Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P13232 (Interleukin-7)
 580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of hydrocortisone on blood-borne tumor metastasis was studied in an i.v. inoculation experiment with Ehrlich hypotetraploid clone 1, Ehrlich hypotetraploid stock, and Ehrlich hyperdiploid stock tumors. The administration of hydrocortisone before tumor inoculation resulted in increased tumor take, reduced mean survival time of mice, and concentration of tumor metastasis in a specific organ (i.e., lung metastasis for Ehrlich hypotetraploid clone 1 tumor, and liver metastasis for Ehrlich hypotetraploid stock and Ehrlich hyperdiploid stock tumors). Enhancement of tumor metastasis, as induced by hydrocortisone pretreatment, was not reproduced by the administration of 6-mercaptopurine, testosterone, or estradiol. The progress of tumor death in hydrocortisone-conditioned mice was not affected by either heparin or dextran sulfate. This indicated that the effect of hydrocortisone on tumor metastasis was independent of the effect of these agents on immune reaction or blood coagulation. In the tracer experiment with 125-I-labeled tumor cells, hydrocortisone pretreatment significantly increased over the control the intrapulmonary retention of Ehrlich hypotetraploid clone 1 tumor cells from 1 through 72 hr after tumor inoculation, the time lag required for the establishment of metastatic foci in the lung. The arrest of Ehrlich hypotetraploid stock and Ehrlich hyperdiploid stock tumors in the liver was also temporarily increased by hydrocortisone pretreatment. No correlation was found between tumor cell size and differential distribution of metastatic tumors with 3 Ehrlich tumors. An attempt was made to use this blood-borne metastasis system for chemotherapeutic study. Administration of cyclophosphamide gave rise to a significant prolongation of survival time and often to complete prevention of tumor metastasis in hydrocortisone-conditioned mice.
Cancer Res 1975 Apr
PMID:Enhancing effect of hydrocortisone on hematogenous metastasis of Ehrlich ascites tumor in mice. 111 40

The purpose of this study was to test the validity of our working hypothesis that the stress of radical surgery may affect the prognosis of a cancer patient by precipitating hematogenous tumor metastasis, and that enhancement of this type of tumor metastasis is mediated by an increase of glucocorticoid activity that is induced in a cancer patient by surgical stress. Practically, we looked for the presence of glucocorticosteroid excess in cervical cancer patients in the course of radical surgery, and also tested the possible impact of glucocorticoid excess on the development of tumor metastasis in mice with i.v. inoculated Ehrlich ascites clone 1 tumor cells. The results obtained indicated that: 1) a state of glucocorticoid excess was observed in cancer patients at an early stage of postoperative convalescence. 2) Development of lung metastasis of blood-borne Ehrlich ascites tumor cells was facilitated in mice by hydrocortisone pretreatment--a substitute for surgical stress conditioning. 3) In the enhancement of lung metastasis, the hormone was found to induce constriction of the lung capillary lumen on the one hand, and acceleration of microvillus growth of the tumor cell surface on the other hand two morphological changes that may facilitate intrapulmonary retention of tumor cells. 4) Cyclophosphamide, as tested in a series of adjuvant chemotherapy experiments, was effective in either retarding or arresting the progress of tumor metastasis in hydrocortisone-conditioned mice. The possible impact of surgical stress on the spread of blood-borne tumor cells to the lung and liver, as well as on the therapeutic effect of cyclophosphamide for the prevention of postoperative micrometastasis, is discussed in the light of glucocorticoid actions on its target tissues.
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PMID:Does surgical stress cause tumor metastasis? 144 28

