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PubMed2006

Histopathology and histomorphometry of the urogenital tract in 15-month old male and female rats treated neonatally with SERMs and estrogens.

In this study, two selective estrogen receptor modulators (SERMs), tamoxifen (TAM) and toremifene (TOR) or two estrogens, ethinylestradiol (EE) and diethylstilbestrol (DES) were administered to newborn male and female Sprague-Dawley rats (days 1-5) to investigate the occurrence of developmental abnormalities in the adulthood. The compounds were dosed (s.c.) at an equimolar dose of 24.9 micromol/kg. During the follow-up period, mortality occurred mainly in DES-treated male rats (3/4), associated with obstructive urinary calculi and suppurative renal inflammation in 2/3 rats. Similar lesions were not evident in other groups. At the age of 15 months, the animals were necropsied and organs were collected for histopathology and histomorphometry. Treatment-related abnormalities were restricted to the reproductive organs. Chronic prostatitis and epithelial abnormalities in the vas deferens were observed in all treatment groups. The columnar epithelium of vas deferens showed hyperplasia and development of subepithelial glandular structures resembling epididymal cysts reported in humans exposed in utero to DES. Testicular atrophy was observed especially in estrogen-treated rats. Mainly in SERM-treated female rats, the uterus showed luminal dilation or obstruction, loss of endometrial glands and myometrium disorganization including foci of muscular disruption. TOR-treated female rats showed polyp-like nodules (incidence 4/15) and a high incidence (9/15) of a simple cuboidal epithelium in cervical regions normally occupied by multilayered epithelia. In conclusion, the vas deferens is a main target organ following neonatal administration of SERMs and estrogens. In addition, female rats were significantly more susceptible to SERM treatment than to treatment with estrogens.

Animals↗
PubMed1996

Effect of antiestrogen regimen on prostacyclin and thromboxane A2 in postmenopausal patients with breast cancer: evidence of significance of hypertension, smoking or previous use of estrogen therapy.

To explore the mechanism(s) by which antiestrogens may protect against the development of cardiovascular disorders, we measured the production of vasodilatory, antiaggregatory prostacyclin (PGI2) and that of vasoconstrictive, proaggregatory thromboxane A2 (TxA2) before and after 6 months' use of antiestrogens in postmenopausal patients after operation for stage II breast cancer (n = 38). Urine samples were assayed by high performance liquid chromatography and radio-immunoassays for 2,3-dinor-6-ketoprostaglandin F1 alpha (= metabolite of PGI2, dinor-6-keto) and for 2,3-dinor-thromboxane B2 (= metabolite of TxA2, dinor-TxB2). In addition, in 35 of these 38 patients we assayed the capacity of platelets to produce thromboxane A2 during standardized blood clotting. The 4 patients using low-dose aspirin had low thromboxane production, and were excluded from further analysis of the data. An antiestrogen regimen consisting either of tamoxifen (n = 15) or of toremifene (n = 19) caused no changes in production of PGI2 or TxA2, or in their ratio, and in this regard, these antiestrogens behaved similarly. Hypertensive patients (n = 7) using different anti-hypertensive agents were characterized by reduced urinary out-put of dinor-6-keto (18.5 +/- 6.1 vs 35.5 +/- 18.5 ng/mmol, mean +/- SD, p < 0.05) and reduced platelet capacity to produce TxA2 (62.6 +/- 67.8 vs 134.6 +/- 75.6 ng/mL, p < 0.05). The patients (n = 15) who had used estrogen replacement therapy (ERT) up until diagnosis of breast cancer showed reduced dinor-TxB2 excretion (15.5 +/- 12.7 vs 29.9 +/- 20.9 ng/mmol, p < 0.05) before initiation of antiestrogens, and elevated dinor-6-keto output during the antiestrogen regimen (32.4 +/- 21.2 vs 22.7 +/- 8.7 ng/mmol, p = 0.07). Smokers (n = 6) had elevated dinor-TxB2 output before and during antiestrogen use. Thus we conclude that the cardiovascular protection provided by an antiestrogen regimen is unlikely to be mediated through vaso- and platelet active PGI2 and TxA2.

Aged↗
PubMed1998

Antiestrogen stimulated human endometrial cancer growth: laboratory and clinical considerations.

