Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0598934 (tumor growth)
 58,965 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A study was undertaken to observe morphological changes and viral morphogenesis during the growth of the mouse preputial gland tumor ESR 586. The acinar cells of the normal preputial gland have an extensive agranular endoplasmic reticulum and Golgi apparatus and large lipid droplets. No viral particles are present. During tumor growth, and numerous lipid droplets never attain the size of those found in the normal gland. There is a decrease in the Golgi apparatus and agranular endoplasmic reticulum and an increase in the rough endoplasmic reticulum which could reflect a change in composition of tumor secretory product from the normal gland. Indeed, there is a decrease in triglycerides as the tumor ages and an increase in the sterol esters and waxes. In addition, intracisternal A-particles are observed budding from thickened endoplasmic reticulum membranes. Thickening of these membranes occur early in A-particle formation. One side of the membrane is first thickened while the opposing membrane appears is first thickened while the opposing membrane appears morphologically unaffected. The thickening of the affected membrane is initially confined to the outer (cytoplasmic) face of the membrane. In the older tumor, both opposing membranes of the reticulum are thickened and can assume an elongated whorled pattern.
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PMID:Ultrastructural changes and viral morphogenesis during the growth of the mouse preputial gland tumor ESR 586. 83 78

An increasing number of polypeptide growth factors have been identified that regulate not only cell proliferation but also an extraordinary range of cell activities, including matrix protein deposition and resolution, the maintenance of cell viability, cell differentiation, inflammation, and tissue repair. Normal cells appear to require growth factors for proliferation and for maintenance of viability. Cells that secrete a polypeptide growth factor have an advantage in growth. These factors can act either externally through cell surface receptors or internally during the transport of receptors and growth factors through the endoplasmic reticulum and Golgi apparatus, causing autocrine stimulation of cell growth. Depending on the cell type, growth factors can also be potent inhibitors of cell growth rather than stimulators of growth, and the effect can depend on the presence or absence of growth factors. Among the growth factors considered, IGFs are unusual in that they function both as endocrine and as autocrine/paracrine agents. IGF-II, which is associated with fetal growth, is the IGF most frequently expressed by tumors. There is now convincing evidence that some tumors secrete sufficient IGF-II to have systemic endocrine effects as recognized as nonislet cell tumor hypoglycemia. PDGF is normally highly concentrated in platelets and has major significance in stimulation of cellular proliferation in inflammation and wound repair. Normally, this proliferation is self-limited, but the secretion of PDGF by tumors and its effects on cell proliferation of tumors persist. The fact that PDGF B monomer has an identical structure with that of the proto-oncogene C-cis further strengthens the connection between PDGF and tumor growth. EGF has a restricted role in normal physiology, but its close relative, TGF-alpha, is widely distributed in normal and neoplastic tissues. The common receptor for EGF and TGF-alpha is present in many normal and neoplastic cell types. The EGF receptor is the product of the C-erb gene. The oncogene V-cis is a truncated form of the EGF receptor whose tyrosine kinase activity is not dependent on ligand binding. TGF-beta exists in multiple forms. Although it can transform the morphology of certain cell lines in culture, it probably does not act generally as a mitogenic agent. Its major physiologic role in the body appears to be the stimulation of mesenchymal matrix formation. It is of special importance in the regulation of bone matrix formation. Its expression is increased in many tumors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Tumor secretion of growth factors. 171 47