The purpose of this study is to investigate the relation between the fine structure of the tumor cell surface and the tumor malignancy by scanning electron microscopy. Practically, comparison was made between the invasive Ehrlich ascites clone 1 tumor and the non-invasive Ehrlich ascites clone 3 tumor, and also between the 4th postinoculation day and the 6th postinoculation day as regards the growth of microvilli on the cell surface. On the 4th postinoculation day, an invasive clone 1 tumor cell was indistinguishable from a non-invasive clone tumor cell because of their common paucity of microvilli development. On the 6th postinoculation day, the former was associated with exuberant growth of microvilli, and was clearly distinguished from the latter in which the density of microvilli stayed low as before. The appearance of dense microvilli growth in the invasive clone 1 tumor cells chronologically coincided with the stage of fatal bleeding into the abdominal cavity. Hydrocortisone with a dose of 1 mg/mouse, when given subcutaneously to a tumor-bearing mouse on the 4th postinoculation day, stimulated the development of microvilli in both clone 1 and clone 3 tumors. The enhancing effect of the hormone on this process was detectable 2 hours after hormone injection. It was indicated that the dense growth of microvilli in the clone 1 tumor facilitated its tumor invasion into visceral organs, and that the enhancing effect of hydrocortisone on microvilli development was to be related to the promotion of malignant transformation. The possible implications of glucocorticoid in mammocarcinogenesis are discussed from the point of view of comparative endocrinology.
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PMID:Differential surface structures of invasive and non-invasive Ehrlich ascites tumor cell lines with special reference to the effect of hydrocortisone treatment. 150 12

Biliary glycoprotein I (BGP I) is a member of carcinoembryonic antigen (CEA) gene family consisting of at least 11 related genes. The transcription of BGP I gene was analysed in malignant and non-malignant human liver tissues with a 396-bp 3'-untranslated region probe from a cDNA clone 4-13 which was newly isolated from an adult human colon cDNA library. Among 21 tissue samples from 14 patients with hepatocellular carcinoma, 16 samples were clearly shown to express a single 3.9-kb message. This message was also found in the hepatoma cell line HuH-7. When the malignant tissues were compared to the non-malignant ones for the intensity of the band, no significant difference was observed. mRNAs of CEA and non-specific cross-reacting antigen (NCA) were not detected in 5 samples which were shown to have the message of the BGP I gene. These data suggest that the human hepatocyte and its malignant transformant produce BGP I, and that this could correspond to the cross-reacting antigen previously detected in the liver.
Int J Cancer 1990 May 15
PMID:Transcription of biliary glycoprotein I gene in malignant and non-malignant human liver tissues. 233 90

To characterize differences in gene expression between hormone-dependent and hormone-independent mammary carcinoma, we cloned complementary DNAs of genes expressed in a hormone-independent breast carcinoma cell line that were not expressed in a hormone-dependent line. One clone, which was isolated in many copies, coded for the intermediate filament protein vimentin. A complementary DNA clone 1.8 kilobases long included the entire protein-coding region for vimentin. Vimentin was expressed by more than one-half of the hormone-independent breast carcinoma cell lines tested but not by the hormone-dependent cell lines. The cell lines which expressed vimentin expressed only low levels of cytokeratins. The correlation between vimentin expression and more advanced stages of mammary cell transformation was tested in a model system in which immortal, nontumorigenic human mammary epithelial cells or derivative lines transformed with v-ras-H or SV40 T-antigen were found not to express vimentin, whereas a derivative highly tumorigenic cell line transformed by both v-ras-H and T-antigen did express vimentin. Analysis of several other kinds of epithelial carcinoma cell lines showed only rare examples of vimentin expression.
Cancer Res 1989 Aug 01
PMID:Vimentin rather than keratin expression in some hormone-independent breast cancer cell lines and in oncogene-transformed mammary epithelial cells. 247 76

