Expression of prolactin and prolactin receptors by non-Hodgkin's lymphoma cells

Matera, Lina; Geuna, Massimo; Pastore, Cristina; Buttiglieri, Stefano; Gaïdano, Gianluca; Savarino, Andrea; Marengo, Simona; Vonderhaar, Barbara K.

doi:10.1002/(sici)1097-0215(20000101)85:1<124::aid-ijc22>3.0.co;2-u

Cited by 27 publications

(18 citation statements)

References 24 publications

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“…Clinical and pathological information were obtained from pathology reports. For carcinomas, this also included oestrogen (ER) and progesterone (PgR) receptor status in all cases, as assessed by immunohistochemistry, 16 and axillary lymph node status in most cases. In all malignant cases, the original sections were reviewed to confirm the histological type and grade of the tumours.…”

Section: Methodsmentioning

confidence: 99%

“…Although patients with positive tumours had an older mean age than those with negative tumours, the diVerence was not significant (p = 0.1396). A significant direct correlation was found between PrlR and ER staining when only cases that scored more than 100/300, using the H scoring system, 16 were considered (p = 0.0207; Only one of the three cases examined, which were all of the invasive ductal type, showed PrlR positivity in more than 10% of the tumour cells. All three cases were strongly positive for ER.…”

Section: Female Invasive Breast Carcinomamentioning

confidence: 96%

“…13 This antibody has been used successfully for the demonstration of PrlR in gastrointestinal 14 and breast 15 tissue, and non-Hodgkin's lymphoma cell lines. 16 In our study, we have used B6.2 to investigate the expression of PrlR in a wide variety of normal, benign, and malignant breast tissue sections, to explore the possible presence of alterations that could be useful in studying the biology of breast cancer.…”

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confidence: 99%

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Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study

Gill

Peston²,

Vonderhaar³

et al. 2001

Journal of Clinical Pathology

117

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Aims-Prolactin plays an important role in the proliferation and diVerentiation of normal breast epithelium, and possibly in the development of breast carcinoma. The eVects of prolactin are mediated by its receptor; thus, alteration in the expression of this receptor could be important in studying the biology of breast cancer. This investigation was aimed at comparing the expression of prolactin receptors in normal, benign, and malignant breast tissue. Material/Methods-The expression of prolactin receptors was studied in paraYn wax embedded sections of 102 breast biopsies (93 female and nine male), using the monoclonal antibody B6.2, and the avidin-biotin immunoperoxidase technique. Six biopsies were normal, 34 had benign lesions, and 62 were malignant. Results-In normal cases, prolactin receptor positivity was seen only on the luminal borders of the epithelial cells lining ducts and acini. In most benign lesions, variable degrees of luminal and cytoplasmic staining were seen. Cells showing apocrine metaplasia and florid regular ductal epithelial hyperplasia were mostly negative. In malignant cases, the staining pattern was mostly cytoplasmic and heterogeneous. Forty one of the 59 carcinomas in women showed a degree of positivity involving 10-100% of the tumour cells. A significant direct correlation was found between prolactin receptor and oestrogen receptor staining when only cases that scored more than 100/300 for the latter receptor, using the H scoring system, were considered (p = 0.0207). No correlation was found between prolactin receptors and progesterone receptors, patient's age, tumour size, tumour grade, or axillary lymph node status. Conclusions-Prolactin receptors seem to be expressed at diVerent cellular sites in normal, benign, and malignant breast epithelial cells. The receptor is expressed in more than two thirds of female breast carcinomas, suggesting that it may play a role in the pathogenesis of the disease. The positivity is correlated with moderate and strong staining for oestrogen receptors in tissue sections, but not with other prognostic factors. (J Clin Pathol 2001;54:956-960)

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Section: Methodsmentioning

confidence: 99%

Section: Female Invasive Breast Carcinomamentioning

confidence: 96%

mentioning

confidence: 99%

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Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study

Gill

Peston²,

Vonderhaar³

et al. 2001

Journal of Clinical Pathology

117

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“…Receptors with high affinity for PRL were expressed on human B and T cells by direct binding of PRL, and PRL-or IL-2-induced activation of these cells resulted in a further induction of PRL receptor expression [5][6][7]. PRL and the corresponding mRNA were present in human T-and B-lymphocyte as well as in B-lymphoblastoid line and T leukemia cells, which has been suggested to act as an autocrine growth factor for lymphoid cell proliferation [8][9][10][11]. Specific inhibition of PRL release by bromocriptine or in the presence of anti-PRL antibodies were associated with decreased T cell and NK cell function [12,13].…”

