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PubMed1989

Inhibition of tumor angiogenesis activity in C3H mouse mammary tumor by medroxyprogesterone acetate.

The growth of the C3H mouse mammary tumor (MMT) is considered to be hormone independent. Medroxyprogesterone acetate (MPA) had no effect on the growth of transplanted autochthonous MMT or the colony-formation of MMT cells. The tumor angiogenesis factor (TAF) activity of tumor-extract prepared from C3H mouse with transplanted autochthonous MMT and injected with 0.67 mg of MPA (in vivo MPA group) and that prepared from the colony of MMT cells treated with 10(-6) M MPA (in vitro MPA group) was lower (100.0% and 9.8%) than those of the in vivo and in vitro cortisol groups (325.5% and 44.3%), and the in vivo and in vitro groups without treatment (393.5% and 46.8%), respectively. The fibroblast growth factor (FGF) activity of the in vivo and in vitro MPA groups was lower (23.7% and 2.7%) than those of the in vivo and in vitro cortisol groups (54.7% and 11.3%), and the in vivo and in vitro groups without treatment (49.6% and 11.3%), respectively. Therefore, MPA may reduce neovascularization induced by TAF and FGF, although it had no effect on the growth of this MMT, and it had a glucocorticoid action similar to that of cortisol.

Angiogenesis Inducing Agents↗

PubMed1989

Inhibition of tumor angiogenesis activity by medroxyprogesterone acetate in gynecologic malignant tumors.

More than 30% of the colony formation of dispersed tumor cells was inhibited by medroxyprogesterone acetate (MPA) in 2 out of 6 cases of endometrial cancer, in 1 out of 6 cases of cervical cancer, and in 3 out of 12 cases of ovarian cancer. The colony formation inhibited by MPA was not related to clinical stage or histological type. There was no significant difference in the tumor angiogenesis factor (TAF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. TAF activity was inhibited by MPA in 4 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 9 out of 12 cases of ovarian cancer. There was no significant difference in the fibroblast growth factor (FGF) activity of any case of endometrial, cervical and ovarian cancer between the cortisol-treated group and the controls. FGF activity was inhibited by MPA in 3 out of 6 cases of endometrial cancer, in 5 out of 6 cases of cervical cancer, and in 10 out of 12 cases of ovarian cancer. The cases in which the colony formation was inhibited by MPA were not related to the cases in which TAF or FGF activity was inhibited by MPA. Therefore, MPA may reduce neovascularization induced by TAF and FGF, and can depress secondary spreading of some endometrial, cervical and ovarian cancer via the mechanism of terminal process of secondary spreading, regardless of the presence of glucocorticoid actions similar to that of cortisol, and the reduction of cell proliferation.

Adenocarcinoma↗

PubMed1989

Sequential hormone therapy with medroxyprogesterone acetate for 7, 12-dimethylbenz [alpha] anthracene-induced rat mammary tumors.

Two types of sequential hormone therapy with medroxyprogesterone acetate (MPA) were examined in female 93 Sprague--Dawley (SD) rats with 7,12-dimethylbenz [alpha] anthracene (DMBA)-induced mammary tumors. Estradiol (E2) priming induced progesterone receptors (PgR) in most cases and, after induction of PgR, MPA often showed an augmented antitumor effect. For this reason, E2 priming + MPA had a more marked antitumor effect on DMBA tumors than MPA alone. Tamoxifen (TAM) (0.1 mg/kg) priming induced PgR more frequently than TAM (0.4 mg/kg) priming. Furthermore, treatment with TAM priming (0.1 mg/kg) + MPA showed a more marked antitumor effect than with TAM priming (0.4 mg/kg) + MPA or MPA alone. In the above two priming therapies with MPA, the latter is more practical for the clinical treatment of breast cancer than the former because the mechanism of action of E2 is usually thought to show tumorigenic activity on breast cancer, while the mechanism of action of TAM is thought to show an antitumor effect. It is suggested that the sequence of administration of MPA after TAM priming may be favorable for the treatment of breast cancer.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1989

[Combination therapy with medroxyprogesterone acetate and tegafur in tamoxifen- and adriamycin-resistant advanced breast cancers].

Medroxyprogesterone acetate (MPA) plus Tegafur (TGF) therapy was performed to evaluate the efficacy in a treatment for Tamoxifen- and Adriamycin-resistant advanced breast cancers. The patients were medicated in different doses on 800 mg or 1,200 mg daily po for MPA and TGF. Sixteen patients were evaluable in this trial. According to criteria of the Japan Mammary Cancer Society, one was regarded as CR and five as PR. The response rate was 37.5%. There was no difference in response rates between premenopausal and postmenopausal patients or ER positive and negative patients. No difference was noted either in response rates and incidence of side effects between two different doses of MPA. This means that an 800 mg daily dose of MPA lower than the recommended 1,200 mg might be better in the treatment for Japanese patients with advanced breast cancers. Gastrointestinal disorders, bone marrow suppression and liver dysfunction which could be found in high-dose TGF therapy, were not frequently observed in this trial. Patients could expect good quality of life during the treatment because of fewer side effects. This combination therapy with MPA and TGF was regarded as a good modality for the treatment of Tamoxifen- and Adriamycin-resistant advanced breast cancers.