The new antiestrogen toremifene (TOR) is currently on the market for the treatment of advanced breast cancer in postmenopausal women. TOR is known to exhibit a similar efficacy profile as tamoxifen (TAM) in the treatment of advanced breast cancer and there are studies to suggest that the beneficial side effects of TAM on bone and blood lipids are also achieved with TOR. However, the data concerning the action of TOR on the endometrium is sorely lacking. In light of the estrogenic effect of TAM on the uterus and the 2-3-fold increased incidence in endometrial carcinoma detected in patients receiving TAM therapy, it is imperative to investigate the effect of TOR on endometrial carcinoma. We compared the actions of TAM and TOR on the EnCa101 human endometrial tumor model and find that both antiestrogens have similar growth stimulatory effects. To investigate a potential mechanism of antiestrogen-stimulated endometrial tumor growth, we have examined known activators of the AP-1 signal transduction pathway, the protein kinase C (PKC) family of isozymes, in the EnCa101 human endometrial tumor model. We find that increased PKC isozyme expression correlates with hormone-independent breast cancer as well as antiestrogen-stimulated endometrial cancer.

Antineoplastic Agents, Hormonal↗
PubMedDate not supplied

Selective estrogen receptor modulators (SERMs) in clinical practice.

The objective of this literature review is to familiarize the reader with the clinical data on selective estrogen receptor modulators (SERMs) and antiestrogens currently in use in the US, excluding data on breast effects. Four compounds in the SERM and antiestrogen families are presently in clinical use in the US: clomiphene (CC), tamoxifen (TAM), toremifene (TOR), and raloxifene (RLX). The clinical database on these compounds is among the largest available. Each compound demonstrates a specific profile for its target tissue effects, and this may differ between premenopausal and postmenopausal women. CC is the most widely used agent for ovulation induction. TAM is indicated in the management of breast cancer and for prevention in women at high risk. TAM may have additional effects on the cardiovascular and skeletal systems. TOR also is used for its effects on breast tissue and may have positive cardiovascular effects. RLX is approved in the management of osteoporosis with data supporting favorable effects on the cardiovascular system and breast tissue. TAM and TOR appear to have stimulatory effects on the uterus and endometrium, whereas RLX is neutral. Few adverse events have been attributed to these agents, with hot flashes being the most common one. There appears to be an increased risk of thromboembolic events with continuous use of TAM, TOR, and RLX. SERMs and antiestrogens continue to be studied extensively. Their evolving profiles support key roles for these agents in modern day medicine, particularly in the management of postmenopausal women's health.

Breast Neoplasms↗
PubMed2001

Nuchal aggressive fibromatosis in childhood: two instructive case reports.

Aggressive fibromatosis is a rare, benign tumour with a capacity for infiltration of surrounding structures and a propensity for local recurrence. The cornerstone of therapy is surgery, with various other treatment modalities having ill-defined roles. Assessment of the efficacy of these interventions is difficult. The natural history of the condition is variable and different treatment modalities are often used concurrently. Childhood cases pose particular management problems because of their tendency to occur in the head and neck region and the potential for treatment-related morbidity. Two children presented after surgery with recurrent disease threatening the airway. One remitted spontaneously and remains disease free at 20 years. The other achieved a complete remission with radiotherapy and toremifene. The role of non-surgical treatment, particularly radiotherapy, is reviewed.

Adolescent↗
PubMed2001

Non-steroidal anti-oestrogens inhibit the differentiation of synovial macrophages into dendritic cells.

BACKGROUND: Dendritic cells (DC) have been suggested to play an important role in the pathogenesis of rheumatoid arthritis (RA). Agents that inhibit DC differentiation and function may have a therapeutic value in the treatment of RA. OBJECTIVE: To examine the effect of the non-steroidal anti-oestrogens toremifene and tamoxifen on the differentiation of synovial fluid (SF) macrophages into DC. METHODS: SF macrophages from patients with RA were cultured with interleukin (IL)-4 and granulocyte/macrophage colony-stimulating factor (GM-CSF) in the presence or absence of anti-oestrogens. The expression of cell surface markers on SF antigen-presenting cells (APC) was studied by flow cytometry. The capacity of SF APC to stimulate allogeneic T cells was studied using the mixed lymphocyte reaction. The production of tumour necrosis factor-alpha, IL-10 and transforming growth factor-beta1 was studied using ELISA. RESULTS: Anti-oestrogens inhibited the differentiation of SF macrophages into DC and the capacity of SF macrophage-derived DC to stimulate allogeneic T cells. CONCLUSIONS: By inhibiting the differentiation of SF macrophages into DC, non-steroidal anti-oestrogens may have beneficial effects in RA.

