Progestational Agents in the Treatment of Carcinoma of the Endometrium

Kelley, Rita M.; Baker, William H.

doi:10.1097/00006254-196108000-00040

Cited by 6 publications

(7 citation statements)

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“…[1][2][5][6][7][8][9][10][11]28 More to the point, ovarian hormones have been known to regulate proliferation and survival of the endometrial cancer as well as the cancer invasion. [12][13][14][15][16][17][18][19] The purpose of this study, therefore, is to identify how ovarian hormones, especially estrogen, would regulate the FIGURE 5 -Regulation of stromal expression of HGF by ovarian hormones. HEC-1A and KLE cells were cocultured in pair with stromal cells under 3 different ovarian hormonal conditions.…”

Section: Discussionmentioning

confidence: 99%

“…As seen in Figure 1a, estrogen increased the invasion of both HEC-1A and KLE cells significantly compared with the control (No) (p < 0.05) whereas progesterone opposed it. Albeit progesterone's anti-invasive effects, [14][15][16][17][18][19] the invasion of the endometrial cancer cells appeared little affected in the P 4 milieu vs. in the control (No), thus hereafter being referred to as ''basal invasion.'' Intriguingly, little invasion was also detected when cancer cells (HEC-1A cells) were cultured alone without stromal counterparts under the otherwise identical condition and even in the presence of 100 nM estradiol (Supp.…”

Section: Endometrial Cancer Invasion Is Enhanced By Estrogenmentioning

confidence: 99%

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Endometrial cancer invasion depends on cancer‐derived tumor necrosis factor‐α and stromal derived hepatocyte growth factor

Choi

Kim

Yoon

et al. 2009

Intl Journal of Cancer

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Cancer invasion is an outcome of interactions of the cancer and the host cell. It is now becoming increasingly clear that ovarian hormones have a huge influence on such intercommunications in various types of cancers. Estrogen is known to aggravate the aggressiveness of the endometrial cancer whereas progesterone seems to act as a negative factor. Insight into the mode of ovarian hormonal actions could come from the studies of its regulation of the paracrine interactions between the endometrial cancer and the normal stromal cells during the cancer invasion. In this context, we report here that estrogen promotes the endometrial cancer invasion by inducing humoral interactions between the cancer and the stromal cells, i.e., estrogen stimulates tumor necrosis factor-a expression from the endometrial cancer cells, which, in turn, induces the stromal expression of hepatocyte growth factor (HGF), conferring the enhanced NK4 (HGF-antagonist/angiogenesis inhibitor)-sensitive invasion characteristic of the endometrial cancer cells. Additionally, we demonstrate a close correlation of the invasion of endometrial cancer cells with the expression and dimerization of integrin a v b 5 as well as the activation of focal adhesion kinase as the consequences of paracrine interactions. Thus, understanding of paracrine interactions of cancer cells with host stromal cells can yield new insight into the architecture and function of cancer invasion and metastasis, leading to a development of a new cancer therapeutic intervention. '

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Section: Discussionmentioning

confidence: 99%

Section: Endometrial Cancer Invasion Is Enhanced By Estrogenmentioning

confidence: 99%

Endometrial cancer invasion depends on cancer‐derived tumor necrosis factor‐α and stromal derived hepatocyte growth factor

Choi

Kim

Yoon

et al. 2009

Intl Journal of Cancer

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“…5A-C) also showed that progesterone significantly reduced the growth of progesterone receptor-positive NSCLC cells starting from 50 mg of progesterone pellet (f350 nmol/L serum progesterone concentration). Progesterone treatment is an established endocrine therapy in human hormone-dependent breast (9) and endometrial cancers (40), and at present, oral progestins such as medroxyprogesterone acetate are widely employed. Thigpen et al (10) reported that serum level of medroxyprogesterone acetate became 600 and 1,900 nmol/L in endometrial cancer patients who have received oral medroxyprogesterone acetate in a dose of 200 mg/d (low dose; n = 145) and 1,000 mg/d (high dose; n = 154), respectively, and the overall clinical response rate was not significantly different in these groups (25% in the low-dose group and 15% in the high-dose group).…”