Adult↗

PubMed1989

Effect of medroxyprogesterone acetate on secondary spreading of endometrial cancer.

We examined the effect of medroxyprogesterone acetate (MPA) on secondary spreading of endometrial cancer. There was no significant difference in the adhering capacity of dispersed Ishikawa cells (derived from well-differentiated endometrial cancer) to a cell basement membrane matrix, fibronectin or laminin between cells treated with MPA, with cortisol, and without treatment. The adhering capacity of cells treated with cortisol to collagen type IV was higher than that without treatment. However, the adhering capacity was little affected by treatment with MPA. These results indicate that although cortisol may induce the initial process of metastasis by inducing the attachment of tumor cells to the basement membrane of vascular endothelium, MPA has no influence on the attachment, although it has a glucocorticoid action similar to that of cortisol. There was no significant difference in tumor angiogenesis factor (TAF) or fibroblast growth factor (FGF) activity of the tumor extract from Ishikawa cell colonies between cortisol-treated and control group. TAF or FGF activity of the MPA-treated group was lower than that of the control group. MPA may reduce the neovascularization in the terminal process of metastasis via the reduction of TAF and FGF produced by tumor cells, in spite of its glucocorticoid action.

Angiogenesis Inducing Agents↗

PubMed1989

[Effect of medroxyprogesterone acetate on side effects of CAP therapy in gynecological malignant tumors].

We concomitantly administered a large dose of medroxyprogesterone acetate (MPA) to gynecological malignant tumor patients undergoing CAP therapy (CAP). Hematological changes in the peripheral blood were compared between concomitant MPA patients and those not receiving MPA to examine the effect of MPA in reducing the marrow depression which is the major side effect of CAP. 1) Leukocyte count reached minimum at the second week of CAP in both groups. There was no significant difference in the count between the two groups. At the third week of CAP, the count improved to 84% of the pre-CAP level in patients receiving MPA and to 68% in those not receiving MPA, a significant difference (p less than 0.01). At the fourth week, leukocyte counts were 105% and 96% of pre-CAP levels, respectively. There was no difference between the two groups, but the leukocyte count returned to the pre-CAP level in the patients receiving MPA. 2) Platelet count showed changes similar to those in the leukocyte count. In patients receiving MPA, the count improved more rapidly within three weeks (118%, p less than 0.01), and was significantly higher at the fourth week (107%, p less than 0.05) than in patients not receiving MPA. 3) Reticulocyte count reached minimum in the first week, thereafter improving rapidly in both groups. No differences were noted between the two groups. 4) The periods needed for one course of CAP were 27.7 +/- 3.3 days in the patients receiving MPA and 29.5 +/- 3.7 days in the patients not receiving MPA, making for a significant difference between the two groups (p less than 0.05). These results show that MPA accelerates recovery from marrow depression caused by CAP. It is anticipated, therefore, that MPA will be helpful in the application of various chemotherapies which are expected to be frequently conducted in the future.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1989

[Mammary gland carcinoma treated by large-dose medroxyprogesterone acetate of which pulmonary metastases disappeared and a selection of hormone, chemoimmunological treatment].

A patient who underwent radical mastectomy was treated by tegafur and tamoxifen. Pulmonary metastases were found four months after operation. Lymphokine activated killer (LAK) and auxiliary interleukin-2 (IL-2) administration was performed, with no change (NC). However, administration of large-dose medroxyprogesterone acetate induced complete disappearance of pulmonary metastases after more than nine months.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1989

[Combination with medroxyprogesterone acetate and chemotherapy making possible complete removal of uterine corpus carcinoma].

A case of uterine corpus carcinoma (stage III) after surgical resection of her primary lesion was treated with a medroxyprogesterone acetate (MPA) and PAE (CDDP, adriamycin and etoposide) regimen. The patient has been given MPA during a three-month period and received four courses of PAE regimen. The residual tumor was decreased and removed completely at the second-look operation. Pathologically, the carcinoma cells were clearly changed in loss of atrophy or degeneration by MPA or PAE regimen. After the second-look operation, the patient underwent 4 courses of PAE regimen and was given MPA continuously. We have not recognized any recurrence of carcinoma for seven months after the second look operation.

Adenocarcinoma↗

PubMed1989

[Progesterone receptors in endometrial carcinoma and their response to medroxyprogesterone acetate].