Aged↗
PubMed2001

Sex difference in alcohol-related organ injury.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Nobuhiro Sato and Kai O. Lindros. The presentations were (1) Sex differences in ethanol pharmacokinetics, by E. Baraona; (2) Estrogen regulates the sensitivity to endotoxin in hepatic Kupffer cells, by K. Ikejima; (3) Sex difference in alcohol-related organ injury, by E. Mezey; (4) Aggravated ethanol-induced liver injury in female rats: Protection by the antiestrogen toremifene, by Harri A. Järveläinen; and (5) Alcohol metabolism in Asian subjects: Sex differences and flushing response, by V. A. Ramchandani.

Alcohol Dehydrogenase↗
PubMed1996

Modification of growth of desmoid tumours in tissue culture by anti-oestrogenic substances: a preliminary report.

BACKGROUND: Tamoxifen and toremifene have been used in patients with advanced desmoid tumours with response rates of 51%. METHODS: We developed an experimental model of desmoid tumour cells in tissue culture to study their effect. Four cell lines were established in tissue culture. All native and corresponding cultured tumours were oestrogen receptor negative. Tumour 1 was from a 22 year old with familial adenomatous polyposis (FAP) and recurrent abdominal wall desmoid tumours. She remains disease free on tamoxifen 4 years following surgery. Both her mother and sister also have shown regression of their FAP-associated desmoid tumours at the menopause and on tamoxifen, respectively. We assessed the effect of tamoxifen on desmoid tumours in tissue culture at 780 ng/mL. The results were assessed by cell density counting. RESULTS: Tumours 1 and 2 have responded with an approximately. 50% reduction in growth to tamoxifen at 780 ng/mL. CONCLUSIONS: This apparent growth inhibitory effect of tamoxifen on two desmoid tumour cell lines appears to be independent of oestrogen and correlates with the in vivo effect of tamoxifen on three desmoid tumours in an FAP family.

Abdominal Neoplasms↗
PubMed2001

Okadaic acid-sensitive activation of Maxi Cl(-) channels by triphenylethylene antioestrogens in C1300 mouse neuroblastoma cells.

1. The regulation of Maxi Cl(-) channels by 17beta-oestradiol and non-steroidal triphenylethylene antioestrogens represents a rapid, non-classical effect of these compounds. In the present study we have investigated the signalling pathways used for the regulation of Maxi Cl(-) channel activity by oestrogens and antioestrogens in C1300 neuroblastoma cells. 2. Whole-cell Maxi Cl(-) currents were readily and reversibly activated by tamoxifen, toremifene and the membrane-impermeant ethyl-bromide tamoxifen, only when applied to the extracellular medium. 3. Pre-treatment of C1300 cells with oestrogen or cAMP prevented the antioestrogen-induced activation of Maxi Cl(-) channels. The inhibitory effect of 17beta-oestradiol and cAMP was abolished by the kinase inhibitor staurosporine. 4. Current activation was unaffected by the removal of intracellular Ca(2+) and Mg(2+), but was completely abolished in the presence of okadaic acid. These results are consistent with the participation of an okadaic acid-sensitive serine/threonine protein phosphatase in the activation of Maxi Cl(-) channels. However, neither oestrogen or antioestrogen treatment modified the total activity of the two major serine/threonine phosphatases, PP1 and PP2A, in C1300 cells. 5. Although the role of these Maxi Cl(-) channels remains unknown, our findings suggest strongly that their modulation by oestrogens and antioestrogens is linked to intracellular signalling pathways.

Animals↗
PubMed1991

The effects of anti-estrogen therapy on lymphocyte functions in breast cancer patients.

The effects of anti-estrogen therapy (tamoxifen or toremifene) on in vitro lymphocyte functions were investigated in breast cancer patients. We found that the amount of DNA synthesis, with or without PWM stimulation, was decreased in all cancer patient groups compared to normal controls. The number of Ig-secreting cells was enhanced in unstimulated peripheral blood lymphocyte cultures but decreased in PWM-stimulated cultures. This occurred in all cancer patient groups investigated, with or without anti-estrogen therapy, as compared to healthy controls. On the other hand, subsequent samples with two-month intervals showed that anti-estrogens can increase PFC responses and inhibit DNA synthesis of peripheral blood lymphocytes in more than half of the patients. Interestingly, the enhancing dexamethasone effect, which usually causes an increase in the number of Ig-secreting cells in PWM-stimulated cultures, was also seen more often in anti-estrogen-treated patients. These results suggest that anti-estrogens may have immunoregulatory effects in vivo.

