[Hemodynamics in patients with neoplastic and suppurative processes of the lungs, based on data obtained by catheterization of the pulmonary circulation].
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Catheterization↗
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Results for “Neoplastic Processes”
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[Arteriography in neoplastic and inflammatory processes of the testis].
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Angiography↗
The insulin-like growth factor system in regulation of normal and malignant hematopoiesis.
The published data available on the insulin-like growth factor (IGF) family of peptides, its receptors and binding proteins in connection with normal and neoplastic hematopoietic processes are reviewed. It is found that nearly all the different hematopoietic cells, either normal or neoplastic, express IGF receptors. The IGFs are involved in normal erythropoiesis, granulopoiesis and lymphopoiesis. IGFs, especially IGF-1, are mitogenic for cell lines of myeloid and lymphoid leukemias and Burkitt's lymphoma. Differentiation of certain immature malignant cell lines is associated with a decrease in the number and affinity of IGF receptors. It might be concluded that the IGFs have an important role in the physiologic and neoplastic processes of the hematopoietic system, and the expanding knowledge of this issue will contribute to the understanding of proliferation and differentiation processes in specific hematologic disorders.
Animals↗
Transdifferentiation of neoplastic cells.
Transdifferentiation is a process in which a stable cell's phenotype changes to that of a distinctly different cell type. It occurs during certain physiological processes and leads to transition of tumor cell phenotypes. The latter process includes neoplastic epithelial-epithelial transition, neoplastic epithelial-mesenchymal transition, neoplastic mesenchymal-epithelial transition and transition between non-neural and neural neoplastic cell. This phonomenon is exemplified in some origin-debated tumors, such as carcinosarcoma, pleomorphic adenoma, synovial sarcoma, Ewing's/pPNET, and malignant fibrohistiocytoma. We propose that differentiation disturbance of cancer cells should include not only undifferentiation and dedifferentiation, but also transdifferentiation as well. Tumor cell transdifferentiation may be influenced or determined by cellular genetic instabilities, proliferation and apoptosis, as well as by extracellular matrix and growth factors.
Animals↗
Post-translational processing of gastrin in neoplastic human colonic tissues.
Gastrin has been postulated to stimulate proliferation in colorectal neoplasms. Although gastrin mRNA has been demonstrated to be present in colon cancer cell lines, the intact peptide had not been recovered from human colorectal neoplasms. We demonstrate that gastrin and its precursors are present in both colorectal neoplasia and adjacent normal-appearing colonic mucosa. In colonic tissue, the glycine-extended precursor form of the peptide is over 10-fold more abundant than the amidated gastrin, and progastrin is more than 700-fold more abundant. In contrast, amidated gastrin in the human antrum is the predominant form of gastrin by a factor of 10. Furthermore, the ratio of gastrin precursors to gastrin is significantly increased in neoplastic colonic mucosa when compared with normal colonic tissue. These data suggest that the processing of gastrin is unique in the human colon and that further differences in processing occur in neoplastic colonic tissue.
Amino Acid Sequence↗
Immunohistochemical localization of chromogranins A and B and secretogranin II in normal, hyperplastic and neoplastic prostate.
Routinely processed normal, hyperplastic and neoplastic prostatic tissue was immunohistochemically investigated with antibodies against chromogranin A and B and secretogranin II. In normal and hyperplastic prostates all three peptides were immunolocalized in scattered neuroendocrine cells situated within the glandular epithelium. In 17 prostatic carcinomas with pronounced neuroendocrine differentiation and in a case of prostatic carcinoid, chromogranin B was the major component whereas chromogranin A and secretogranin II were virtually absent in poorly differentiated (grade III) tumours. Neuroendocrine differentiation in prostatic cancer is most likely to be associated with a poor clinical outcome; thus, chromogranin B appears to be a useful marker in the histopathological diagnosis of these neoplasms.
Chromogranin A↗
Dermatofibroma is a clonal proliferative disease.
