Treatment of advanced refractory ovarian carcinoma with a gonadotropin-releasing hormone analogue

Bruckner, Howard W.; Motwani, Bina T

doi:10.1016/0002-9378(89)90669-8

Cited by 39 publications

(12 citation statements)

References 13 publications

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“…The results of receptor assays in the first experiment are shown in Table 5 (1,20,26,27 (10,(12)(13)(14), but in a study involving 41 patients with advanced ovarian cancer, the response rate was only about 15% (28). The reduction in blood levels of gonadotropins and sex steroids, induced by LH-RH analogs, may be useful for the treatment of ovarian cancer.…”

Section: Resultsmentioning

confidence: 99%

“…It was reported that gonadotropins and estradiol increased the growth rate of some ovarian cancer cell lines (8,9), but the exact mechanism of endocrine regulation ofthe growth of ovarian cancer is still unclear. Some experimental and clinical findings indicate that the suppression of the secretion of gonadotropins produced by LH-RH agonists may inhibit the growth of epithelial ovarian cancers (1,(10)(11)(12)(13)(14). The inhibitory action of [D-Trp6]LH-RH on ovarian cancer growth was thought to be mediated mainly by the suppression of the pituitary-gonadal axis, but some of the inhibitory effects could be direct, since human ovarian epithelial cancers have LH-RH-binding sites (1,3,7).…”

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confidence: 99%

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Inhibition of growth of OV-1063 human epithelial ovarian cancer xenografts in nude mice by treatment with luteinizing hormone-releasing hormone antagonist SB-75.

Yano¹,

Pinski²,

Halmos³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Inhibition of growth of OV-1063 human epithelial ovarian cancer xenografts in nude mice by treatment with luteinizing hormone-releasing hormone antagonist SB-75.

Yano¹,

Pinski²,

Halmos³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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“…Previously, reduction in tumor growth or regression of cancers by treatment with peptide analogues has been seen in patients (34)(35)(36) and animal models (17,34), suggesting that such responses might occur. In addition, apoptosis has been observed in response to analogue treatment in some cancers (37,38 (11).…”

Section: Discussionmentioning

confidence: 99%

Peptide analogues alter the progression of premalignant lesions, as measured by Photofrin fluorescence.

Liebow¹,

Crean²,

Mang³

1993

Proc. Natl. Acad. Sci. U.S.A.

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Somatostatin analogue RC-160 and bombesin/gastrin-releasing peptide antagonist RC-3095 were infused at 2 jug per day via miniosmotic pumps implanted s.c. in hamsters with premalignant disease to examine the effect of these peptides on cancer promotion and progression. These analogues have been shown to inhibit growth ofcertain tumors, especially those that overexpress tyrosine kinase activity. Progression of premalignant lesions initiated by applying 0.5% 9,10-dimethyl-1,2-benzanthracene (DMBA) to the hamster buccal cheek pouch was measured by Photofrin-induced fluorescence 24 hr after ihjecting the porphyrin (1.0 mg/kg) by using in vivo fluorescence photometry. This method of monitoring progression was reaffirmed by the observations that fluorescence increased significantly as compared with controls in lesions receiving 4 additional weeks of continuous promotion by DMBA application (P < 0.01 in two independent trials) and in lesions receiving transient promotion by laser incision (P < 0.01 and < 0.05 at the same time in the two trials). Twelve weeks after treatment, fluorescence had decreased silfcantiy among animals treated for 2 weeks with RC-3095 (control, 0.53 ± 0.03 V vs. RC-3095, 0.28 ± 0.03 V; P < 0.0005) or with RC-160 (control, 0.85 ± 0.03 V vs. RC-160, 0.24 ± 0.03 V; P < 0.0001). These data were obtained 20 weeks after DMBA initiation. Thus, treatment with RC-160 and RC-3095 decreased the progression, measured by fluorescence, compared with control animals. In addition, there was also an absolute continuous decrease in fluorescence for the 22 weeks after the cessation of RC-160 treatment. That the changes in tumor progression produced by RC-160 extended beyond the treatment period supports the hypothesis that the changes were irreversible. Histopathological analysis revealed normal tissue and/or mild-moderate dysplasia in hamster buccal mucosa treated with the RC-160 (an improvement compared to pretreatment), whereas 40% of the animals receiving no treatment after DMBA initiation developed invasive squamous ceil carcinomas after 20 weeks.