A monoblastic cell line U-937 (clone 4), was induced to differentiate along the monocytoid lineage by 12-O-tetradecanoylphorbol-13-acetate (TPA), retinoic acid (RA), and vitamin D3 (VD3). By immunochemical and morphological criteria the cells were found to differentiate into macrophage-like cells in the presence of all three inducers. The expression of proteoglycans was investigated in control cultures and in cells differentiated in the presence of both TPA, RA, and VD3. The cells were labeled with [35S]sulfate and cell and medium-associated 35S-macromolecules were either solubilized in sodium dodecyl sulfate or subjected to proteolytic digestion. By use of chondroitinase ABC digestions and deaminative cleavage at pH 1.5 it was demonstrated that all cell cultures incorporated [35S]sulfate exclusively into chondroitin sulfate proteoglycan (CSPG). The expression of CSPG was found to decrease with differentiation to 60% in the presence of TPA, 67% in RA, and 40% in VD3 of control cultures on a cellular basis. The CSPG synthesized was consistently recovered from the medium fractions, whereas free glycosaminoglycan (GAG) chains were found in the cell fraction in all the cell cultures. GAG chains from both control and TPA-, RA-, and VD3-induced cultures were found to be exclusively of the chondroitin 4-sulfate type. However, the CSPGs from RA- and VD3-treated cells were found to differ in molecular size from those of control and TPA-induced cultures, as judged by Sepharose CL-6B gel chromatography. This difference in macromolecular properties following the induced differentiation of the monoblastic cells into macrophage-like cells was found to reside in expression of CSPGs (in the presence of RA and VD3) with smaller GAG chains. Control cells and TPA-induced cells synthesized CSPGs with GAG chains of approximate Mr of 30,000, contrasted by approximate Mr of 17,000 and 16,000 in RA- and VD3-induced cells, respectively. Accordingly, all three agents used in this study were found to induce differentiation of the U-937-4 cells and a decrease in the expression of CSPG, but only RA and VD3 were found to influence the structure of the proteoglycans synthesized.
Cancer Res 1988 Nov 01
PMID:Differentiation-associated changes in the expression of chondroitin sulfate proteoglycan in induced U-937 cells. 284

DNA from a human laryngeal carcinoma was molecularly cloned in Lambda L47. The gene library was screened for human papillomavirus (HPV)-related sequences by hybridization analysis with 32P-labelled HPV 16 DNA at conditions of low stringency (Tm -40 degrees C). One of the clones (4-5) with an insert of 7.8 kb showed cross-hybridization with most of the known HPV types (Tm -40 degrees C), and with several of them even under more stringent conditions (Tm -30 degrees C). No signal was detected under high-stringency conditions (Tm -20 degrees C). The co-linear alignment of clone 4-5 with HPV 16 DNA could be demonstrated by hybridization experiments and also by partial DNA sequence analysis. We conclude that clone 4-5 represents a new HPV type tentatively designated HPV 30. HPV 30 DNA was also detected in 2 genital lesions but not in 41 laryngeal carcinomas analyzed so far. Its presence in other tumor DNA is now under investigation.
Int J Cancer 1986 Jan 15
PMID:Molecular cloning and characterization of the DNA of a new human papillomavirus (HPV 30) from a laryngeal carcinoma. 300 Sep 55

The biological activities of Epstein-Barr virus (EBV) from a human epithelial hybrid cell line derived from a nasopharyngeal carcinoma (NPC-KT) were studied. Low concentrations of virus from the NPC-KT cell line stimulated DNA synthesis of human cord blood lymphocytes (CBL) and induced CBL to form EBV nuclear antigen-positive continuous cell lines. The CBL exposed to higher doses of virus showed stimulated DNA synthesis 2 days after infection, followed by cell lysis. Virus from the NPC-KT cell line induced EBV-specific antigens in nonproducer Raji cells and reduced the colony-forming ability of the super-infected cells. The ratio of transforming activity to early antigen-inducing ability was not constant during cell passage. The data obtained suggest that NPC-KT clone 1 cells are producing virus with cytotoxic and transforming properties.
J Natl Cancer Inst 1986 Jun
PMID:Heterogeneity of Epstein-Barr virus derived from a nasopharyngeal carcinoma that has transforming and lytic properties. 301 75