Section: Introductionmentioning

confidence: 99%

Expression of prolactin receptor and response to prolactin stimulation of human NK cell lines

Sun

Wei

et al. 2004

Cell Res

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We have previously shown a critical role of prolactin (PRL) during maturation and anti-tumor effects of murine natural killer (NK) cells in vitro and in vivo. We extended that study by exploring the ability of human NK cell lines (NK-92 and YT cell) to express PRL receptor (PRL-R) and to respond to PRL stimulation in vitro. Both human NK cell lines constitutively expressed PRL-R on membrane and mRNA transcripts, NK-92 cells contained higher level of PRL-R than YT cells, which correlated to the enhanced capacity of the cells to proliferate and to lyse target cells in response to PRL stimulation in the presence of trace amount of IL-2 or IL-15 in vitro. Two differences between IL-2 and IL-15 in functioning on human NK cells were for the first time observed. PRL synergized with IL-15 to improve proliferation of NK cells in a dose-dependent manner without double peak manifesting like IL-2. Although PRL enhanced the cytotoxicity of IL-2 or IL-15 activated NK cells, it exerted the function through up-regulating gene expression of perforin without influence of FasL in IL-2-stimulated NK cells, while in IL-15-stimulated NK cells, PRL did the function through up-regulating gene expression of both perforin and FasL but not IFNγ. PRL increased expressions of IL-2Rα on membrane and of IL-2 mRNA in cells, indicating that PRL up-regulated NK cell function by improving positive feedback between IL-2 and IL-2R. The similar results were also observed in network between IL-15 and IL-15R. These data indicate a potential role of PRL in human NK cell modulation.

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“…While the main function of prolactin is to regulate the growth and differentiation of the mammary gland and the ovary [2], it also acts as an important connection between the endocrine and immune systems [4]. Prolactin receptors, which can be found in many cell types including monocytes and lymphocytes, mediate the signal transduction of prolactin [5][6][7][8]. The initial signaling events include prolactin ligand binding, receptor dimerization, and recruitment of cytoplasmic molecules, such as JAK2 and STAT family members, to bind to receptors [9].…”

Section: Introductionmentioning

confidence: 99%

Diminished prolactin from chlordecone treatment in ovariectomized (NZB×NZW)F1 mice

Wang¹,

Roberts²,

Butfiloski³

et al. 2007

International Immunopharmacology

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In murine models of systemic lupus erythematosus (SLE), administration of either prolactin or estradiol (E2) increases autoimmunity, and there is evidence that elevated prolactin in response to E2 administration may contribute substantially to E2 effects. Hormonal influence on SLE can extend to environmental agents, as demonstrated by the ability of estrogenic organochlorine pesticides such as chlordecone to accelerate the development of lupus in female (NZB x NZW)F 1 mice. In order to evaluate a potential role for prolactin in chlordecone effects on SLE, it was necessary to first determine whether treatment with chlordecone, like E2, results in elevated prolactin levels. Ovariectomized (NZB x NZW)F 1 mice were treated for 5-6 weeks with chlordecone or E2 in doses shown previously to significantly shorten the time to onset of SLE. At the end of the treatment period, serum prolactin levels were increased 10-to 20-fold in E2-treated mice compared to untreated controls, but decreased in an apparent dose-dependent manner in mice treated with chlordecone. Prolactin receptor in purified B and CD4 T cells from treated animals, assessed through measurement of mRNA using quantitative real-time PCR, was increased by E2 treatment but unchanged in response to chlordecone. These observations suggest that the role of prolactin in eliciting autoimmunity in E2-treated animals is absent in the case of chlordecone, and by implication, that chlordecone possesses other actions that can replace the contribution of prolactin to development of SLE.

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Expression of prolactin and prolactin receptors by non-Hodgkin's lymphoma cells

Cited by 27 publications

References 24 publications

Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study

Expression of prolactin receptors in normal, benign, and malignant breast tissue: an immunohistological study

Expression of prolactin receptor and response to prolactin stimulation of human NK cell lines

Diminished prolactin from chlordecone treatment in ovariectomized (NZB×NZW)F1 mice

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