Progesterone receptors (PR) were measured in 18 cases of endometrial carcinoma using the dextran-coated charcoal assay. The histological changes and PR levels of the endometrial carcinoma after the medroxyprogesterone acetate (MPA) treatment were studied. A higher PR levels were observed in well-differentiated tumors. After treatment with MPA, the PR content was reduced and histological appearance similar to normal endometrium was noticed. The histological changes of the tumor was closely related to the receptor levels.

Adult↗

PubMed1989

[Results of tamoxifen-medroxyprogesterone acetate sequential therapy in 22 patients with recurrent breast cancer].

Effects of tamoxifen (TAM)-medroxyprogesterone (MPA) sequential therapy were evaluated in 22 patients with recurrent breast cancer. TAM-MPA therapy was given in the form of TAM 20 mg b.i.d. for 14 days followed by MPA 1200 mg t.i.d. for the subsequent 14 days, in alternating sequence. The response rate was 27% (6/22). Weight gain (greater than 5 kg) was observed in 18% (4/22) and this incidence was lower than that reported for MPA therapy. These results demonstrate that TAM-MPA therapy offers fewer side effects than MPA therapy, but response rate is unlikely to be improved.

Adult↗

PubMed1989

Mechanism of antitumoral activity of medroxyprogesterone acetate for endometrial cancer.

The colony-formation of Ishikawa cells, which originate from well differentiated endometrial cancer, and produce progestogen receptors (PR), was inhibited by high concentrations of medroxyprogesterone acetate (MPA). However, the colony-formation was not inhibited by norethindrone (ENT), as a luteohormone or 17 beta-hydroxy-11 beta-(4-dimethylaminophenyl-1)-17 alpha(prop-1-ynyl)-estra-4, 9-dien-3-one (RU-486), as an antiprogestogen. Colony-formation in cells treated with MPA alone was not significantly different from that in those treated with MPA combined with either ENT or RU-486. ENT and RU-486 have high affinity with PR as does MPA. If the suppressive effect by MPA on colony-formation is mediated via PR, then this suppression should be competitively inhibited by ENT or RU-486. Our findings indicate that the effect of MPA is not mediated via PR.

Antineoplastic Agents↗

PubMed1987

Mouse mammary tumors induced by medroxyprogesterone acetate: immunohistochemistry and hormonal receptors.

Mammary adenocarcinomas induced by medroxyprogesterone acetate (MPA) in female BALB/c mice were investigated as to their morphology and immunohistochemistry and their content of steroid, prolactin (PRL), and epidermal growth factor (EGF) receptors. Histologically, these tumors were mainly of ductal origin, since hyperplastic alveolar nodules were observed only in 3 cases. No viral particles were encountered in electron microscopic studies. Estrogen and/or progesterone, PRL, and EGF receptors were detected in MPA-induced tumors, as well as in the occasional spontaneous mammary tumors of multiparous females. EGF was detected, by a radioimmunoassay, in the cystic fluid of 12 mammary adenocarcinomas. MPA treatment was found to induce uterine secretory changes, glandular cystic hyperplasia, and eventually deciduomas that stained strongly for desmin and to a lesser degree for vimentin, suggesting a muscular differentiation. Consequently, MPA-induced adenocarcinomas can be considered as ductal tumors that possess estrogen and/or progesterone, PRL, and EGF receptors. Whether MPA induces tumor growth directly via progesterone receptors remains to be investigated.

Adenocarcinoma↗

PubMedDate not supplied

The effect of ethynyloestradiol and medroxyprogesterone acetate on the in vivo uptake and metabolism of 3H-oestradiol by breast tumour tissue in postmenopausal women.

The uptake and metabolism of 3H-oestradiol by breast tumour tissue was studied in three postmenopausal women before, after 1 week of treatment with ethynyl-oestradiol (EE, 10 micrograms/day) and again two weeks later after treatment with medroxyprogesterone acetate (MPA, 500mg/day, i.m.). Treatment with EE reduced the tissue: plasma gradients for both 3H-oestradiol and 3H-oestrone and little further change in these ratios occurred after MPA treatment. The proportion of oestrogen present as 3H-oestrone increased in tumours from 2/3 women after treatment with MPA but not EE, although no increase in the activity of oestradiol 17 beta-hydroxysteroid dehydrogenase (E2DH) was detected. Plasma and tissue concentrations of 5-androstenediol, dehydroepiandrosterone and dehydroepiandrosterone sulphate were all reduced after MPA treatment. The results from this study show that treatment with EE and MPA can reduce the uptake of oestradiol by breast tumours. No increase in E2DH activity was detected but it is possible that MPA influences other enzymes involved in oestradiol metabolism.

17-Hydroxysteroid Dehydrogenases↗

PubMedDate not supplied

[Medroxyprogesterone acetate. Contributive treatment in congenital adrenal hyperplasia caused by 21-hydroxylase deficiency in children].

