MCF-7: A human breast cancer cell line with estrogen, androgen, progesterone, and glucocorticoid receptors

Horwitz, Kathryn B.; Costlow, Mark E.; McGuire, William

doi:10.1016/0039-128x(75)90110-5

Cited by 365 publications

(124 citation statements)

References 17 publications

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“…The human breast carcinoma line MCF-7, a gift from Dr. M. Lippman (National Cancer Institute, Bethesda, MD), was established from a pleural effusion in a patient previously treated with radiation and hormone therapy. These cells have receptors for oestrogens, glucocorticoids, and insulin (14). MCF-AZL is a clone from the MCF-7 line, which has been isolated and established at our Institution and shows different growth properties, morphology, and DNA content.…”

Section: Methodsmentioning

confidence: 99%

Subdivision of S‐phase by analysis of nuclear 5‐bromodeoxyuridine staining patterns

et al. 1989

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After pulse labeling of mammalian cells in vivo or in vitro with 5-bromodeoxyuridine (BrdUrd), followed by immunostaining with a monoclonal antibody to DNA-incorporated BrdUrd, various intranuclear staining patterns are observed. These results are obtained in various labeling, fixation, denaturation, and staining conditions. We defined five different patterns in immunoperoxidasestained monolayers of human and rodent cancer cells and compared mean nuclear areas as measured by computerized planimetry. Furthermore, we evaluated frequency distributions of these patterns in partly synchronized cell populations and correlated these results with flow cytometric DNA histograms.The results indicate that the observed patterns reflect the spatial and temporal organization of DNA synthesis, which seems to be characterized by at least three successive stages of replication. Evaluation of these patterns may have various applications in studies on cell cycle kine tics.Key terms: DNA replication, B-bromodeoxyuridine, monoclonal anti-BrdUrd antibodies, interphase nucleus There is much evidence from (3H)-thymidine (3HTdR) labeling studies that DNA synthesis in an eukaryotic nucleus consists of an ordered cascade of initiations of replicons (4), controlled by an intranuclear mechanism (36). This is particularly clear from studies on polytene chromosomes of dipteran larvae, describing various patterns of DNA synthesis, tentatively assigned to specific periods of the S-phase (1,2,28). In general, GC-rich euchromatin replicates early, whereas AT-rich heterochromatic DNA replicates late (13); these early and late DNA synthesizing sites roughly correspond to R-and G-bands on trypsinGiemsa-stained chromosomes, respectively (6). However, also in euchromatin, distinct early-and late-replicating DNA fractions have been decribed (24); Goldman et al. (1 1) have presented evidence that genes that are obligatory or potentially active in a given cell type replicate early in that cell type, whereas genes that are permanently inactive replicate late.The characteristic grain distributions observed in eukaryotic nuclei after in situ autoradiography of incorporated 3HTdR (35) may reflect both the structural organization of replicon domains and a nonrandom localization of chromosomes in the interphase nucleus (12,161. In particular, centromeric and other highly repeated nontranscribed sequence domains may be positioned on the nucleolus or nuclear membrane and act as general organizing centers for cell type-specific interphase patterns (21). Multiple adjacent replicons appear to be clustered on fixed sites of the nuclear matrix (17,271, and it has been suggested that clustered replication origins are activated simultaneously (25). Early DNA synthesis then seems to occur in replicon clusters evenly distributed over the nucleus, whereas late DNA synthesis, being primarily heterochromatic, is preferentially restricted to domains on the periphery of the nucleus and in nucleoli (35,361. However, the assignment of autoradiographic labeling patterns to spe...

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Section: Methodsmentioning

confidence: 99%

Subdivision of S‐phase by analysis of nuclear 5‐bromodeoxyuridine staining patterns

et al. 1989

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“…The following cell lines were characterized for MUC1 expression by flow cytometry and tested as target cells in the ADCC: human breast tumor cell lines ZR-75-1, 39 T-47D, MCF-7, 42 CAMA-1, 43 , the ovarian tumor cell line IGROV-1, the MUC1-transfected human breast cell line HBL 100, clone HCA 1.3 ϩ 44 and its low MUC1 producing revertant HCA 1.3 Ϫ (kindly provided by Dr. J. Hilkens, The Netherlands Cancer Institute, Amsterdam, The Netherlands), the bone marrow derived tumor cell lines KM22, 1590 and HG15 (kindly provided by Dr. S. Kaul, Universitätsfrauenklinik Heidelberg, Germany) and the MUC1-transfected Chinese hamster cell line (CHO-MUC1) and its parent CHO-WT (both kindly provided by Dr. T. van den Berg, Free University, Amsterdam, The Netherlands). We also used the erythroleukemic cell line K562 (American Tissue Type Collection, Manassas, VA), known to be very sensitive for NK-mediated killing.…”

