UMLS:C0432222 - FACTA Search

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The effect of somatostatin analogue RC-160 on the growth of hepatic metastases of colon cancer was investigated in rats using magnetic resonance imaging. Experimental liver metastatic tumors were established in syngeneic BDIX rats after intrasplenic injection of DHD/K12 colon adenocarcinoma cells. Each rat with implanted liver tumors received s.c. injections of somatostatin analogue RC-160 (50 micrograms/kg) or the vehicle (control) twice a day for 4 weeks, starting 3 weeks after tumor inoculation. During the treatment with RC-160, the growth of liver tumors was studied quantitatively by measuring liver tumor volumes in vivo with magnetic resonance imaging at intervals of 7 days. Chronic administration of RC-160 inhibited the growth of hepatic metastases of colon cancer in rats. Significant inhibition of liver tumor growth in RC-160-treated rats was observed throughout the treatment. The final liver tumor volume in the treated rats was decreased by 56.1% as compared to the controls. The treatment with RC-160 reduced the percentage increase in liver tumor volume from 1575 +/- 674% (mean +/- SEM) for the control to 1034 +/- 727% in the treated group. The tumor volume doubling time in treated rats was 3.7 days longer than the controls. The liver tumor growth delay time was 15.1 days. At the end of the treatment, the incidence of ascites and the weights of tumorous livers were also decreased by RC-160 treatment. Administration of RC-160 prolonged the median survival time by 13 days in treated rats. In cell cultures, significant inhibitory effects of somatostatin-14 and RC-160 on the growth of DHD/K12 colon cancer cells were determined by MTT assay and [3H]-thymidine incorporation assay, indicating direct effects of these peptides on the growth of colon cancer cells in vitro. These data suggest that administration of RC-160 could inhibit the growth of colon cancer and their hepatic metastases in rats. Somatostatin analogue RC-160 might be considered as a potential new agent for the treatment of patients with hepatic metastases of colorectal cancers.
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PMID:Inhibitory effect of somatostatin analogue RC-160 on the growth of hepatic metastases of colon cancer in rats: a study with magnetic resonance imaging. 135 23

Hormonally active neuroendocrine tumors may easily be diagnosed by elevated serum levels of their specific peptides and hormonal products, but there are no reliable markers for neuroendocrine tumors without hormonal activity. Chromogranin A (CgA), a secretory protein of neuroendocrine cells, has recently been characterized as a valuable tissue marker in hormonally active and non-functioning neuroendocrine tumors. This study analyzes the role of CgA as a serum marker for different neuroendocrine tumors. Thirty-three patients with neuroendocrine tumors of the stomach (n = 7), the ileum (n = 18), and the pancreas (n = 8) were investigated. Serum CgA levels were analyzed by radioimmunoassay at the time of diagnosis and during follow-up under different therapeutic regimens. Serum CgA was elevated in 30 (91%) patients. Mean CgA serum levels varied with tumor location (pancreas: 7068 +/- 3008 ng/ml, ileum: 5381 +/- 1740 ng/ml, stomach: 529 +/- 179 ng/ml, x +/- SEM ng/ml) but did not differ between functioning and non-functioning tumors. Eight of 10 patients treated with either somatostatin or interferon-alpha showed changes of CgA concentrations corresponding to tumor growth. We conclude that CgA is a useful broad-spectrum tumor marker in gastroenteropancreatic neuroendocrine tumors. Its determination is especially recommended in tumors without hormonal activity.
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PMID:Serum chromogranin A in the diagnosis and follow-up of neuroendocrine tumors of the gastroenteropancreatic tract. 141 39

