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Gunter Emons - One of the best experts on this subject based on the ideXlab platform.

  • Luteinizing Hormone-Releasing Hormone Receptor-Targeted Chemotherapy Using AN-152
    Neuroendocrinology, 2009
    Co-Authors: Gunter Emons, Andrew V. Schally, Herbert Sindermann, Jürgen Engel, Carsten Grundker
    Abstract:

    The luteinizing Hormone-Releasing Hormone (LHRH; also known as gonadotropin-Releasing Hormone) receptor can be utilized for targeted chemotherapy with cytotoxic LHRH analogues such as AN-152, in which

  • expression of receptors for luteinizing Hormone Releasing Hormone in human ovarian and endometrial cancers frequency autoregulation and correlation with direct antiproliferative activity of luteinizing Hormone Releasing Hormone analogues
    American Journal of Obstetrics and Gynecology, 2002
    Co-Authors: Peter Volker, Carsten Grundker, Oswald Schmidt, Klausdieter Schulz, Gunter Emons
    Abstract:

    Abstract Objective: Several recent reports have demonstrated the expression of luteinizing Hormone-Releasing Hormone receptors by human ovarian and endometrial cancers. Controversy persists on the relevance of this finding, in particular whether these receptors mediate direct antiproliferative effects of luteinizing Hormone-Releasing Hormone analogues. We correlated the expression of luteinizing Hormone-Releasing Hormone receptors by well-characterized ovarian and endometrial cancer cell lines with the ability of luteinizing Hormone-Releasing Hormone analogues to reduce their proliferation and studied the autoregulation of luteinizing Hormone-Releasing Hormone receptor expression by luteinizing Hormone-Releasing Hormone agonist triptorelin and antagonist cetrorelix. The expression of luteinizing Hormone-Releasing Hormone receptors was assessed in a series of specimens from primary ovarian and endometrial cancers. Study Design: Luteinizing Hormone-Releasing Hormone receptor expression was assessed by semiquantitative reverse transcriptase–polymerase chain reaction and radioligand binding assay. Antiproliferative effects were ascertained by proliferation assays in the absence or presence of luteinizing Hormone-Releasing Hormone analogues. Results: Ovarian (4/6 cell lines) and endometrial (5/6 cell lines) cancer cell lines expressed luteinizing Hormone-Releasing Hormone receptors. The proliferation of these luteinizing Hormone-Releasing Hormone receptor–positive cell lines was dose- and time-dependently reduced by agonistic and antagonistic luteinizing Hormone-Releasing Hormone analogues. Luteinizing Hormone-Releasing Hormone receptor density was reduced to 80% of controls (control, 100 %; P Conclusion: These findings suggest that luteinizing Hormone-Releasing Hormone receptors that are expressed by human ovarian and endometrial cancer cell lines mediate direct antiproliferative effects of luteinizing Hormone-Releasing Hormone analogues. Because most respective primary cancers expressed luteinizing Hormone-Releasing Hormone receptors, these receptors might be used for novel antiproliferative therapeutic approaches and should be further evaluated. (Am J Obstet Gynecol 2002;186:171-9.)

  • Antitumor effects of the cytotoxic luteinizing Hormone-Releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
    American journal of obstetrics and gynecology, 2002
    Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter Emons
    Abstract:

    Abstract Objective: Most human endometrial and ovarian cancers express receptors for luteinizing Hormone– Releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic luteinizing Hormone–Releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]luteinizing Hormone–Releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human luteinizing Hormone–Releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the luteinizing Hormone–Releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–Releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of luteinizing Hormone–Releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic luteinizing Hormone–Releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on luteinizing Hormone–Releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)

Carsten Grundker - One of the best experts on this subject based on the ideXlab platform.