Benign fibrous histiocytoma of the skin or dermatofibroma (DF) has been regarded as a fibrohistiocytic tumor. Whether DF is a neoplastic growth or a reactive process has not been settled. Since a neoplastic process is clonal in nature, clonal analysis of DF was conducted to see if DF is a clonal disease. Fresh specimens of 13 DFs and 2 hypertrophic scars obtained from female patients were studied. The adjacent nonlesional skin tissues served as controls. The clonal analysis was based on the methylation pattern of the polymorphic X-chromosome linked androgen-receptor gene (HUMARA). Eight DFs and 1 hypertrophic scar were heterozygous at the androgen receptor gene and could be analyzed. All 8 informative DFs showed a significant reduction in one of the allelic bands compared with the corresponding bands of the nonlesional tissue after Hha I digestion. Therefore, DF is a clonal proliferative disease. In contrast, 1 hypertrophic scar showed a polyclonal pattern of X-chromosome inactivation. We conclude that DF is a clonal disease favoring a neoplastic process.
Alleles↗
[Imbalance between pro-oxidative and anti-oxidative processes in children with neoplastic disease].
UNLABELLED: THE AIM of the study was to assess the concentration of malondialdehyde (MDA), vitamin E and total antioxidant status (TAS) of serum and activity of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in erythrocytes. MATERIAL AND METHODS: a total of 56 children, aged 1,5-18 years, treated between 2001-2002, were diagnosed as having malignant disease. Of these, 27 patients had leukemia, 20 had solid tumours and 9 -lymphoma. These patients were examined before treatment and on achieving remission during therapy. RESULTS: the imbalance between pro-oxidative and antioxidative processes were found in all the children with neoplastic disease. TAS was lower and GPX was higher than normal in all children with cancer; MDA was higher in the newly diagnosed children before treatment. CONCLUSIONS: the role of vitamin E in the pathogenesis of childhood neoplastic disease need to be evaluated. Further studies on a larger group of patients are needed.
Adolescent↗
Modulation of mouse fibroblast adipocyte differentiation by X-rays and TPA.
The purpose of this study was to determine whether X-rays and the tumor promoter TPA which, in combination, are more effective at transforming cells in vitro than is either alone, may also be more effective at inhibiting differentiation in combination. Previous studies with 3T3 T proadipocytes have shown that both the tumor promoter 12-o-tetradecanoylphorbol-13-acetate (TPA) and a classical initiator, UV light, can inhibit differentiation. We have now extended these studies by examining the effects of X-rays and TPA administered singly and in combination on differentiation of 3T3 T proadipocytes caused by incubation in medium containing 25% human plasma and on 5-azacytidine induced differentiation of C3H/10T1/2 cells. X-rays alone caused a dose-dependent inhibition of differentiation of 3T3 proadipocytes from 1.0 to 9.0 Gy. Low doses of X-rays (1.0 Gy) also inhibited differentiation of C3H/10T1/2 cells treated with 5-azacytidine but high doses (6.0 Gy) actually caused differentiation in the absence of 5-azacytidine treatment. TPA also inhibited differentiation of both 3T3 T and 5-azacytidine-treated C3H/10T1/2 cells at a dose of 0.1 micrograms/ml. At the lower dose of 0.001 micrograms/ml TPA, 3T3 T differentiation was inhibited only 10%, while 2.5 Gy of X-rays inhibited differentiation approximately 20%. Combined treatment of cells with X-rays and TPA caused more than 60% inhibition of differentiation, i.e., approximately twice the inhibition that would be expected if the effects of these two agents were additive. This synergistic effect suggests that in some systems there may be a closer association between the multistage process of neoplastic transformation and the inhibition of processes involved in cell differentiation than previous experiments, performed with initiators or promoters administered separately, have indicated.
Adipose Tissue↗
Osteochondrosis of the temporomandibular joint presenting as an apparent parotid mass.