Very recently a subset of human GH-secreting pituitary adenomas carrying a somatic mutation in the alpha subunit of the stimulatory regulatory protein of adenylyl cyclase (Gs) was identified. In all these tumors (Group 2; about 30% of all the GH secreting tumors studied) the alpha s cDNAs contained mutations; in 8 tumors mutations replaced Arginine 201 with either Cystein or Histidine while in the remaining tumors Glutamine 227 was replaced by either Arginine or Leucine. No mutations were observed in the remaining adenomas (Group 1). The two mutations caused a constitutive activation of adenylyl cyclase and a turn on of cAMP synthesis by inhibiting GTPase activity. The transformed phenotype was reflected in adenomatous cells with high rate of cAMP production and in vitro GH secretion. No difference in age, sex, clinical features, duration of the disease and cure rate were observed between the patients without (Group 1) or with alpha s mutation (Group 2), while higher serum GH levels and smaller tumor size were present in Group 2 patients. Moreover, hypersecretory activity in Group 2 tumors was also apparent at electron microscopy; cells of Group 2 tumors were densely granulated and showed prominent rough endoplasmic reticulum and Golgi complex. With respect to Group 1, Group 2 patients were less responsive to GH-releasing hormone (GHRH), while they were more sensitive to somastostatin. The former finding is in agreement with the hypothesis that the oncogenic proteins mimic the effects of extracellular growth factors, so removing the requirement for GHRH; the latter might explain the low rate of tumor growth as due to the counteracting role of endogenous inhibitory factors.
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PMID:Mutations in the alpha subunit of the stimulatory regulatory protein of adenylyl cyclase (Gs) in human GH-secreting pituitary adenomas. Biochemical, clinical, and morphological aspects. 192 49

Somatic mutations in the alpha-chain (alpha s) of the stimulatory regulatory protein of adenylyl cyclase (Gs) causing constitutive activation of the enzyme have been identified in a subset of human GH-secreting pituitary adenomas. This study reports on the differences between acromegalic patients bearing tumors without (group 1; n = 51) or with (group 2; n = 29) this alteration. No difference in age, sex, clinical features, duration of the disease, or cure rate was observed between the two groups. By contrast, group 2 patients had higher basal GH levels than group 1. Moreover, a significant difference in sellar morphology was found; group 2 patients more frequently showed sellas of normal size (grade I) than group 1. Hypersecretory activity of group 2 tumors was also apparent at electron microscopy; contrary to those of group 1, cells of group 2 tumors were densely granulated and showed prominent rough endoplasmic reticulum and Golgi complex. With respect to group 1, group 2 patients were less responsive to GH-releasing hormone, while they were more sensitive to somatostatin- and dopamine-induced GH inhibition. These results suggest that patients with constitutively active adenylyl cyclase have hyperactive tumors; the sensitivity of these tumors to inhibitory agents (somatostatin and dopamine), possibly counteracting the expression of activating mutations, might explain the low rate of tumor growth.
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PMID:Clinical, biochemical, and morphological correlates in patients bearing growth hormone-secreting pituitary tumors with or without constitutively active adenylyl cyclase. 197 58

Chemotaxis is an important step in monocyte recruitment in inflammation, wound healing, and tumor growth. We reported previously that monocyte chemotactic activity secreted by malignant cells and normal smooth muscle cells is associated with a protein or family of proteins that are related to the monocyte-specific smooth muscle cell-derived chemotactic factor (SMC-CF) (Graves, D. T., Jiang, Y. L., Williamson, M. J., and Valente, A. J. (1989) Science 245, 1490-1493). Similar monocyte chemotactic proteins (MCP-1) produced by U-105MG human glioma cells have also been identified (Yoshimura, T., Robinson, E. A., Tanaka, S., Appella, E., Kuratsu, J., and Leonard, E. J. (1989) J. Exp. Med. 169, 1449-1459). We now report that the MCP-1 gene is expressed in MG-63 human osteosarcoma and vascular smooth muscle cells and that SMC-CF antiserum specifically immunoprecipitates proteins synthesized by U-105MG glioma cells. Experiments were undertaken to elucidate the processing pathway of MCP-1/SMC-CF-like proteins in each of these cell types. These experiments demonstrate that larger MCP-1/SMC-CF-like proteins are derived from a Mr = 9000 precursor. Post-translational modification involves the addition of O-linked carbohydrates and sialic acid residues. Differences in carbohydrate processing account for the heterogeneity in MCP-1/SMC-CF-like proteins produced by different cell types. Secretion of these proteins occurs rapidly following processing events in the endoplasmic reticulum-Golgi compartment.
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PMID:Post-translational modification of a monocyte-specific chemoattractant synthesized by glioma, osteosarcoma, and vascular smooth muscle cells. 221 4