  • Luteinizing Hormone-Releasing Hormone Receptor-Targeted Chemotherapy Using AN-152
    Neuroendocrinology, 2009
    Co-Authors: Gunter Emons, Andrew V. Schally, Herbert Sindermann, Jürgen Engel, Carsten Grundker
    Abstract:

    The luteinizing Hormone-Releasing Hormone (LHRH; also known as gonadotropin-Releasing Hormone) receptor can be utilized for targeted chemotherapy with cytotoxic LHRH analogues such as AN-152, in which

  • expression of receptors for luteinizing Hormone Releasing Hormone in human ovarian and endometrial cancers frequency autoregulation and correlation with direct antiproliferative activity of luteinizing Hormone Releasing Hormone analogues
    American Journal of Obstetrics and Gynecology, 2002
    Co-Authors: Peter Volker, Carsten Grundker, Oswald Schmidt, Klausdieter Schulz, Gunter Emons
    Abstract:

    Abstract Objective: Several recent reports have demonstrated the expression of luteinizing Hormone-Releasing Hormone receptors by human ovarian and endometrial cancers. Controversy persists on the relevance of this finding, in particular whether these receptors mediate direct antiproliferative effects of luteinizing Hormone-Releasing Hormone analogues. We correlated the expression of luteinizing Hormone-Releasing Hormone receptors by well-characterized ovarian and endometrial cancer cell lines with the ability of luteinizing Hormone-Releasing Hormone analogues to reduce their proliferation and studied the autoregulation of luteinizing Hormone-Releasing Hormone receptor expression by luteinizing Hormone-Releasing Hormone agonist triptorelin and antagonist cetrorelix. The expression of luteinizing Hormone-Releasing Hormone receptors was assessed in a series of specimens from primary ovarian and endometrial cancers. Study Design: Luteinizing Hormone-Releasing Hormone receptor expression was assessed by semiquantitative reverse transcriptase–polymerase chain reaction and radioligand binding assay. Antiproliferative effects were ascertained by proliferation assays in the absence or presence of luteinizing Hormone-Releasing Hormone analogues. Results: Ovarian (4/6 cell lines) and endometrial (5/6 cell lines) cancer cell lines expressed luteinizing Hormone-Releasing Hormone receptors. The proliferation of these luteinizing Hormone-Releasing Hormone receptor–positive cell lines was dose- and time-dependently reduced by agonistic and antagonistic luteinizing Hormone-Releasing Hormone analogues. Luteinizing Hormone-Releasing Hormone receptor density was reduced to 80% of controls (control, 100 %; P Conclusion: These findings suggest that luteinizing Hormone-Releasing Hormone receptors that are expressed by human ovarian and endometrial cancer cell lines mediate direct antiproliferative effects of luteinizing Hormone-Releasing Hormone analogues. Because most respective primary cancers expressed luteinizing Hormone-Releasing Hormone receptors, these receptors might be used for novel antiproliferative therapeutic approaches and should be further evaluated. (Am J Obstet Gynecol 2002;186:171-9.)

  • Antitumor effects of the cytotoxic luteinizing Hormone-Releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
    American journal of obstetrics and gynecology, 2002
    Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter Emons
    Abstract:

    Abstract Objective: Most human endometrial and ovarian cancers express receptors for luteinizing Hormone– Releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic luteinizing Hormone–Releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]luteinizing Hormone–Releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human luteinizing Hormone–Releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the luteinizing Hormone–Releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–Releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of luteinizing Hormone–Releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic luteinizing Hormone–Releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on luteinizing Hormone–Releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)

Andrew V. Schally - One of the best experts on this subject based on the ideXlab platform.

  • Growth Hormone-Releasing Hormone Receptor Antagonist Modulates Lung Inflammation and Fibrosis due to Bleomycin.
    Lung, 2019
    Co-Authors: Chongxu Zhang, Andrew V. Schally, Renzhi Cai, Aaron Lazerson, Gaëtan J.-r. Delcroix, Medhi Wangpaichitr, Mehdi Mirsaeidi, Anthony J. Griswold, Robert M. Jackson
    Abstract:

    Purpose Growth Hormone-Releasing Hormone (GHRH) is a 44-amino acid peptide that regulates growth Hormone (GH) secretion. We hypothesized that a GHRH receptor (GHRH-R) antagonist, MIA-602, would inhibit bleomycin-induced lung inflammation and/or fibrosis in C57Bl/6J mice.