A mass in the preauricular area usually indicates the presence of a neoplastic or inflammatory process within the parotid gland. Osteochondrosis is an unusual disease process affecting large joints, particularly the knee. Rarely, the temporomandibular joint (TMJ) may be affected. The disease process involves the synovial lining of the TMJ and is commonly ascribed to a benign neoplastic process or metaplasia, although trauma and inflammation have also been implicated. This process can result in single or multiple loose cartilage bodies (joint mice) within the joint cavity. Symptoms are usually those of a mass in the preauricular area, or those of TMJ dysfunction (pain, dislocation, click, decreased range of motion). Physical findings are limited to presence of a mass in the pre-auricular parotid area with a paucity of other parotid findings. Treatment involves removal of the loose cartilage bodies from the TMJ and possibly the synovial lining, if it appears to be severely damaged.
Biopsy, Needle↗
DNAase I encapsulated in liposomes can induce neoplastic transformation of Syrian hamster embryo cells in culture.
We have used liposomes to deliver DNAase I inside normal Syrian hamster embryo (SHE) cells. We showed the entrance of DNAase I inside the cell by dose-dependent cytotoxicity; and the entrance of DNAase I into the nucleus by the induction of chromosomal aberrations and somatic mutation at the HPRT locus (but not at the Na+/K+ ATPase locus). The induction of neoplastic transformation in cultures treated by DNAase I-in-liposomes was manifested by increased saturation density, colony formation at low seeding density, colony formation in 1% serum and 0.3% agar, and tumorigenicity in 100% of injected animals. The acquisition of anchorage-independent growth became apparent only after 39-57 posttreatment population doublings. Thus damage to DNA alone can initiate the neoplastic transformation process; but for full expression of the neoplastic phenotypes, a long progression time is required for the acquisition of anchorage-independent growth and tumorigenicity.
Animals↗
Requirement of long progression time for the expression of neoplastic phenotypes following direct perturbation to specific region(s) of DNA of Syrian hamster embryo cells.
We have studied the neoplastic transformation of early passage Syrian hamster embryo cells in culture, which were initiated by a specific perturbation of DNA replicated during different periods of S phase. The cells were treated with a "1-h pulse" of 5-bromodeoxyuridine (BrdUrd), followed by a "5-min" irradiation with near ultraviolet (near UV) light. The treated cells were successively subcultured and tested for growth in soft agar and tumorigenicity in newborn hamsters. Neoplastic transformation was induced by treatment with BrdUrd followed by near UV irradiation within the first 4 h of S phase, which was 5 h in duration. Cells treated with BrdUrd plus near UV irradiation during late S phase (the last hour) or during the absence of DNA synthesis (outside of the S phase) were not transformed. In addition, cultures treated in either G1, G2, or S phase with BrdUrd alone or with near UV alone also were not transformed. While morphological transformation, somatic mutation, and DNA and chromosomal aberrations can be observed either immediately or after a few cell divisions, 100 to 200 population doublings after the treatment were required for the emergence of a neoplastic subpopulation, as measured by anchorage independent growth and tumorigenicity. Furthermore, cellular DNA replicated during the first 4 h of S phase is sensitive to the perturbation which leads to neoplastic transformation. These results indicate that the direct perturbation of specific region(s) of cellular DNA can initiate the neoplastic transformation process; but for full expression of the neoplastic phenotypes, a long progression time is required for the acquisition of anchorage-independent growth and tumorigenicity.
Animals↗
[Data on the problem of bilateral lesions of the ovaries caused by a tumor process].
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Female↗
Melanocortin signaling and anorexia in chronic disease states.
Data from both rodent models and humans suggest that intact neuronal melanocortin signaling is essential to prevent obesity, as mutations that decrease the melanocortin signal within the brain induce hyperphagia and excess body fat accumulation. Melanocortins are also involved in the pathogenesis of disorders at the opposite end of the spectrum of energy homeostasis, the anorexia and weight loss associated with inflammatory and neoplastic disease processes. Studies using melanocortin antagonists (SHU9119 or agouti-related peptide) or genetic approaches (melanocortin-4 receptor null mice) suggest that intact melanocortin tone is required for anorexia and weight loss induced by injected lipopolysaccharide (an inflammatory gram-negative bacterial cell wall product) or by implantation of prostate or lung cancer cells. Although the precise mechanism whereby peripheral inflammatory/neoplastic factors activate the melanocortin system remains unknown, the proinflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha) that are produced in the hypothalamus of rodents during both inflammatory and neoplastic disease processes likely play a role. The data presented in this paper summarize findings that implicate neuronal melanocortin signaling in inflammatory anorexia.