Breast Neoplasms↗
PubMed2004

A high serum matrix metalloproteinase-2 level is associated with an adverse prognosis in node-positive breast carcinoma.

PURPOSE: The aim of this study was to determine whether serum matrix metalloproteinase (MMP) -2 and MMP-9 levels could predict overall and disease-free survival in primary node-positive breast cancer. EXPERIMENTAL DESIGN: MMP-2 and MMP-9 levels were quantitatively measured in serum after surgery from 133 patients with primary node-positive breast cancer using enzyme-linked immunoassays. All of the patients received adjuvant therapy, postmenopausal endocrine treatment (tamoxifen or toremifen for 3 years) and premenopausal six cycles of CMF chemotherapy. The follow-up time for all of the patients was 5 years. RESULTS: Overall survival (OS) and disease-free survival (DFS) rates were better among patients with low MMP-2 levels than in patients with high levels (OS, 91% versus 75%, P = 0.020; DFS, 82% versus 58%, P = 0.005). The appearance of bone and visceral metastases was also significantly lower in patients with low serum MMP-2 levels (bone metastases, 10% versus 23%, P = 0.050; visceral metastases, 12% versus 34%, P = 0.018). The prognostic value of MMP-2 levels was most pronounced among a subgroup of estrogen receptor-positive patients (OS, 96% versus 78%, P = 0.052; DFS, 85% versus 58%, P = 0.014), whereas no significant difference was found among estrogen receptor-negative patients (OS, 73% versus 69%, P = 0.25; DFS, 73% versus 63%, P = 0.32). In multivariate analysis, MMP-2 level together with nodal status (NS), progesterone receptor (PgR), and tumor size (T) remained independent predictors for DFS (NS, P = 0.002; PgR, P = 0.004; T, P = 0.023; MMP2, P = 0.039) and OS (NS, P = 0.0002; PgR, P = 0.004; T, P = 0.004; MMP2, P = 0.032). MMP-9 levels did not correlate with survival. CONCLUSIONS: The results suggest that serum postoperative MMP-2 level is a predictor of DFS and OS, and could help to stratify breast cancer patients with primary node-positive disease into low- and high-risk groups.

Adult↗
PubMed1991

Estrogen and prolactin regulation of rat dorsal and lateral prostate in organ culture.

Besides androgens, estrogen (E) and PRL are thought to have important roles in the regulation of the growth and function of the prostate. We have established organ cultures of rat dorsolateral prostate for the analysis of the multiple hormone actions. Explants of dorsal prostate (DP) and lateral prostate (LP) were cultured in a serum-free basal medium containing insulin and corticosterone with or without the hormones studied. The viability and overall integrity of the tissues were maintained for at least 14 days. The morphology of the explants showed castration-like changes in the basal medium, but the addition of testosterone (T) prevented them. Androgen receptors in the prostate cultured with T were demonstrated by immunohistochemistry. When the explants were grown with E the epithelium became stratified, and the cells were flat. The epithelium was also layered when the explants were grown with PRL, but the epithelial cells were hypersecretory and large. The glandular morphology of the cultured prostate was, however, best preserved if T was added along with E or PRL. The wet weights and DNA contents of the explants declined during the culture, but they were better maintained if T, E, or PRL were added to the medium. The rate of DNA labeling with [3H]thymidine was activated in the cultured explants, but it was higher in those grown with T, E, or PRL than in those grown in the basal medium. The tissue specific functions were evaluated by measuring the expression of the genes RWB and M-40.3 encoding androgen-regulated secretory proteins. The steady state levels of RWB and M-40.3 mRNA were low in the explants grown in the basal medium but in the presence of T they were high. E and PRL also increased the expression of RWB and M-40.3 messenger RNA, although the responses in DP and LP were somewhat different. The antihormones cyproterone and toremifene opposed the increase of M-40.3 messenger RNA by T and E, respectively. The results show that the cultured DP and LP of the rat maintain the androgen responsiveness and tissue-specific functions in vitro. In addition, E and PRL have androgen-independent, direct effects in them. Rat dorsolateral prostate in culture thus provides a useful model for the studies on the mechanisms of hormone regulation of the prostate.

