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M Landström

Publications and source records attributed to M Landström.

27 records · Page 2Linked to original sources
PubMed1992

Dose/response study of the effects of oestrogens on tumour growth and morphology in the Dunning R3327 prostatic adenocarcinoma.

The present study was undertaken to investigate to what extent the oestrogen-induced effects on growth and morphology of the Dunning R3327 rat prostatic adenocarcinoma are dose-dependent. Castrated and testosterone-supplemented rats were used in order to study effects of increasing doses of oestrogens on the tumour. It was found that the lowest dose of oestradiol-17 beta that reduced the overall growth, the volume density of the epithelium and epithelial cell area in Dunning R3327 prostatic tumours is 10 micrograms given as daily injections. Higher oestrogen doses (50 micrograms, 200 micrograms, and 500 micrograms), in addition to reducing the volume of tumour epithelium, also induced an increase of the volume density of tumour stroma. The area of stroma cell nuclei was increased by 50 micrograms and 200 micrograms oestradiol-17 beta. These observation, may indicate that the lowest effective oestrogen dose is different in the epithelium and stroma of Dunning tumours and that large doses of oestrogen stimulate the stromal compartment. This stimulatory effect did not influence the inhibitory effects seen on the overall growth of the tumour and on the tumor epithelium.

Adenocarcinoma↗
PubMed1991

Treatment of rat prostatic adenocarcinoma with medroxyprogesterone acetate (MPA): effects on growth and morphology.

Rats bearing the Dunning R3327H prostatic carcinoma were castrated and supplemented with testosterone propionate. These rats were then treated with estradiol benzoate or medroxyprogesterone acetate alone or in combination with estradiol. During the treatment period of six weeks, the growth rate of the prostatic tumors was measured. At the end of the treatment period the morphology of the tumors was also studied. It was found that medroxyprogesterone acetate is as effective as estradiol in inhibiting the growth of the Dunning prostatic carcinoma and that the combination of medroxyprogesterone acetate and estradiol was more efficient in that respect than estradiol alone. Morphometric evaluation of the tumor epithelium and stroma showed a decrement of epithelial growth in all treatment groups, while the groups treated with medroxyprogesterone acetate, both alone or in combination with estradiol, also showed an inhibited growth of the tumor stroma. It was concluded that medroxyprogesterone acetate probably has direct inhibitory effects on prostatic tumor cells in the Dunning model and that medroxyprogesterone acetate may act in an additive manner with estradiol.

Adenocarcinoma↗
PubMed1990

Estrogen treatment combined with castration inhibits tumor growth more effectively than castration alone in the Dunning R3327 rat prostatic adenocarcinoma.

This study was designed to investigate whether the combination of castration with estrogen treatment for 6 weeks (combined treatment) further inhibits growth of the Dunning R3327 rat prostatic adenocarcinoma as compared with castration alone. Combined treatment arrested tumor growth more effectively than castration. Combined treatment also induced morphological changes in both tumor stroma and epithelium that were not found in tumors from castrated animals. The volume density of the tumor epithelium was reduced and the volume density of the tumor stroma was increased by the combined treatment as compared with castration alone. The number of tumor epithelial cells was calculated by morphological methods: combined treatment lowered the number as compared with castration alone. The number of tumor epithelial cells was similar in castrated and intact rats. Both combined treatment and castration alone reduced tumor epithelium cell size as compared with tumors from intact rats. These findings suggest that estrogen may have direct effects on total number and function of prostatic tumor cells.

Adenocarcinoma↗
PubMed1988

Antiestrogens do not counteract the inhibitory effect of estradiol-17 beta on the growth of the Dunning R3327 prostatic adenocarcinoma.

The purpose of this study was to investigate if the local effects of estradiol on the Dunning R3327 prostatic adenocarcinoma were estrogen-receptor mediated. All rats with the transplantable Dunning R3327 prostatic adenocarcinoma were castrated on the first day of treatment and were supplemented with daily s.c. injections of testosterone propionate (0.1 mg) during the treatment period, lasting for 6 weeks. The following treatment groups were studied: castration + testosterone supplementation (C + T, control group), C + T and estradiol-17 beta (50 micrograms/daily s.c.), C + T and tamoxifen (1 mg twice a week s.c.), and C + T and estradiol-17 beta in combination with tamoxifen. Tumor volumes were measured every week. At the end of the treatment period, pieces of the tumors were taken for morphological studies and estrogen-receptor analysis. In the groups of rats given tamoxifen treatment no estrogen-receptor binding was detectable in prostatic tumors, but, despite this, tamoxifen did not prevent either the inhibitory effect of estradiol-17 beta on the tumor growth rate or the estrogen-induced decrease of volume density of prostatic glandular epithelium. In contrast, the estrogen-induced increase of volume density of the stroma was abolished by tamoxifen, suggesting that this effect may be mediated by the estrogen receptor. A morphometrical method for estimating the growth of different tumor compartments is presented. Treatment with estradiol-17 beta, both with or without combined treatment with tamoxifen, reduced the growth of both the tumor epithelium and stroma. The direct effect of estradiol-17 beta on the growth and morphology of the Dunning R3327 prostatic adenocarcinoma seemed not to be mediated by the estrogen receptor.

