Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolactin iodinated by lactoperoxidase method showed immunologically, electrophoretically and biolo9gically similar properties to native prolactin and possessed enough specific radioactivity for receptor studies. 1251-prolactin was incubated with mouse mammary tissues at 8 days of lactation. Both binding and release of 1251-prolactin depended on incubation time and temperature and were maximal at 37 degrees C. Michaelis constant was estimated to be 1.4 X 10(-9) M from Lineweaver-Burk plot and to be 1.2 X 10(-9) M from id-value of the dose-response curve for displacement with native prolactin. Total number of binding sites for prolactin was 1.38 X 10(-15) mole per mg weight of tissue. Ovine prolactin, human growth hormone and human placental lactogen complete with 1251-prolactin and dose-response curves for these three hormones were all parallel. These results suggest the existence of a specific receptor site with high affinity for prolactin in lactating mouse mammary glands.
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PMID:A receptor site for prolactin in lactating mouse mammary tissues. 17 1

This study was carried out as a step toward clarifying the hormone responsiveness of mammary tumors in the F1 hybrid mice of the GR/A and SHN strains. Mammary tumors in SHN mice are pregnancy-independent while mammary tumors of GR/A mice are pregnancy-dependent. Females of each strain were mated with males of the other strain to produce F1 hybrids. They were subjected to forced breeding without subsequent lactation. Only animals with palpable mammary tumors during 2nd and 4th pregnancies were used. Mice received sc injections of several hormones, singly or in combination, daily from 1 day after parturition, i.e., .5 mcg of estradiol benzoate (EB) and of 100 mcg human placental lactogen (HPL). The dose of progesterone (P) before parturition was 100 mcg and after parturition 1 mg. A group received grafts of isologous pituitary glands under kidney capsules (3 AP) during Days 12-34 of pregnancy. 1 day after parturition each mouse was given a single ip injection of 50 micro Ci tritiated-thymidine (tritiated-TdR; 5 Cim/mole) along with the last injection of hormones. Animals were killed 2 hours later. Cyclic SHN mice with mammary tumors received tritiated-TdR, after 2 daily injections of hormones, for 3 days, or after 7-8 days of 3AP. The index of DNA synthesis was determined by a liquid scintillation countermeasuring tritiated-TdR incorporated with DNA. Some of the mice were bled 1 day after parturition and plasma prolactin assayed. Hormone responsiveness was similar among GR/A and both F1 hybrids in either normal or neoplastic glands. DNA synthesis of mammary tumors did not respond to any hormone used but normal glands were stimulated by the hormones. EB injection or 3AP did not alter tritiated-TdR incorporation. HPL injection stimulated DNA synthesis of normal glands but not of tumors. P significantly increased the synthesis of both normal and neoplastic mammary glands. EB and HPL injected with P also significantly promoted DNA synthesis of tumors, but did not increase synthesis in normal glands cuased by P. Plasma prolactin levels were significantly increased by EB injection or by 3AP but were not altered by P. In SHN mice DNA synthesis in mammary tumors was not altered by any hormone treatment but synthesis in normal glands was increased by all treatments. Findings suggest that the hormone-responsiveness of pregnancy-dependent mammary tumors in GR/A and its F1 hybrids is different from some other mammary tumors in mice and rats. Progesterone was more important than prolactin or estrogen for tumor growth. Although EB injection was without effect, intact mice were used so some endogenous estrogen may have participated in the effect. While hormone responsiveness of mammary tumors was different between GR/A and SHN mice, the tumors in both hybrids (BR/A with SHN F1 and SHN with GR/A F1) showed responses quite similar to those of tumors of GR/A mice. This suggests the dominance of the GR/A genotype over the SHN genotype for determining the biological characteristics of mammary tumors.
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PMID:Importance of progesterone in DNA synthesis of pregnancy-dependent mammary tumors in mice. 98 72

Serum SP1 (pregnancy specific beta 1 glycoprotein), hPL (human placental lactogen) and beta-hCG (beta-human chorionic gonadotropin) in patients with choriocarcinoma, invasive mole, and hydati-diform mole were determined by radioimmunoassay (RIA), and compared with those in normal males, non-pregnant women and normal pregnant women in order to evaluate the clinical significance of SP1, hPL and beta-hCG determinations. Serum SP1 levels at the time of admission were highest in hydatidiform mole (5.1 +/- 0.6 micrograms/L) and lowest in choriocarcinoma (0.5 +/- 0.3 micrograms/L). Serum hPL levels were 68.2 +/- 9.7 ng/L in hydatidiform mole and 26.4 +/- 8.3 ng/L in choriocarcinoma. Serum SP1 and hPL levels in trophoblastic diseases were lower than in normal pregnancies (SP1 11.5 +/- 5.1 micrograms/L, hPL 216.8 +/- 48.1 ng/L). SP1/beta-hCG ratios were less than 1.5 in 4/43 (9.3%) cases of hydatidiform mole and 17/19 (89.5%) cases of invasive mole and choriocarcinoma. The beta-hCG/hPL ratios were below 15 in 35/43 (81.4%) cases of hydatidiform mole and 4/19 (21.1%) malignant trophoblastic diseases. The prognosis after operation and chemotherapy was favourable if patient's SP1 and beta-hCG levels gradually decreased.
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PMID:Serum SP1, hPL and beta-hCG levels in trophoblastic diseases. 172 74