Section: Discussionmentioning

confidence: 99%

Progesterone Receptor in Non–Small Cell Lung Cancer—A Potent Prognostic Factor and Possible Target for Endocrine Therapy

Suzuki²,

et al. 2005

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A possible involvement of gender-dependent factors has been postulated in development of human non-small-cell lung cancers (NSCLC), but its details remain unclear. In this study, we examined biological significance of progesterone receptor in NSCLCs. Progesterone receptor immunoreactivity was detected in 106 of 228 NSCLCs (46.5%). Progesterone receptorpositive NSCLC was frequently detected in female and adenocarcinoma, and was inversely associated with tumornode-metastasis stage and histologic differentiation. Progesterone receptor status was also associated with better clinical outcome of the patients, and a multivariate analysis revealed progesterone receptor status as an independent prognostic factor. Progesterone-synthesizing enzymes were detected in NSCLCs, and tissue concentration of progesterone was higher in these cases (n = 42). Immunoblotting analyses showed the presence of progesterone receptor in three NSCLC cell lines (A549, LCSC#2, and 1-87), but not in RERF-LC-OK or PC3. Transcriptional activities of progesterone receptor were increased by progesterone in these three progesterone receptorpositive NSCLC cells by luciferase assays. Cell proliferation was inhibited by progesterone in these progesterone receptorpositive NSCLC cells in a dose-dependent manner, which was inhibited by progesterone receptor blocker. Proliferation of these tumor cells injected into nude mice was also dosedependently inhibited by progesterone, with a concomitant increase of p21 and p27 and a decrease of cyclin A, cyclin E, and Ki67. Results of our present study suggested that progesterone receptor was a potent prognostic factor in NSCLCs and progesterone inhibited growth of progesterone receptorpositive NSCLC cells. Therefore, progesterone therapy may be clinically effective in suppressing development of progesterone receptor-positive NSCLC patients. (Cancer Res 2005; 65(14): 6450-8)

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“…Reported response rates include 14%-53% for MPA, 9%-34% for hydroxyprogesterone caproate, and 11%-56% for megestrol acetate [41][42][43][44][45][46][47][48]. Overall, response rates of 30%-35% have been reported [41][42][43][44][45][46][47][48]. Recent data suggest that the response rate to progestational therapy may be only 15%-20% [47,49].…”

Section: Hormonal Therapymentioning

confidence: 99%

Treatment for Advanced and Recurrent Endometrial Carcinoma: Combined Modalities

Rauh‐Hain

Carmen

2010

The Oncologist

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After completing this course, the reader will be able to:1. Discuss the role of radiation therapy for advanced stage endometrial cancer in order to differentiate between patients who should receive only radiation therapy and patients requiring surgery and/or chemotherapy in addition to radiation.2. Evaluate the role of surgery for stage IV and recurrent endometrial cancer in order to select patients most likely to benefit from cytoreductive surgery.3. Evaluate the role of chemotherapy, particularly in conjunction with radiotherapy, in advanced stage endometrial carcinoma and select appropriate candidates for multimodality therapy.This article is available for continuing medical education credit at CME.TheOncologist.com. CME CME ABSTRACTWomen with recurrent or advanced endometrial cancer constitute a heterogeneous group of patients. Depending on previous treatment, women with recurrent endometrial cancer may be appropriate candidates for surgery, radiation therapy, hormonal therapy, or chemotherapy. Women with advanced stage disease at presentation may also be appropriate candidates for systemic and local therapies. We review the treatment options available to treat recurrent and locally advanced endometrial cancer. Treatment choice depends largely on the localization of disease, the patient's performance status and previ-

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Progestational Agents in the Treatment of Carcinoma of the Endometrium

Cited by 6 publications

References 0 publications

Endometrial cancer invasion depends on cancer‐derived tumor necrosis factor‐α and stromal derived hepatocyte growth factor

Endometrial cancer invasion depends on cancer‐derived tumor necrosis factor‐α and stromal derived hepatocyte growth factor

Progesterone Receptor in Non–Small Cell Lung Cancer—A Potent Prognostic Factor and Possible Target for Endocrine Therapy

Treatment for Advanced and Recurrent Endometrial Carcinoma: Combined Modalities

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