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“…It was reported that gonadotropins and estradiol increase the growth rate of some ovarian cancer cell lines (4,5), but the processes involved in the growth of ovarian cancer are still unclear. Experimental and clinical findings indicate that LH-RH agonists may inhibit the growth of epithelial ovarian cancers (6)(7)(8)(9)(10). The inhibitory action of [D-Trp6]LH-RH on ovarian cancer growth was thought to be mediated mainly by suppression of pituitary gonadotropin secretion, but some of the inhibitory effects could be direct, since human ovarian epithelial cancers have LH-RH binding sites (3,11).…”

mentioning

confidence: 99%

“…LH-RH agonists have been used for the treatment of women with epithelial ovarian cancer (6,(8)(9)(10) (27). However, the binding sites for gonadotropins in some human ovarian cancers are localized in the stromal tissue and not in the epithelium (28).…”

mentioning

confidence: 99%

Inhibition of human epithelial ovarian cancer cellgrowth in vitro by agonistic and antagonistic analogues of luteinizinghormone-releasing hormone.

Yano¹,

Pinski²,

Radulović³

et al. 1994

Proc. Natl. Acad. Sci. U.S.A.

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In this study, we investigated the effects of luteinnimig hormone-releasing hormone (LH-RH) agonist ]LH-RH, LH-RH antagonist [Ac-D-Nal(2)1,DPhe(pCI)2,n-Pal(3)3,D-Cit',D-Ala"'JLU-RH (SB-75), and estradiol on the growth of human epithellal ovarian cancer cell line OV-1063. Cells were cultured under estrogen-deprived conditions. Estradiol inhibited cell proliferation, as measured by cell number at 10-9-10-7 M and Epithelial ovarian cancer is the most common cause of death from gynecologic malignancies in the United States. It is estimated that 21,000 cases ofovarian cancer were diagnosed and 13,000 deaths from this disease occurred in 1992 (1). Treatment of ovarian cancer is based on surgery and chemotherapy but is far from satisfactory and new approaches must be explored to improve the therapy.The normal ovary is a hormone-dependent organ and receptors for estrogen, progesterone, androgen, luteinizing hormone (LH), and luteinizing hormone-releasing hormone (LH-RH) are found in ovarian cancers (2, 3). It (12, 13). The use of LH-RH antagonists in cancer therapy would prevent the temporary clinical "flare-up" of disease that occurs initially in response to LH-RH agonists in some malignancies such as prostate cancer (11-13).OV-1063 human epithelial ovarian cancer cell lines originated from a metastatic papillary cystadenocarcinoma of the ovary in a 57-year-old woman (14). OV-1063 cells are positive for carcinoembryonic antigen (14).The purpose of the present study was to investigate the presence of LH-RH binding sites on OV-1063 Cell Culture. OV-1063 cells were originally kindly provided by S. Biran (Hadassah University, Jerusalem) and were maintained in phenol red-free RPMI 1640 medium supplemented with 10% heat-inactivated and dextran-coated charcoal-treated FBS (DCC/FBS), which was prepared as described (15). RPMI 1640 medium also contained 25 mM Hepes buffer, 2 mM glutamine, penicillin (100 units/ml), streptomycin (100 pg/ml), and amphotericin B (0.25 pu/ml). 1701The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Treatment of advanced refractory ovarian carcinoma with a gonadotropin-releasing hormone analogue

Cited by 39 publications

References 13 publications

Inhibition of growth of OV-1063 human epithelial ovarian cancer xenografts in nude mice by treatment with luteinizing hormone-releasing hormone antagonist SB-75.

Inhibition of growth of OV-1063 human epithelial ovarian cancer xenografts in nude mice by treatment with luteinizing hormone-releasing hormone antagonist SB-75.

Peptide analogues alter the progression of premalignant lesions, as measured by Photofrin fluorescence.

Inhibition of human epithelial ovarian cancer cellgrowth in vitro by agonistic and antagonistic analogues of luteinizinghormone-releasing hormone.

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