Clinical trials of radioimmunotherapy (RIT) of lymphoma have produced frequent tumor regressions and remissions, but it has been difficult to determine to what extent these tumor responses have been due to antibody-specific targeted radiation, nontargeted radiation, and/or cytotoxicity mediated by the carrier monoclonal antibody (MoAb). In this report, RIT was studied in athymic nude mice bearing s.c. Raji human Burkitt's lymphoma xenografts using two different pan-B-cell MoAbs, MB-1 (anti-CD37) and anti-B1 (anti-CD20), which differ in isotype (and thus the potential for interaction with host effector mechanisms) and isotype-matched control antibodies either in the unlabeled state or labeled with 131I. When a single i.p. injection of 300 microCi 131I-labeled MB-1 (IgG1) was compared to treatment with unlabeled MB-1 or 300 microCi 131I-labeled MYS control IgG1 MoAb, an antibody-specific targeted radiation effect of RIT was seen. 131I-labeled MB-1 produced a 44 +/- 19% (SEM) reduction in tumor size at 3 weeks posttreatment, while unlabeled MB-1 or 300 microCi 131I-labeled MYS control IgG1 antibody treatment resulted in continued tumor growth over this period of time. In vitro studies demonstrated that MB-1 was incapable of mediating antibody-dependent cellular cytotoxicity using Raji tumor cell targets and human peripheral blood mononuclear cells. Similar to the MB-1 studies, treatment with 300 microCi 131I-labeled anti-B1 produced a 64% reduction in mean tumor size, while 300 microCi of control antibody resulted in a 58% increase in tumor size over the same 3-week period. In contrast to MB-1, however, unlabeled anti-B1 (an IgG2a MoAb which in vitro studies showed to be capable of antibody-dependent cellular cytotoxicity) also had a substantial antitumor effect. Indeed, 300 microCi 131I-labeled anti-B1 and unlabeled anti-B1 treatment (using an equivalent amount of total protein in the treatment dose) produced a similar specific reduction in tumor size. Increasing the radionuclide dose of anti-B1 to 450 microCi in another experiment did not produce a significant difference in tumor regression compared to a 300-microCi dose. These results suggest that the antitumor effects of 131I-labeled anti-B1 treatment were dominated by antibody-mediated cytotoxicity mechanisms, such that an antibody-specific targeted radiation effect could not be distinguished. In contrast, antibody-specific targeting of radiation was the dominant mechanism of tumor killing with 131I-labeled MB-1.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Therapy with unlabeled and 131I-labeled pan-B-cell monoclonal antibodies in nude mice bearing Raji Burkitt's lymphoma xenografts. 142 95

The potential of the adrenal androgens androstenedione (A) and dehydroepiandrosterone (DHEA) to stimulate prostate tumor growth was investigated in the hormone-dependent human prostate tumor model PC-82, propagated in nude mice. Substitution of castrated mice bearing growth-arrested tumors with DHEA for 28 days, resulting in peripheral levels of 9.2 +/- 1.7 nmol/liter (mean +/- SEM), led to a decline of tumor burden comparable to that observed in castrated controls. Intratumor testosterone (T) and 5 alpha-dihydrotestosterone were similar to those detected in the castrated group. In contrast, high-dose A supplementation (peripheral level of 13.5 +/- 1.3 nmol/liter) in androgen ablated tumor-bearing mice resulted in tumor growth, although less pronounced than in T-resubstituted mice (T level of 18.8 +/- 1.5 nmol/l). Intraprostatic levels of androgens were not different between both groups. Substitution of castrated PC-82 tumor-bearing mice with low-dose A (2.5 +/- 0.4 nmol/l) neither stimulated growth of tumors nor did it lead to regression of PC-82 tumors. Proliferative activity as estimated by BrdU incorporation (S-phase cells) was not induced in these tumors. In conclusion, DHEA does not have a stimulatory effect on growth of PC-82 tumor tissue, but A is capable of inducing PC-82 tumor growth, most likely through peripheral conversion of A into T and 5 alpha-dihydrotestosterone.
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PMID:Effects of adrenal androgens on the transplantable human prostate tumor PC-82. 144 27

Beagles were exposed to aerosols of 239PuO2, 238PuO2, or 239Pu(NO3)4. Exponential growth constants for 50 primary lung tumors (23 bronchioloalveolar carcinomas, 22 papillary adenocarcinomas, 5 adenosquamous carcinomas) were calculated in 37 dogs, using sequential thoracic radiography. A wide range in doubling time (6 to 287 days) was observed. Mean +/- SEM doubling time was 93 +/- 10 days for bronchioloalveolar carcinoma, 107 +/- 13 days for papillary adenocarcinoma, and 101 +/- 36 days for adenosquamous carcinoma. Lung tumor growth rate in dogs was comparable to that in human patients with similar histologic tumor types. Linear regression analysis revealed significant (P < or = 0.0001) correlation between doubling time and survival of individual dogs. Doubling time was not significantly dependent on tumor type, sex, age at time of diagnosis, initial lung deposition, or isotope. Extrapolating time to tumor onset from tumor doubling time cannot be used to reliably predict the onset of malignancy.
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PMID:Radiographically determined growth dynamics of primary lung tumors induced in dogs by inhalation of plutonium. 145 11