Section: Cell Linesmentioning

confidence: 99%

Antibody-dependent cell-mediated cytotoxicity can be induced by MUC1 peptide vaccination of breast cancer patients

et al. 2001

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Key words: MUC1; breast cancer; ADCC; NK cells; vaccination; immunotherapyMUC1 is a transmembrane O-linked glycoprotein present on the apical surface of normal secretory epithelial cells. 1 The extracellular domain of MUC1 consists mainly of a variable number of tandem repeats 2 and it has a cytoplasmatic tail of 69 amino acids. 3 In the vast majority of human adenocarcinomas this protein is over-expressed and hypo-glycosylated 4 exposing an immunodominant repetitive amino acid sequence. The overproduction and secretion of MUC1 is correlated with the progression of breast, 5 ovarian 6,7 and colon 8 carcinoma. In breast cancer patients MUC1 serum levels are used to monitor therapy and for early detection of recurrences. 9,10 Proliferative responses to MUC1 and its tandem-repeat peptides have been demonstrated with peripheral blood mononuclear cells (PBMC) of patients with ovarian adenocarcinoma 11 and MUC1 specific cytotoxic T lymphocytes (CTL) have been isolated from tumor-draining lymph nodes of breast 12 and ovarian 13 cancer patients. In patients with ovarian, breast and pancreatic adenocarcinomas cytotoxic T cells can be induced that are specific for the MUC1 tandem repeat. 14,15 Recognition of MUC1 by T lymphocytes may be due to exposure of the immunogenic PDTRP region of the tandem repeat that is normally not exposed due to extensive O-glycosylation of the peptide core. The cytotoxic action of these T cells has also been described to be MHC-nonrestricted, due to crosslinkage to poorly glycosylated MUC1 tandem repeats on tumor cells. 16 Not only cellular but also humoral responses to MUC1 are found in breast, ovarian, colon and pancreatic carcinomas. [17][18][19] Moreover, the presence of immune-complexed MUC1 in breast cancer patients is related to a favorable disease outcome 20 and survival in early breast cancer patients is favorably influenced by a natural humoral immune response to MUC1. 21 These findings point to MUC1 and its repeat peptide as a target for immunotherapy of carcinomas. One possible approach is the use of MAbs against tumor-associated antigens, 22,23 another the use of tumorassociated antigens such as MUC1 as a vaccine and target for cellular and humoral immune responses.MUC1 MAbs have already been used in a number of vaccination trials as carrier molecule of radioactive elements 24,25 and recently a clinical trial has been set up with unlabeled humanized (Hu)HMFG-1 MAb for adjuvant therapy of breast cancer patients (Dr. D.W. Miles, Guy's Hospital, London). Also active vaccination trials with MUC1 tandem-repeat peptides 26 have been initiated. Recently, in 3 phase I vaccination trials executed by Dr. P.O. Livingston in the Memorial Sloan-Kettering Cancer Center, NY, breast cancer patients with no evidence of disease were repeatedly injected with a 30-mer 27,28 a 33-mer or a 106-mer MUC1 tandem repeat peptide conjugated to KLH plus adjuvant QS-21. In these patients high MUC1 IgG and IgM could be induced. 21 MAbs specific for tumor-associated antigens (TAA) can induce a complement-depende...

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“…3) (Pertschuk et al, 1978;Lee, 1980 (Watson & Muldoon, 1977) and lysosomal (Szego, 1974) receptors which cannot be detected in the cytosol assay are included in the cytoplasmic steroid-binding sites Besides binding to RP, progesterone also binds to androgen and glucocorticoid receptors (Horwitz et al, 1975;Ojasoo & Raynaud, 1978); the positive immunofluorescent reactions for RP seen in our tests possibly represent a summation of the reactions with all 3 receptors. This could be an explanation for the high proportion of immunofluorescent RP+ cells in the 2 nodules from Patient 4, compared with the negative or low (15 fmol/mg protein) values detected by biochemical assay (Table).…”

Section: Biochemical Assaysmentioning

confidence: 74%

Immunofluorescent detection of hormone receptors in cutaneous melanocytic tumours

Thompson¹,

Cook²,

Gill³

1981

Br J Cancer

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Summary.-Immunofluorescent assessment of hormone receptors in melanocytic tumours is quite feasible without loss of diagnostic material, in contrast to the impracticability of quantitative biochemical assays. Using this method, oestrogen receptors were demonstrated in 4/6, and progesterone receptors in 3/5 patients with metastatic melanoma. Receptors were not found in 3 patients with primary cutaneous melanomas of the superficial spreading type. Progesterone receptors were present in the junctional component of a naevus from one healthy person.

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MCF-7: A human breast cancer cell line with estrogen, androgen, progesterone, and glucocorticoid receptors

Cited by 365 publications

References 17 publications

Subdivision of S‐phase by analysis of nuclear 5‐bromodeoxyuridine staining patterns

Subdivision of S‐phase by analysis of nuclear 5‐bromodeoxyuridine staining patterns

Antibody-dependent cell-mediated cytotoxicity can be induced by MUC1 peptide vaccination of breast cancer patients

Immunofluorescent detection of hormone receptors in cutaneous melanocytic tumours

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