Among 59 children presenting with congenital adrenal hyperplasia due to 21-hydroxylase deficiency observed between 1976 and 1982, 12 (9 males, 3 females) aged 3 1/2 to 12 years, were treated with medroxyprogesterone acetate (MPA) associated with the usual glucocorticoid and eventually mineralo-corticoid treatment. There were two indications: precocious puberty after the onset of the gluco-mineralo-corticoid treatment; Unbalanced biological status with advancement of bone maturation. After the onset of MPA, a decrease in plasma 17-hydroxyprogesterone (17 OHP) and testosterone levels is observed, the bone maturation speed decreases when growth in height continues. MPA may be a contributive treatment for congenital adrenal hyperplasia due to 21-hydroxylase deficiency, permitting restoration of biological balance by restraining adrenal function and improving the final height prognosis.

Adrenal Hyperplasia, Congenital↗

PubMed1985

Effect of medroxyprogesterone acetate on steroid reductases in rat liver.

Male and female rats were treated with medroxyprogesterone acetate (17 alpha-acetoxy-6 alpha-methyl-pregn-4-ene-3,20-dione, MPA) 600 mg/kg body weight i.p. daily for seven days. The steroid metabolizing enzymes in liver microsomes and liver homogenate were measured following MPA treatment and in control rats. The specific activity of NADPH- and NADH-5 alpha-reductase in female rats and of NADPH-5 alpha-reductase in male rats decreased by the treatment. NADP+- and NAD+-3-hydroxysteroid dehydrogenase activities were lower in female MPA rats if compared to untreated animals. In male rats only NADP+- and NAD+-3 beta-hydroxysteroid dehydrogenase activities (substrate 5 beta-dihydrotestosterone) were diminished by MPA administration. There was no effect on the cytoplasmatic 5 beta-reductases. Plasma concentrations of luteinising hormone (LH), testosterone and androstenedione were lowered by MPA treatment.

3-Hydroxysteroid Dehydrogenases↗

PubMed1985

Effective sequential administration of tamoxifen and medroxyprogesterone acetate for 7,12-dimethylbenz[a-anthracene-induced rat mammary tumors in relation to hormone receptors.

The effects of two hormonal agents with different mechanisms of action, medroxyprogesterone acetate (MPA) and tamoxifen (TAM), on the tumor growth and hormone receptor status were evaluated in rat mammary tumors induced by 7,12-dimethylbenz[alpha]anthracene (DMBA). All estrogen receptor-positive (ER(+)) tumors became ER-negative (ER(-)), and 3 out of 4 progesterone receptor-negative (PgR(-)) and ER(+) tumors became PgR-positive (PgR(+)) after daily, oral administration of TAM for 2 weeks. In contrast, ER and PgR remained unchanged after daily administration of MPA for 2 to 4 weeks. All the ER(+) and PgR(-) tumors were transformed into PgR(+) after daily treatment with MPA for 2 weeks and then with TAM for another 2 weeks, but tumor regression was modest and none disappeared completely. In contrast, complete remission was achieved in all ER(+) tumors in the group treated with TAM for 2 weeks and then with MPA for another 2 weeks. The results suggest that the antitumor activity of the latter treatment regimen was significantly higher than that of the former. The possible mechanisms of antitumor activity of two hormonal agents are discussed.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed1986

Lipoprotein changes during treatment of pelvic endometriosis with medroxyprogesterone acetate.

Ten women with endometriosis were treated with medroxyprogesterone acetate (MPA), 150 mg intramuscularly every second week. After 2 weeks, there was a significant (8%) decrease in the high-density lipoprotein (HDL) concentration. This reduction became more pronounced after 8 and 24 weeks' medication. The HDL reduction was confined to the HDL2 subfraction, which was decreased by 15%, 33%, and 58% after 2, 8, and 24 weeks, respectively; there was no significant change in the HDL3 concentration. During treatment, there was a continuous increase in the mean MPA plasma level and a strong inverse correlation between this level and the mean HDL and HDL2 cholesterol concentrations. It was concluded that MPA affects HDL metabolism in a dose-dependent way and in the same direction as other progestins.

Adult↗

PubMed1986

Modalities and results of a combined anti-estrogenic therapy by means of tamoxifen and medroxyprogesterone in gynecologic cancerology.

In the therapeutic schemes of the hormone-dependent gynecologic cancers, the combined administration of tamoxifen and medroxyprogesterone, generally, scores better results. The highly hormone-dependent tumors (ER+, PgR+) respond very well to a combined, simultaneous treatment. The strictly hormone-dependent (ER+, PgR-) and the potentially hormone-dependent (ER-, PgR-) tumors seem to be most efficiently treated by means of a combined, successive scheme.

Adenocarcinoma↗