Transforming growth factor alpha (TGF-alpha) is a polypeptide regulator of cell growth produced by many malignant tumors. It stimulates osteoclastic resorption in bone organ culture and osteoclast-like cell formation in marrow culture. To determine whether tumor production of TGF-alpha can cause hypercalcemia in vivo, we used Chinese hamster ovarian (CHO) cells transfected with the human TGF-alpha gene (TCHO), which stably express and secrete TGF-alpha. We used nontransfected CHO cells as controls (CCHO). TCHO and CCHO were inoculated intramuscularly into one hindlimb of nude mice and grew as local solid tumors. After 4 weeks of TCHO tumor growth, plasma ionized calcium (Ca2+) increased to reach 1.48 +/- 0.03 mM (mean +/- SEM), whereas mice bearing similarly sized CCHO tumors and non-tumor-bearing mice (NTB) remained normocalcemic (normal range for Ca2+, 1.15-1.30 mM). Plasma TGF-alpha was undetectable by an ELIFA assay in all NTB mice, was markedly increased in all TCHO mice (5.75 +/- 0.78 ng/ml), and was slightly increased in CCHO mice (0.50 +/- 0.22 ng/ml). Quantitative bone histomorphometry showed a prominent increase in osteoclastic bone resorption in TCHO mice. These data suggest that TGF-alpha is a mediator of hypercalcemia and increased osteoclastic bone resorption in tumors that produce it in sufficient quantity.
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PMID:Expression of human transforming growth factor alpha by Chinese hamster ovarian tumors in nude mice causes hypercalcemia and increased osteoclastic bone resorption. 164 53

The effect of repeated, intermittent hepatic vascular occlusion on liver tumor growth was studied in 32 rats. An adenocarcinoma was inoculated in the left liver lobe. After 8 days, the tumor size was measured and then, in three groups, the hepatic artery was occluded intermittently during 5 days for 15 min, 1 hr, or 2 hr daily, respectively. The tumor growth after 6 days in these groups was compared with that in a group where instead the portal vein was occluded intermittently during 5 days for 15 min, and with that in a group of sham-operated control rats. In the control rats, the tumor volume (mean +/- SEM) increased from 0.16 +/- 0.03 to 1.34 +/- 0.15 cm3 during the 6 days of experiment. It was found that repeated, intermittent occlusion of the hepatic artery or the portal vein, retarded the liver tumor growth to 30-60% of the growth rate in sham-operated controls (P less than or equal to 0.015). The 15-min daily hepatic artery or portal vein occlusion was found to reduce the tumor growth rate as much as daily hepatic artery occlusion for 2 hr. It is suggested that short, daily, intermittent hepatic vascular occlusions might be efficient in the palliative treatment of liver malignancy.
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PMID:Intermittent hepatic arterial or portal occlusion reduces liver tumor growth. 199 Feb 19

