growth factor (EGF) receptor. Although tissue from the primary tumor contained low levels of estrogen receptor activity, no receptor activity was detected in the cell lines. Nevertheless, both lines were sensitive to growth inhibition by tamoxifen. This effect was not reversible by estradiol, indicating an estrogen-receptor-independent mechanism. The tumors were both hypotetraploid, contained the same chromosome rearrangements and had stable karyotypes in vitro. Each contained inv(1)(p36.3q32.1), del(4)(q12), dic(4;11)(q12;p11.2), i(5p), der(6)t(3;6)(q25.1;p21.1), several rearrangements involving chromosomes 8 and 14, + i(13), i(18p), a dicentric t(11;19), and 2 or 3 unidentified markers. Since the karyotypes of both tumors were the same, no major karyotypic change was associated with metastatic spread. These paired primary and metastatic SCC lines from an unusually aggressive vulvar carcinoma provide an in vitro model for analysis of the biological basis of this tumor's behavior.

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Section: Time (Days)mentioning

confidence: 54%

Section: Steroid Hormone Receptorsmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Growth Rate and Growth Inhibition By Tamoxifenmentioning

confidence: 99%

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Phenotypic characterization, karyotype analysis and in vitro tamoxifen sensitivity of new ER‐negative vulvar carcinoma cell lines, UM‐SCV‐1A and UM‐SCV‐1B

Grénman

Dyke

Worsham

et al. 1990

Intl Journal of Cancer

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“…However, in early experiments in our laboratory, we also encountered poor results in soft agar clonogenic assays using fully viable cell suspensions from established SCC cell lines that were derived from patients with head and neck cancer. Thus, to study the response of these tumor lines to chemotherapeutic drugs (Speigel et al, 1984) and anti-hormones (Shapira et al, 1986;Grenman et al, 1987) we have used in vitro growth-inhibition experiments. However, as these tests are labor-intensive, expensive, require a large number of cells, and are difficult to apply to radiation survival experiments, we sought alternatives.…”

mentioning

confidence: 99%

Clonogenic cell assay for anchorage‐dependent squamous carcinoma cell lines using limiting dilution

Grénman

Burk

Virolainen

et al. 1989

Intl Journal of Cancer

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Clonogenic assays under either anchorage-dependent or -independent conditions are very useful for testing the sensitivity of tumor cells to cytotoxic drugs and radiation. These assays have not been widely used with squamous-cell carcinomas (SCC) because of poor tumor-cell viability and poor cloning efficiency, especially in semi-solid media. To find a clonogenic assay suitable for use with human squamous cancers we tested SCC lines, derived in our laboratory from patients with head and neck cancer, for the capacity to form colonies in soft agar and in 96-well plates. Of 13 UM-SCC lines tested for colony formation in agarose, only UM-SCC-11A was capable of growth in conventional semi-solid media. One other line, UM-SCC-14C, produced colonies in agarose only in the presence of epidermal growth factor. In contrast, all 17 of the SCC lines tested exhibited colony formation in adherent cell culture using limiting dilution in 96-well plates. The plating efficiencies of the SCC lines in the 96-well plate assay ranged from 0.02 to 0.52 colonies (wells)/cell whereas the PE values in soft agar were lower, ranging from 0.0055 to 0.0086 colonies/cell. The 96-well plate assay is not affected by cell migration, a problem encountered with some cell lines when clonogenic assays are performed in Petri dishes. UM-SCC-11A was tested for radiation sensitivity both in soft agar and in the 96-well plate assay. Comparable results were obtained. In summary, the majority of SCC cell lines did not form viable colonies in soft agar but the 96-well plate assay was applicable to a broad spectrum of anchorage-dependent human SCC cell lines and provides an efficient method for evaluating clonogenic cell survival.

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Sex Steroid Receptor Distribution in the Human Larynx and Laryngeal Carcinoma

Ferguson¹,

Hudson²,

McCarty³

1987

Archives of Otolaryngology - Head and Neck Surgery

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\s=b\Previous reports of estrogen receptor (ER) and progesterone receptor (PgR) in the human larynx and laryngeal carcinoma have relied on ligand-binding techniques using cytosol from tissue homogenates. These methods obscure the contribution of different tissue components to total receptor content. Recently developed, highly specific monoclonal antibodies to human ER and PgR were able to discern the presence of ER and PgR at the cellular level in 12 specimens of normal laryngeal tissue and eight laryngeal squamous cell carcinomas. Localization of ER and PgR was observed in the nuclei of vocalis muscle. No evidence of ER or PgR was found in epithelial components of the normal larynges or in laryngeal carcinomas. These results extend previous findings in lower primates and rodents to the human larynx and clarify previously reported receptor analyses of laryngeal carcinomas.

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Growth Inhibition of Laryngeal UM-SCC Cell Lines by Tamoxifen: Comparison With Effects on the MCF-7 Breast Cancer Cell Line

Cited by 23 publications

References 21 publications

Phenotypic characterization, karyotype analysis and in vitro tamoxifen sensitivity of new ER‐negative vulvar carcinoma cell lines, UM‐SCV‐1A and UM‐SCV‐1B

Phenotypic characterization, karyotype analysis and in vitro tamoxifen sensitivity of new ER‐negative vulvar carcinoma cell lines, UM‐SCV‐1A and UM‐SCV‐1B

Clonogenic cell assay for anchorage‐dependent squamous carcinoma cell lines using limiting dilution

Sex Steroid Receptor Distribution in the Human Larynx and Laryngeal Carcinoma

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