Adenocarcinoma↗
PubMed1987

Effect of medroxyprogesterone acetate, alone or in combination with epirubicin hydrochloride, on the growth of the Dunning R3327H prostatic adenocarcinoma.

Rats bearing the Dunning R3327H prostatic adenocarcinoma were castrated and supplemented with testosterone propionate. Some of the testosterone-supplemented rats were treated with medroxyprogesterone acetate (MPA) alone or in combination with epirubicin hydrochloride. During the treatment period of 4 weeks, the growth rate of the prostatic tumors was measured. The testosterone-supplemented rats showed a tumor growth rate similar to that found in intact control rats. It was found that MPA has an inhibitory effect on the tumor growth rate in castrated testosterone-supplemented animals. This effect was more pronounced if the MPA treatment was combined with epirubicin hydrochloride, where the tumor growth rate was slower than that found in rats castrated as the only treatment.

Adenocarcinoma↗
PubMedDate not supplied

Antiproliferative activity and toxicity of 2-methoxyestradiol in cervical cancer xenograft mice.

2-methoxyestradiol (2-ME) is considered to be an effective anticancer compound for many types of tumors. We have previously demonstrated that 2-ME inhibits the growth of human cervical cancer HeLaS3 cells in vitro. In this study, we investigated the antitumoral effects of 2-ME on human cervical carcinoma in severe combined immune deficient (SCID) mice. The potential side effects of 2-ME on the SCID mice were also investigated. SCID mice were injected with HeLaS3 cells (3 x 10(6) to 4 x 10(6)/mouse) and a 15-day administration of 2-ME followed after a 1-week cell implantation. Tumor weight, volume, body weight, and blood chemistry were determined. Tumor tissues were examined with an antibody against the proliferative cell nuclear antigen and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Liver, spleen, kidney, heart, and lung were screened by pathologic examinations. 2-ME (75 mg/kg p.o.) inhibited growth of human cervical carcinoma by 34% (P < 0.05) as compared with control. Necrosis was found in both 2-ME-treated and untreated tumor tissues, but the necrotic area was larger in 2-ME-treated mice. A low expression of proliferative cell nuclear antigen and an increased number of apoptotic cells were found in 2-ME-treated tumor sections as compared to those in controls. No significant difference was detected in blood chemistry. In addition, the liver showed hyperplastic Kupffer cells, hydropic swelling of hepatocytes, and liquefactive necrosis. The spleen showed an increased number of megakaryocytes and apoptotic cells after 2-ME treatment. Thus, 2-ME has an antitumor effect on human cervical carcinoma, and it is toxic to liver and spleen in this mouse model.

2-Methoxyestradiol↗
PubMedDate not supplied

Alterations of tumour cells, stroma and apoptosis in rat prostatic adenocarcinoma following treatment with histamine, interleukin-2 and irradiation.

The present study was designed to determine whether IL-2 and histamine alone, or in combination could modulate the effects of irradiation on Dunning (R3327) rat adenocarcinomas at the cellular level. Copenhagen x Fisher rats carrying bilateral tumours in the flank were used. When the tumours had a median volume of 150 mm3, one group of rats was treated with histamine alone (4 mgkg-1 subcutaneously on week days), another group with interleukin-2 (IL-2) alone (425 IU kg-1 continuous infusion) and a third group with both histamine and IL-2 during 6 weeks. Irradiation was given one week after the onset of treatment with histamine and/or IL-2, with a linear accelerator 6 MV, in a dose of 6 Gy/day for 3 days to the tumour of one side, while the other side served as control. Morphometric analyses of the amount of cystic structures, volume density for tumour epithelium, stroma and acinar lumina, the number of activated macrophages and natural killer cells (NK-cells) and in situ detection of apoptotic cells was carried out 5 weeks after the irradiation, when the experiment was ceased. The combination of IL-2 with histamine and irradiation significantly augmented the reduction of tumour cells (p < 0.002) and increased the number of apoptotic cells (p < 0.007) compared to irradiation alone. The number of cystic structures within tumour tissue increased in all tumours that received histamine, but was most pronounced in the three combination group. A strong negative correlation between the epithelial cells and the apoptotic index (rs = -0.61, p < 0.0001) and a strong positive correlation between the stroma and the apoptotic index (rs = 0.59, p < 0.001) was found. A prominent infiltration of activated macrophages was observed in the irradiated group. This infiltration was impaired by the drugs. The results suggested that the used three modality treatment could be of value in increasing the efficacy of local radiotherapy concomitantly with a most plausible effect on micrometastatic spread. The results also propose that volume measurements alone are not an optimal parameter when evaluating effects of new treatment modalities.

Adenocarcinoma↗