Animals↗
Detection of human herpes virus type 8 DNA sequences as a valuable aid in the differential diagnosis of Kaposi's sarcoma.
The occurrence of human herpes virus type 8 (HHV-8) DNA sequences was evaluated by polymerase chain reaction in 36 cases of cutaneous Kaposi's sarcoma (KS) (classic and associated with the acquired immunodeficiency syndrome) and in 88 pathologic entities that can histologically mimic KS, such as reactive and neoplastic vascular processes and lesions featuring focal or extensive spindle cell pattern. A positive reaction was detected in 16 (70%) of 23 samples of classic KS and 10 (77%) of 13 KS cases related to the acquired immunodeficiency syndrome. In particular, 4 (50%) of 8 samples in the patch stage were found to be positive, whereas in the plaque and nodular stages, HHV-8 DNA sequences were observed in 8 (67%) of 12 and 14 (87%) of 16 cases, respectively. KS cases that had yielded previous negative results were found to be positive for HHV-8 on nested polymerase chain reaction, except two cases of classic KS in the patch stage (6% of the total number of KS, 25% of cases in the patch stage). Reactive and neoplastic vascular processes and cutaneous lesions with a spindle cell component were consistently negative. HHV-8 detection by polymerase chain reaction can represent a valuable method for diagnosing KS, particularly in small skin biopsy samples that might show histologic overlap with non-KS lesions. In early patch stage lesions, however, the diagnostic value of the method is hampered by the occurrence of cases in which HHV-8 sequences are still undetectable.
DNA, Viral↗
Relationship between contact inhibition and intranuclear S100C of normal human fibroblasts.
Many lines of evidence indicate that neoplastic transformation of cells occurs by a multistep process. For neoplastic transformation of normal human cells, they must be first immortalized and then be converted into neoplastic cells. It is well known that the immortalization is a critical step for the neoplastic transformation of cells and that the immortal phenotype is recessive. Thus, we investigated proteins downregulated in immortalized cells by two-dimensional gel electrophoresis. As a result, S100C, a Ca(2+)-binding protein, was dramatically downregulated in immortalized human fibroblasts compared with their normal counterparts. When the cells reached confluence, S100C was phosphorylated on threonine 10. Then the phosphorylated S100C moved to and accumulated in the nuclei of normal cells, whereas in immortalized cells it was not phosphorylated and remained in the cytoplasm. Microinjection of the anti-S100C antibody into normal confluent quiescent cells induced DNA synthesis. Furthermore, when exogenous S100C was compelled to localize in the nuclei of HeLa cells, their DNA synthesis was remarkably inhibited with increase in cyclin-dependent kinase inhibitors such as p16(Ink4a) and p21(Waf1). These data indicate the possible involvement of nuclear S100C in the contact inhibition of cell growth.
Amino Acid Sequence↗
[Change in the generation time of neoplastic cells in the process of development of sarcoma 45].
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Animals↗
[Immune complexes in neoplastic diseases and autoimmune processes].
The level and possible pathologic relevance of circulating immune complexes (ICs) were investigated by polyethylene glycol precipitation method in sera of 109 untreated cancer patients (melanoblastoma, lung and breast cancer) and 118 patients with various immune complex diseases (collagenosis, nephropathia, vasculitis and immune hemocytopenia). The highest level of ICs was established in all patients with melanoblastoma. The raised concentration of ICs was registered in patients with malignancies of lung and breast (42 and 44%, respectively). A relationship between increased level of ICs and the rate of its growth in breast cancer patients, on the one hand, and clinical stage of the disease, on the other, was shown. The pathogenic effects of ICs in malignancies and immune complex diseases are compared.
Antigen-Antibody Complex↗