The effects of the androgen dihydrotestosterone (DHT) and of the androgenic steroid medroxyprogesterone acetate were studied on the growth of human ZR-75-1 breast carcinoma in athymic mice. The possibility of additive inhibitory effects of DHT and the new steroidal antiestrogen N-n-butyl, N-methyl-11-[16' alpha-chloro-3',17' alpha-dihydroxyestra-1',3',5'(10')trien-7' alpha-yl]undecanamide (EM-170) was also investigated on tumor growth. Removal of the high dose 17 beta-estradiol (E2) implants used to optimally stimulate initial ZR-75-1 tumor development in ovariectomized mice led to a progressive decrease in tumor area to 50.2 +/- 8% (SEM) of original tumor size 40 days after E2 deprivation. Additional treatment with the androgen DHT led to a more rapid fall in tumor volume, which already reached 57% of pretreatment values at 11 days. Whereas physiological implants of E2 led to a progressive increase in tumor size to about 180% above original size after 40 days, physiological plasma levels (205 +/- 37.2 pg/ml or approximately 0.67 nM) of DHT completely reversed the stimulatory effect of E2. Similar inhibitory effects on E2-stimulated tumor growth were achieved with the synthetic androgenic steroid medroxyprogesterone acetate. When the steroidal antiestrogen EM-170 at the dose of 30 micrograms/day was used simultaneously with DHT, tumor area was further reduced from 99.0 +/- 9.5% (DHT alone) to 58.8 +/- 18% when both DHT and EM-170 were administered together for 40 days compared with 169 +/- 22.2% in control E2-stimulated animals. The present data show that the androgen DHT as well as medroxy-progesterone acetate are potent inhibitors of E2-stimulated human ZR-75-1 breast cancer cell growth in vivo. Moreover, the inhibitory effect of DHT can be further increased by addition of the antiestrogen EM-170, thus suggesting the interest of combining these 2 classes of compounds acting, at least partially, through different mechanisms, in order to improve breast cancer therapy in women.
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PMID:Additive inhibitory effects of an androgen and the antiestrogen EM-170 on estradiol-stimulated growth of human ZR-75-1 breast tumors in athymic mice. 203 92

The stem cell soft agar culture system provides a biological tool with which to study tumor clones derived from heterogeneous tumor cell populations. For testing the feasibility of this approach in identifying hormone-responsive clones of mammary tumors, a study was done to determine whether estrogen deprivation or supplementation would alter colony formation in sequential breast neoplasms received in the Cell Kinetics Laboratory, The Pennsylvania State University. Single-cell suspensions obtained from 22 freshly excised breast neoplasms (20 malignant, 2 benign) were plated in soft agar with and without tamoxifen (Tam) (10(-7) M) with the use of serum-supplemented media and with and without 17 beta-estradiol (E2) (10(-8) M] under serum-free medium conditions. Twenty tumors successfully grew, producing 42 +/- 8 (mean +/- SEM) colonies in control dishes in the presence of serum and 27 +/- 5 in its absence (P less than .001). Tam inhibited colony formation in 78% of malignant tumors, whereas a stimulatory effect was observed with E2 in 94%. An increase in colony formation was induced by Tam in 4 tumors (2 benign and 2 malignant). The effects of E2 and Tam on tumor growth were not influenced by the estrogen and progesterone receptor status of the tumor. These preliminary results suggest that all tumors, irrespective of their receptor status, may contain clones of hormone-responsive cells.
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PMID:Hormone dependency of human breast neoplasms cultured in vitro in the stem cell assay. 298 56

The effect of piroxicam, a nonsteroidal anti-inflammatory drug, on a transplantable adenocarcinoma in Fischer rats was studied. Forty male Fischer rats were injected with 1 X 10(6) DMH-F317 adenocarcinoma cells, and after 2 weeks were assigned to be treated with piroxicam or carrier solution. The groups were as follows: Group 1, control; Group 2, 4.0 mg/kg piroxicam; Group 3, 6.0 mg/kg piroxicam; and Group 4, 8.0 mg/kg piroxicam. Thirty-nine of forty rats developed measurable tumors during this study. At the conclusion, 60% (6/10) of the rats in Group 2 were tumor free compared to 0/10 controls, 0/10 Group 3 rats, and 1/8 Group 4 rats. (P less than 0.005, chi 2). Mean tumor volumes (mm3) were calculated for each group and converted to log10. At Week 6, the mean log10 tumor volume (+/- SEM) for Group 2 was 1.5 +/- 0.6 vs 4.1 +/- 0.1 for Group 1 (P less than 0.05). The mean log10 volume for Group 3 was 3.8 +/- 0.1 (P less than 0.05 vs Group 2). The mean log10 volume for Group 4 was 3.4 +/- 0.05 and was not significantly different from that for Group 2 (P greater than 0.05). Plasma PGE2 levels for each treatment group were determined at the conclusion of the study and no statistical difference between treatment groups was found. It is concluded that piroxicam inhibits tumor growth in this model, and may have a role as a biological response modifier in cancer therapy.
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PMID:Piroxicam inhibits the growth of an adenocarcinoma isograft in Fischer rats. 316 75

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