Biomedical subjects

S Masamura

Publications and source records attributed to S Masamura.

22 records · Page 2Linked to original sources

PubMed1995

Estrogen deprivation causes estradiol hypersensitivity in human breast cancer cells.

Genetic and environmental factors can modulate the level of sensitivity to various hormones, including estrogens. Enhanced sensitivity to estradiol (E2) has been demonstrated in several biological conditions, such as in sheep during the nonbreeding season, in untreated patients with Turner's syndrome, and in the prepubertal state in normal girls. We postulated that secondary responses to hormonal therapy in patients with breast cancer could also result from enhanced E2 sensitivity, developing as an adaptive mechanism to E2 deprivation. The present study used the MCF-7 human breast cancer cell line as a model system to test the concept that enhanced sensitivity to E2 may occur as a result of adaptation to low E2 levels. After depriving MCF-7 cells of estrogens in tissue culture medium for periods of 1-6 months, we established conditions under which replication could be stimulated maximally by 10(-14)-10(-15) mol/L E2. In contrast, wild-type cells not exposed to estrogen deprivation required 10(-10) mol/L E2 to grow at the same rate. Further, the concentration of the antiestrogen, ICI 164384, needed to inhibit growth by 50% in estrogen-deprived cells was much lower than that required in wild-type cells (i.e. 10(-15) vs. 10(-9) mol/L). Nude mice implanted with these estrogen-deprived cells demonstrated an earlier appearance of palpable tumors in response to E2 than animals bearing wild-type cells. Reexposure to 10(-10)-10(-9) mol/L E2, either in vivo or in vitro, returned these cells to the level of estrogen sensitivity observed in wild-type cells. Taken together, these observations suggest that breast cancer cells can adapt to low levels of estrogens by enhancing their sensitivity to E2.

Animals↗

PubMed1992

Successful aggressive treatment against multiple intra-abdominal metastases from renal cell carcinoma 18 years after nephrectomy.

The management of late metastases from renal cell carcinoma is often difficult because of multiple organ involvement. We report a case of multiple metastases from renal cell carcinoma in the duodenum, pancreas, intestine, falciform ligament and liver, 18 years after nephrectomy. The patient underwent a total pancreatectomy following a gastroduodenal arterial embolization to control duodenal bleeding, a resection of the ileum and falciform ligament at a second laparotomy and repeated hepatic arterial embolizations to control the growth of liver metastases. Aggressive treatment should be undertaken in cases of late recurrence of renal cell carcinoma after nephrectomy because of the possibly slow-growing biological character of the tumor.

Abdominal Neoplasms↗

PubMed1989

[Follow-up study of benign breast diseases].

Follow-up study after surgery of the benign breast disease revealed that rates of the recurrence were 50%, 6%, 4%, 3.5% in those who had phyllodes tumor, duct ectasia, intraductal papillary lesion, and multiple fibroadenoma, respectively. Incidences of the subsequent breast cancer development were 14.3% after ADH, 11.7% after ALH, 1.5% after PDWA, respectively. However no difference was found statistically among those diseases(X2 = 2.89). The longest interval between time of the first surgery and time of detection of subsequently developing cancer was 68 months. Accordingly, checks at three times of postoperative third, fifth and eighth year were required for early detection of such subsequent breast cancer, using image diagnostic methods.

Breast Diseases↗

PubMed1989

[Follow-up study of precancerous lesions of the breast].

A follow-up study of 105 patients with microdochectomy for nipple discharge during the ten year period from 1965 to 1974 revealed that cancer developed in seven of the cases. The histology of the seven cases consisted of atypical hyperplasia in the terminal duct or lobular neoplasia. Accordingly, patients with either of the above histological findings were regarded as high risks for the development of breast cancer. Twenty such high risk patients were selected from 1850 patients biopsied for benign breast disease during the eleven year period from 1975 to 1985. This follow-up study revealed that five of the 13 patients (38%) with atypical hyperplasia in the terminal duct and two of the seven patients (28%) with lobular neoplasia developed breast cancer. Microphotocytometry using TV image analyzed system showed that the mean +/- standard deviation of the nuclear area and the absorbance were, respectively, 46.79 +/- 2.84 and 0.42 +/- 0.01 in fibroadenoma, 62.93 +/- 12.15 and 0.32 +/- 0.02 in precancerous lesion and 86.16 +/- 14.38 and 0.44 +/- 0.07 in breast cancer.

Breast Neoplasms↗