  • Combining Growth Hormone-Releasing Hormone Antagonist With Luteinizing Hormone-Releasing Hormone Antagonist Greatly Augments Benign Prostatic Hyperplasia Shrinkage
    The Journal of urology, 2012
    Co-Authors: Ferenc G Rick, Luca Szalontay, Karoly Szepeshazi, Marta Zarandi, Norman L. Block, Andrew V. Schally, Mehrdad Nadji, Irving Vidaurre, Magdolna Kovacs, Zoltan Rekasi
    Abstract:

    Purpose: Benign prostatic hyperplasia often affects aging men. Antagonists of the neuropeptide growth Hormone-Releasing Hormone reduced prostate weight in an androgen induced benign prostatic hyperplasia model in rats. Luteinizing Hormone-Releasing Hormone antagonists also produce marked, protracted improvement in lower urinary tract symptoms, reduced prostate volume and an increased urinary peak flow rate in men with benign prostatic hyperplasia. We investigated the influence of a combination of antagonists of growth Hormone-Releasing Hormone and luteinizing Hormone-Releasing Hormone on animal models of benign prostatic hyperplasia.Materials and Methods: We evaluated the effects of the growth Hormone-Releasing Hormone antagonist JMR-132, given at a dose of 40 μg daily, the luteinizing Hormone-Releasing Hormone antagonist cetrorelix, given at a dose of 0.625 mg/kg, and their combination on testosterone induced benign prostatic hyperplasia in adult male Wistar rats in vivo. Prostate tissue was examined bio...

  • Luteinizing Hormone-Releasing Hormone Receptor-Targeted Chemotherapy Using AN-152
    Neuroendocrinology, 2009
    Co-Authors: Gunter Emons, Andrew V. Schally, Herbert Sindermann, Jürgen Engel, Carsten Grundker
    Abstract:

    The luteinizing Hormone-Releasing Hormone (LHRH; also known as gonadotropin-Releasing Hormone) receptor can be utilized for targeted chemotherapy with cytotoxic LHRH analogues such as AN-152, in which

  • Antitumor effects of the cytotoxic luteinizing Hormone-Releasing Hormone analog AN-152 on human endometrial and ovarian cancers xenografted into nude mice.
    American journal of obstetrics and gynecology, 2002
    Co-Authors: Carsten Grundker, Andrew V. Schally, Peter Volker, Frank Griesinger, Annette Ramaswamy, Attila Nagy, Gunter Emons
    Abstract:

    Abstract Objective: Most human endometrial and ovarian cancers express receptors for luteinizing Hormone– Releasing Hormone. These receptors can be used for targeted chemotherapy with cytotoxic luteinizing Hormone–Releasing Hormone analogs such as AN-152, in which doxorubicin is linked to [D-Lys 6 ]luteinizing Hormone–Releasing Hormone. Study Design: The antitumor effects of doxorubicin and AN-152 were assessed in vivo in human luteinizing Hormone–Releasing Hormone receptor–positive HEC-1B endometrial cancers and NIH:OVCAR-3 ovarian cancers and in the luteinizing Hormone–Releasing Hormone receptor–negative SK-OV-3 ovarian line. Nude mice bearing these tumors subcutaneously were injected intravenously with saline solution (control), AN-152, or doxorubicin at equimolar doses. Luteinizing Hormone–Releasing Hormone receptor expression in tumors and specimens of human reproductive (n = 5) and nonreproductive (n = 15) normal tissues and in hematopoietic stem cells were analyzed with reverse transcriptase–polymerase chain reaction and radioligand binding assay. Results: The tumor volumes of luteinizing Hormone–Releasing Hormone receptor–positive HEC-1B and NIH:OVCAR-3 cancers were reduced significantly ( P Conclusion: Targeted chemotherapeutic luteinizing Hormone–Releasing Hormone analog AN-152 is more effective and less toxic than cytotoxic radical doxorubicin on luteinizing Hormone–Releasing Hormone receptor–positive tumors. AN-152 could be considered for targeted chemotherapy in patients with ovarian or endometrial cancers. (Am J Obstet Gynecol 2002;187:528-37.)

G Aguilera - One of the best experts on this subject based on the ideXlab platform.

  • single administration of interleukin 1 increased corticotropin Releasing Hormone and corticotropin Releasing Hormone receptor mrna in the hypothalamic paraventricular nucleus which paralleled long lasting weeks sensitization to emotional stressors
    Neuroscience, 2003
    Co-Authors: E D Schmidt, G Aguilera, Rob Binnekade, Fred J H Tilders
    Abstract:

    Abstract Single exposure to the proinflammatory cytokine interleukin-1 induces sensitization of the adrenocorticotropin Hormone and corticosterone responses to stressors weeks later (hypothalamus-pituitary-adrenal sensitization). Hypothalamus-pituitary-adrenal responses are controlled by corticotropin-Releasing Hormone and arginine-vasopressin secreted from parvocellular corticotropin-Releasing Hormone neurons of the hypothalamic paraventricular nucleus and may involve autoexcitatory feedback mechanisms. Therefore, we studied the temporal relationship between resting levels of corticotropin-Releasing Hormone, corticotropin-Releasing Hormone-R1 and arginine-vasopressin receptor (V1a, V1b) mRNAs in the paraventricular nucleus and the development of hypothalamus-pituitary-adrenal sensitization to an emotional stressor (novelty). The adrenocorticotropin Hormone precursor molecule proopiomelanocortin hnRNA in the pituitary gland served as an index for acute activation. Single administration of interleukin-1 induced sensitization of the hypothalamus-pituitary-adrenal to novelty from 3 to 22 days later, but not after 42 days. Single administration of interleukin-1 induced biphasic increases in corticotropin-Releasing Hormone and corticotropin-Releasing Hormone-R1 mRNAs in the paraventricular nucleus: an early peak within 24 h, followed by a delayed (>7 days) increase that peaked after 22 days. Hypothalamic V1a and V1b mRNA levels were unaffected. In contrast, in the pituitary gland, there was an early decrease in corticotropin-Releasing Hormone-R1 mRNA (from 10.5 to 3 h after interleukin-1) and V1b receptor mRNA (3 to 6 h), which returned to control levels from 24 h onwards. Thus, interleukin-1–induced long-lasting hypothalamus-pituitary-adrenal sensitizationis associated with prolonged activation of corticotropin-Releasing Hormone and corticotropin-Releasing Hormone-R1 mRNA expression in the paraventricular nucleus, but not with changes in the expression of proopiomelanocortin hnRNA or V1b receptor or corticotropin-Releasing Hormone R1 mRNAs in the pituitary gland. We propose that transient exposure to immune events can induce long-lasting hypothalamus-pituitary-adrenal sensitization, which at least in part involves long-term hypothalamic adaptations that enhance central corticotropin-Releasing Hormone signaling.

  • central corticotropin Releasing Hormone receptors modulate hypothalamic pituitary adrenocortical and sympathoadrenal activity during stress
    Neuroscience, 1999
    Co-Authors: Daniela Jezova, T Ochedalski, M Glickman, A Kiss, G Aguilera
    Abstract:

    Abstract The role of brain corticotropin-Releasing Hormone receptors in modulating hypothalamic–pituitary–adrenal and sympathoadrenal responses to acute immobilization stress was studied in conscious rats under central corticotropin-Releasing Hormone receptor blockade by intracerebroventicular injection of a peptide corticotropin-Releasing Hormone receptor antagonist. Blood for catecholamines, adrenocorticotropic Hormone and corticosterone levels was collected through vascular catheters, and brains were removed at 3 h for in situ hybridization for tyrosine hydroxylase messenger RNA in the locus coeruleus, and corticotropin-Releasing Hormone and corticotropin-Releasing Hormone receptor messenger RNA in the hypothalamic paraventricular nucleus. Central corticotropin-Releasing Hormone receptor blockade reduced the early increases in plasma epinephrine and dopamine, but not norepinephrine, during stress. Immobilization stress increased tyrosine hydroxylase messenger RNA levels in the locus coeruleus by 36% in controls, but not in corticotropin-Releasing Hormone antagonist-injected rats. In control rats, corticotropin-Releasing Hormone messenger RNA and type 1 corticotropin-Releasing Hormone receptor messenger RNA in the paraventricular nucleus increased after stress ( P The inhibition of plasma catecholamine and locus coeruleus tyrosine hydroxylase messenger RNA responses to stress by central corticotropin-Releasing Hormone receptor blockade supports the notion that central corticotropin-Releasing Hormone regulates sympathoadrenal responses during stress. The attenuation of stress-induced corticotropin-Releasing Hormone and corticotropin-Releasing Hormone receptor messenger RNA responses by central corticotropin-Releasing Hormone receptor blockade suggests direct or indirect positive feedback effects of corticotropin-Releasing Hormone receptor ligands on corticotropin-Releasing Hormone expression, whereas additional mechanisms potentiate adrenocorticotropic Hormone responses at the pituitary level. In addition, changes in neural activity by central corticotropin-Releasing Hormone are likely to modulate adrenocortical responsiveness during stress.

Flora Zagouri - One of the best experts on this subject based on the ideXlab platform.