Animals↗
PubMed1996

Expression and hormone regulation of prolactin receptors in rat dorsal and lateral prostate.

We have studied the receptors that presumably mediate the biological effects of PRL in rat dorsal (DP) and lateral (LP) prostate. The PRL receptor proteins were localized to the glandular secretory epithelium of prostatic tissue by immunohistochemistry. Both the short and the long PRL receptor proteins were detected in DP and LP by Western blot analysis and cross-linking of [125I]human PRL to membrane preparations of DP and LP. Three messenger RNAs (mRNAs) for the long [1.3-1.7, 2.5, and 9.5-10 kilobases (kb)] and short (0.6-0.7, 3.0-4.6, and 10-12 kb) PRL receptors were expressed in dorsal and lateral lobes of rat prostate. Testosterone (T), estrogen (E), and PRL regulation of PRL receptor expression in rat DP and LP was studied in organ culture, which has been shown to be a suitable model to study hormone responses of prostatic tissue in vitro. The mRNAs of the short and long PRL receptors were differentially regulated in rat dorsolateral prostate. T, E, and PRL regulated the level of the long PRL receptor mRNAs in a tissue-specific manner, whereas hormone regulation of the short PRL receptor mRNAs was only modest. Furthermore, the hormonal responses of the different mRNA splicing variants of the long PRL receptor were not all similar; T, E, and PRL each increased the expression of 1.3- to 1.7-kb and 9.5- to 10-kb transcripts in DP, but only T did so in LP, whereas no clear regulation for the 2.5-kb mRNA could be observed in either tissue. This suggests that the hormonal regulation occurs at least at the posttranscriptional level. The effects of T and E were counteracted by the antihormones cyproterone and toremifene, respectively, indicating a specific receptor-mediated manner of steroid action.

Animals↗
PubMed1995

[The diverse effects of hormonal therapeutic agents on the proliferations of human breast cancer cell lines, MCF-7 and its variants].

The author established three variant cell lines which were proliferative in the serum-free medium. These three cell lines were derived from MCF-7, a human breast cancer cell line. These 3 variants (MCF-S1, MCF-S2 and MCF-S3) proliferate estrogen (E2)-dependently, but the amounts of E2 receptor and progesterone receptor in the cells are different from each other among the variants. The author compared the effects of hormonal therapeutic agents, tamoxifen (TAM), 3-hydroxytamoxifen (3-OH-TAM), toremifene (TORE), and medroxyprogesterone acetate (MPA) on MCF-7 and the established variant cells. Although TAM showed little effect on the growth of any cell lines in the absence of E2, it considerably inhibited the growth of MCF-S2 cells and MCF-7 cells in the presence of 10(-10)M E2. TORE also provided no inhibitory effect at less than 10(-7)M concentration on any cells in the absence of E2, but it dose-dependently inhibited DNA synthesis of MCF-S2 cells in the presence of E2. On the other hand, although 3-OH-TAM markedly inhibited the growth of any cell lines at a concentration of less than 10(-6)M in the presence of E2, it dose-dependently inhibited the DNA synthesis of any cell lines in the absence of E2, and the effect was remarkable in the case of MCF-S2 or MCF-S3. MPA showed a tendency to increase the proliferation of any cells in the absence of E2, conversely in the presence of E2, and it slightly inhibited DNA synthesis at concentrations of over 10(-8)M. These results suggest that the effect of hormonal agents on breast cancer cells may depend on either hormonal levels or the characteristics of the cancer cells. The effect of the hormonal agents are diverse, and a hormonal agent which does not work well on one cancer cell population may work well on another population.

Breast Neoplasms↗
PubMedDate not supplied

Treatment of Postmenopausal Breast Cancer with Selective Estrogen Receptor Modulators (SERMs).