Cloned cell strains with adverse patterns of differentiation obtained from 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor tissue were used to study the effects of glucocorticoid hormones on morphology and proliferation. HH-16 clone 2/1 cells apparently reflecting mesenchymal cells of the stromal part of the mammary gland grow as elongated, mostly bipolar fibroblasts in criss-cross patterns. When cultured in the presence of glucocorticoids, the cells flattened, lost bipolarity, extended in size, and showed arrest of growth at confluence, possibly due to contact inhibition. Immunocytochemical examination of dexamethasone-treated cells revealed actin cables which were absent in untreated cells. The hormone-treated cells expressed Mr 50,000-67,000 cytokeratins, and the extracellular matrix proteins fibronectin and laminin were increased. The in vitro effects on morphology and growth were reversible 3-4 days after withdrawal of the glucocorticoids. In dexamethasone-treated animals the growth of fibrosarcomas produced by inoculation of newborn rats with HH-16 clone 2/1 cells was reduced, and the survival time of the tumor-bearing animals was extended. Apparently, morphology and growth of HH-16 clone 2/1 fibrosarcoma cells can be controlled by glucocorticoids. In comparison, epithelioid HH-16 clone 4 cells established simultaneously from 7,12-dimethylbenz(a)anthracene-induced rat mammary tumor were unresponsive to glucocorticoids.
Cancer Res 1988 Dec 15
PMID:Glucocorticoid-induced alterations of morphology and growth of fibrosarcoma cells derived from 7,12-dimethylbenz(a)anthracene rat mammary tumor. 314 85

Cloned lines of Adriamycin (ADR)-sensitive and -resistant P388 leukemia have been established from single cell cultures. A marker chromosome M1 was found in all cells in the heterogeneous resistant P388/ADR parental line as well as in the cloned resistant lines P388/ADR/3 and P388/ADR/7; a different marker chromosome M2 was present in the heterogeneous sensitive P388 parental line as well as the cloned sensitive line P388/4. Dose-survival studies showed that D0, the dose of Adriamycin reducing survival to 1/e (i.e., 37% of the initial population), was 33 +/- 5 (SE) nM for sensitive P388/4 cells, 169 +/- 17 nM for resistant P388/ADR/3 cells, and 336 +/- 28 nM for the more resistant P388/ADR/7 cells. Drug uptake in sensitive P388/4 cells was 1.6-fold greater than in resistant P388/ADR/3 cells and 2.1-fold greater than in resistant P388/ADR/7 cells. The number of DNA single-strand breaks produced per microM Adriamycin was 131 +/- 9 rad equivalents in sensitive clone 4 cells, 41 +/- 8 rad equivalents in resistant clone 3 cells, and 33 +/- 11 rad equivalents in resistant clone 7 cells. The number of DNA double-strand breaks per microM Adriamycin was 1721 +/- 126 rad equivalents in sensitive cells, 117 +/- 36 rad equivalents in resistant P388/ADR/3 cells, and 194 +/- 16 rad equivalents in resistant P388/ADR/7 cells. Differences in drug uptake were insufficient to explain the higher incidence of DNA single- and double-strand breaks in sensitive cells. These findings strongly support the concept that resistance to Adriamycin in P388 leukemia cells is multifactorial; however, this study did not resolve whether these changes arise from a single pleiotropic mutation or from multiple mutations. In sensitive P388/4 cells the number of DNA single-strand breaks formed could all be attributed to double-strand breaks. However, in both resistant cell lines the level of induction of single-strand breaks was in excess of that due to double-strand breaks, and this excess of single-strand breaks appeared to vary directly with the degree of resistance, being greater in the more resistant clone 7 cells than in the less resistant clone 3 cells. In both sensitive and resistant cell lines the ratio of true single- to double-strand breaks varied inversely with the concentration of Adriamycin. Finally, the cytotoxic activity of Adriamycin appeared to correlate more closely with formation of DNA double-strand breaks than with single-strand lesions.
Cancer Res 1986 Jun
PMID:Resistance to adriamycin: relationship of cytotoxicity to drug uptake and DNA single- and double-strand breakage in cloned cell lines of adriamycin-sensitive and -resistant P388 leukemia. 369 20


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