C57BL/6 mice are relatively more resistant to hepatocarcinogens than C3H and C57BL/6 x C3H F1 (hereafter called B6C3F1) mice; however, the basis for this strain-dependent difference is not clear. In order to address this issue, male C57BL/6 mice were treated i.p. with 5 mg/kg diethylnitrosamine when 15 days old and the histological features of induced hepatocellular neoplasms were assessed at intervals over the ensuing 80 weeks. In many respects the natural history of the tumors was similar to that previously reported for hepatic neoplasms in B6C3F1 mice; they invaded hepatic vein branches while still microscopic (18 weeks after diethylnitrosamine) and developed into metastasizing trabecular carcinomas by 80 weeks. However, the tumors in the C57BL/6 mice were unique in their early focal development of cells containing inclusions of secretory protein within the endoplasmic reticulum. At 12 weeks after diethylnitrosamine, more than 90% of the neoplasms contained inclusions. Over the ensuing months, the inclusions increased in size and number and the regions containing them became more sharply defined. In mice killed 48 weeks after carcinogen, the extent of inclusion formation was correlated with [3H]thymidine labeling indices. Mean labeling indices were higher in the inclusion-poor than in the inclusion-rich areas: 5.4% versus 1.5% for the 36 neoplasms smaller than 1 mm in diameter and 14% versus 6% for the 18 neoplasms larger than 1 mm. Thus, we suggest that the focal slowing of hepatocellular tumor growth in C57BL/6 mice contributes to the strain's apparent resistance to hepatocarcinogenicity. However, the impairment does not appear to block tumor progression and the ultimate development of trabecular carcinomas. In addition, the data indicate that, independent of the presence or absence of inclusions, larger tumors have higher labeling indices, and presumably higher growth rates, than smaller ones. While the reason for the association between cytoplasmic inclusions and the low labeling indices is not known at present, at the very least the inclusions serve as unique markers for the growth retardation.
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PMID:Focal impairment of growth in hepatocellular neoplasms of C57BL/6 mice: a possible explanation for the strain's resistance to hepatocarcinogenesis. 273 37

An experimental transplantable canine brain tumor model with the advantages of rapid tumor growth within 10 days and relative safety for the investigator is presently available. The tumor is produced by intracerebral inoculation of cultured cells derived from a canine brain tumor induced by the Schmidt-Ruppin strain of the Rous-Sarcoma virus (SR-RSV). It has potential use as a model in experiments designed to evaluate the effectiveness of chemotherapy and radiotherapy with serial computerized tomography scans. However, characterization of the induced tumor is essential. Ideally, it should have features attributable to glioma and/or neuroectodermal tumors. Utilizing the technique of intracerebral inoculation of cells cultured from the original dog brain tumor induced by SR-RSV, Salcman et al identified the tumor they induced in brains of mongrel puppies as a glioma by light microscopic criteria (Reference). The purpose of our study was to further characterize this experimental tumor by electron microscopic and immunohistochemical techniques. Tumor was induced in 6 mongrel puppies. Stains of the tumor for immunohistochemical reactivity to glial fibrillary acid protein, S-100 protein and 210K neurofilament protein were all negative. With the electron microscope, the intracerebral tumor cells were mostly undifferentiated. They had a few cell processes, occasional punctate adhesions and some microvilli-like structure. The tumor cell nucleus was usually oval shaped and sometimes had nuclear indentations. The cytoplasm contained abundant free ribosomes, some rough endoplasmic reticulum and mitochondria. Collagen fibers and basal lamina were not observed in the intercellular spaces. The capillaries within the tumor were characterized by proliferation of immature endothelial cells which were non-fenestrated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain tumor induced in dogs by intracerebral inoculation of SR-RSV induced cultured tumor cells--electron microscopic study]. 299 91