Macromolecular forms of human placental lactogen have received little attention because it has been thought that such forms either compose only a small fraction of total immunoactive placental lactogen or are merely laboratory artifacts. We examined serum and placental tissue from women with normal pregnancy (first and third trimesters), serum and tissue from women with eutopic tumors (mole and choriocarcinoma), and serum from men with ectopic placental lactogen production. Samples were chromatographed on dextran gel (Sephadex G-100), and placental lactogen was measured in the fractions by radioimmunoassay. In all specimens examined, immunoactive placental lactogen was found at the void volume of the column (molecular weight greater than 150,000 daltons). This macromolecular placental lactogen comprised less than 4% of total placental lactogen in the third trimester, in mole, and in 16 of 18 first-trimester samples but was significantly higher, up to 19%, in the malignant cases. In two first-trimester placental extracts (but not in their matched sera) macromolecular placental lactogen was the dominant (greater than 45% of the total placental lactogen) immunoactive species. Authentic monomeric placental lactogen was not converted to macromolecular placental lactogen by repeated freezing and thawing. Third-trimester placental macromolecular placental lactogen was unstable; only 13% remained at the void on rechromatography. First-trimester placental macromolecular placental lactogen, on the other hand, was stable to rechromatography. The behavior of immunochemical dilutions of macromolecular placental lactogen from first-trimester placenta was similar to that of monomeric placental lactogen in the same sample. Macromolecular placental lactogen is probably not artifact, and it can comprise a large fraction of the total immunoactive placental lactogen in certain conditions.
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PMID:Eutopic and ectopic macromolecular human placental lactogen. 399 4

An immunohistochemical study analyzing distributions of beta-subunit human chorionic gonadotropin (beta HCG), human placental lactogen (HPL), placental alkaline phosphatase (PLAP), and monoclonal anti-cytokeratin (PKK1) was undertaken to determine whether the reactivity of these antigens might assist in the differential diagnosis of molar and non-molar hydropic placentas. A total of 16 complete hydatidiform moles, 15 partial hydatidiform moles, 12 hydropic abortuses and 39 non-hydropic placentas with gestational age ranging from 4 to 40 weeks was examined. In both the complete and partial moles, many syncytiotrophoblasts stained for beta HCG, HPL, PLAP and PKK1 although the staining intensity of beta HCG in the partial moles was weak compared with the complete moles. The staining patterns in the hydropic abortuses were almost the same as those in the normal first trimester placentas and had no distinct features from the partial moles. Trophoblastic hyperplasia is an essential feature in differentiating partial moles from hydropic abortuses. With regard to the immunostaining patterns of these antibodies, there was no significant difference to enable delineation between partial and complete moles, or between a hydropic abortus and a partial mole. Monoclonal anti-cytokeratin was most sensitive for trophoblasts, but less specific for intermediate trophoblasts than HPL. Although an immunohistochemical study using antibodies against beta HCG, HPL, PLAP and PKK1 is very useful for characterizing various trophoblasts, it is considered that an immunohistochemical study may not be a suitable tool for the differential diagnosis of molar and non-molar hydropic placentas.
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PMID:Immunohistochemistry of molar and non-molar placentas with special reference to their differential diagnosis. 750 73

Gestational trophoblastic tumours result from an abnormal proliferation of different types of trophoblasts. The morphological pattern, together with the immunohistochemical aspect, the cytogenetic data and the clinical profile, helps identify each pathological entity. Hydatiform moles represent malformed placentas caused by genetic aberrations of the villous trophoblast. A complete hydatiform mole displays an hydropic degeneration of all the chorionic villi with a more or less marked proliferation of trophoblasts. A partial hydatiform mole is made up of molar vesicles interspersed with normal chorionic villi. In an invasive hydatiform mole or chorioma destruens, molar vesicles penetrate the myometrium giving rise to a mass distorting the uterine wall. A choriocarcinoma is a malignant proliferation of atypical villous trophoblasts without villi formation. Necrosis, haemorrhage, vascular invasion and distant metastases strongly compromise its outcome. A trophoblastic implantation site tumor, clearly less frequent, results from a proliferation of extravillous trophoblasts, particular for their secretion of human placental lactogen hormone (hPL). This tumour, exceptionally malignant, should be differentiated from the exaggerated placental site and its variants. Except for the placental site trophoblastic tumour, and whatever the outcome (benign or malignant), all gestational trophoblastic tumours secrete the beta-subunit of the chorionic gonadotropic hormone (beta-hCG) more or less abundantly. The serum or urinary level of this unit is proportional to the tumour volume and represents a fundamental basis for the follow-up of these tumours. Multidisciplinary care of high-risk cases allows us to cure the disease, and helps the patient recover her reproductive uterine function.
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PMID:[Pathology of gestational trophoblastic tumors]. 1119 98