Endocrine therapy that targets the estrogen receptor (ER) is a standard of care for the treatment of postmenopausal women with ER-positive breast cancer. The selective ER modulator (SERM) tamoxifen has been in use for the treatment of advanced breast cancer for more than 30 years and is currently a treatment option for all stages of ER-positive disease. Tamoxifen blocks the action of estrogen by binding to the ER, and possesses both ER-agonist and antagonist properties. Unfortunately, long-term use of tamoxifen is associated with several important concerns including an increased risk of endometrial cancer and thromboembolic complications. In addition, many patients who initially respond to tamoxifen eventually relapse with resistant disease. New treatment approaches are therefore required. A number of alternative SERMs have been tested as substitutes for tamoxifen. These include; toremifene, droloxifene, idoxifene, and keoxifene. Unfortunately, the SERMs have not proved to be more effective than tamoxifen for the treatment of advanced breast cancer and have shown a high level of cross-resistance with tamoxifen. The subsequent development of the aromatase inhibitors (AIs) is an important therapeutic advance by creating a "no estrogen" environment. Another approach is the development of pure antiestrogens. Fulvestrant is a novel ER antagonist that destroys the ER and its signaling pathway and is not associated with tamoxifen-like agonist effects. It produces high response rates compared with other SERMs and is not cross-resistant to tamoxifen or aromatase inhibitors and is equally as effective as the AI anastrozole in the treatment of postmenopausal women with advanced breast cancer who have progressed on prior adjuvant tamoxifen therapy. This review article discusses the significant and continuing value of SERMs for the treatment of postmenopausal ER-positive breast cancer.

Aged↗
PubMed2002

[Selective estrogen receptor modulators (SERMs) in the practice].

Selective estrogen receptor modulators (SERMs) represent a growing class of compounds that act as either estrogen receptor gonists or ntagonists in tissue-selective manner. SERMs with the appropriate selectivity profile offer the opportunity to dissociate the favorable bone and cardio-vascular effects of estrogen from its unfavorable stimulatory effects on the breast and uterus. The triphenylethylene drug tamoxifen proved to be invaluable to treat and protect against breast cancer and bone loss, probably reduces cardiovascular risk, but had side effects on uterus similar to natural estrogens. The tamoxifen derivate toremifene is also used to treat breast cancer, but has less effect on bone. The non-steroidal benzothiophene derivate, raloxifene, is the best SERM available thus far. It has the potential to prevent breast cancer (like tamoxifen), but has better profile in its actions on bone and cardiovascular system (produces a rapid reduction of serum cholesterol, decreases fibrinogen and lipoprotein, improves the vascular epithelial function, attenuates vascular intimal thickening, etc.). It does not increase the incidence of endometrial cancer. Compounds of this class are the first step in developing the perfect hormone replacement and other multitargeted therapy. This review summarizes the recent important knowledge about SERMs.

Breast Neoplasms↗
PubMed1999

[Recent development of oral anti-cancer drugs for breast cancer].

Oral anti-cancer drugs play an important role in the treatment of breast cancer. Because these hormonal agents are related to mammary carcinogenesis and tumor growth, they are used not only for therapy but also to prevent the onset of the disease. Tamoxifen, toremifene, fadrozole and other aromatase inhibitors, goserelin, leuprolin and MPA are used widely in Japan as hormonal anti-cancer drugs. In addition oral anti-cancer chemotherapeutic agents, such as cyclophosphamide, 5-FU, 5'-DFUR, FT and UFT are used for breast cancer. The combination of these hormonal and chemotherapeutic agents produces good clinical results in curing the disease. Oral drugs are superior to injected drugs with regard to the QOL of patients.

Administration, Oral↗
PubMed1999

[Effective chemo-endocrine combination therapy for obstructive-jaundice caused by multiple liver metastasis of recurrent breast cancer--a case report].

A 68-year-old woman complained of obstructive jaundice 9 years after a radical mastectomy. CT scan demonstrated multiple metastasis of the liver and two coin lesions of the right lung. The biliary tract was completely obstructed at the portal fissure. Multiple liver and lung metastasis of breast cancer were diagnosed because of high CA 15/3 serum levels and normal gastrointestinal study. Following unsuccessful treatment with tamoxifen (TAM), we used toremifene (TORE) and 5'-deoxy-5-fluorouridine (5'-DFUR) followed by percutaneous transhepatic cholangiodrainage (PTCD). The biliary tract was reopening and jaundice disappeared with improvement of the general condition. Then endocrine therapy with medroxy progesterone acetate and UFT and chemotherapy with CAF (Cyclophosphamide, Adriamycin, 5-FU) were begun. A partial response (PR) was obtained with the disappearance of liver metastasis and two coin lesions of the lung 5 months after the first treatment. The effect of chemo-endocrine combination therapy continued for 5 months. Survival time from recurrence was 13 months. In our case, PR was obtained by using chemo-endocrine combination therapy, although a poor prognosis has been reported in patients with obstructive jaundice caused by multiple liver metastasis of recurrent breast cancer.

Aged↗