The Rice H500 tumor is a transplantable nonmetastasizing testicular tumor of Fischer rats associated with hypercalcemia and increased urine cyclic adenosine monophosphate (AMP) excretion, features similar to those of the clinical syndrome of humoral hypercalcemia of malignancy. Tumor cells can be maintained in tissue culture; one million cells grown in culture reinoculated in Fischer rats reproduce the syndrome of tumor growth and lethal hypercalcemia. Infusion of concentrated, serum-free cell culture supernatant into parathyroidectomized rats produced an increase in urine cyclic AMP similar to that produced by an infusion of bovine parathyroid hormone. Light and electron microscopic appearance of the H500 tumor in vivo and in vitro is similar to previous descriptions of a hypercalcemia-associated rat testicular tumor believed to be of Leydig cell origin. Ultrastructural characteristics of microvilli, intracellular glandlike lumina, and cell-cell attachments, however, suggest an epithelial origin. Absence of smooth endoplasmic reticulum typical of steroid-secreting Leydig cells suggest these cells are not actively involved in steroid synthesis and secretion. The ultrastructure of this tumor is sufficiently different from that of normal Leydig cells that the cell of origin is unclear. Nonetheless, this tumor provides a useful model of hormonally mediated tumor-associated hypercalcemia.
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PMID:Morphologic and functional studies of a rat hypercalcemia-associated testicular tumor maintained in cell culture. 300 12

The MtTF4 pituitary tumor has been induced in Fischer rats by chronic estrogen administration. Recently, we reported that sustained pharmacological treatment of Fischer rats with 17 beta-estradiol inhibited the growth of the MtTF4 tumor transplanted s.c. The present work describes the associated morphofunctional changes occurring in the tumor during 17 beta-estradiol inhibition. It is shown that a 7-day 17 beta-estradiol treatment resulted in an increase of the surface area of cells, nuclei, nucleoli, Golgi complexes, and rough endoplasmic reticulum and an increase in the number of euchromatin-rich nuclei. Flow cytometry analysis of DNA distribution suggested that estradiol affects the cell progression through the early S phase. The ratio of RNA to DNA increased significantly, reflecting cell hypertrophy. Moreover, there was a significant increase in tumor prolactin concentration and a marked enhancement in the intensity of the immunocyto-chemical reaction with rat prolactin antiserum. On the other hand, cell mitoses were dramatically decreased. These morphofunctional changes indicate that the inhibition of the tumor growth by estradiol is accompanied by an evolution of the tumor cell population towards a more differentiated state. However, it cannot be decided whether 17 beta-estradiol induces a shift from a proliferative state to a differentiated state or whether 17 beta-estradiol treatment results in a selection of a subpopulation of tumor cells that are slow growing and more differentiated.
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PMID:Morphofunctional modifications associated with the inhibition by estradiol of MtTF4 rat pituitary tumor growth. 674 19

The effects of growth hormone (GH) and/or cortisone and thyroxine (T4) treatment on the ultrastructure of the transplantable Swarm rat chondrosarcoma grown in hypophysectomized rats were studied. Marked atrophy of the tumor occurred when it was grown in hypophysectomized rats. Maximal restoration of tumor growth in hypophysectomized rats was achieved when cortisone, T4, and GH were administered in combination. An intermediate degree of tumor growth restoration was observed when tumor-bearing hypophysectomized rats were given cortisone and T4 or GH alone. Cortisone and T4 treatment was associated with increased rough endoplasmic reticulum and nucleolar enlargement, while GH treatment was associated with marked dilatation of the endoplasmic reticulum. When GH, cortisone, and T4 were given in combination, a marked increase in exocytotic/pinocytotic vesicles and apparent deposition of cartilage matrix were noted. The data indicate that GH has dramatic influences on the tumors and, when GH, cortisone, and T4 are administered together, these hormones have a synergistic effect on the growth of the Swarm rat chondrosarcoma.
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PMID:Hormone responsiveness of a transplantable rat chondrosarcoma: III. ultrastructural evidence of in vivo hormone dependence. 722 63


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