Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0178874 (tumor progression)
 40,807 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A boy with characteristic facial features, pulmonary valvular stenosis, ectodermal abnormalities, growth failure, and mental retardation was admitted for intestinal occlusion at 20 months of age. Clinical findings were consistent with a diagnosis of cardio-facio-cutaneous syndrome (CFC-s), and a huge abdominal mass was evident on computed tomography scan. A biopsy was performed, and embryonal rhabdomyosarcoma was diagnosed. Molecular analysis was performed by reverse transcription (RT) polymerase chain reaction (PCR) on tumor RNA to seek the chimerical transcript of the most common soft tissue sarcoma translocations and analyze neurofibromatosis 1 (NF1) gene expression. Translocations involving 1;13, 2;13, and 11;22 were not found, and the specific transcripts of the NF1 gene were present. Chemotherapy was implemented, but the child died 7 months later of tumor progression. Few patients with CFC-s have been described, and their follow-up is not well known. The association of CFC-s with rhabdomyosarcoma has not been reported previously, but other neoplasms have been reported in patients with Noonan syndrome, a condition similar to CFC-s. More observations are needed, but this and other reports suggest there could be a higher risk of malignancy in patients with syndromes in the Noonan phenotype category.
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PMID:Rhabdomyosarcoma in a patient with cardio-facio-cutaneous syndrome. 1113 27

The relationship between nitric oxide (NO) synthase II (NOS II) expression and the metastatic ability of tumor cells is inconclusive. We determined the role of host NOS II expression in the growth and metastasis of the B16-BL6 murine melanoma and M5076 murine ovarian sarcoma cell lines. The cells were either s.c. or i.v. injected into syngeneic wild-type (NOS H+/+) and NOS II-null (NOS H-/-) C57BL/6 mice. Both cell lines produced slightly larger s.c. tumors in NOS H-/- mice than in NOS II+/+ mice. However, B16- BL6 cells produced more and larger experimental lung metastases in NOS II+/+ mice than in NOS II-/- mice, whereas M5076 cells produced fewer and smaller experimental lung metastases in NOS II+/+ mice than in NOS II-/- mice. After activation with IFN-gamma and lipopolysaccharide, macrophages isolated from NOS II+/+ C57BL/6 mice produced NO-dependent cytotoxicity in sarcoma cells, whereas macrophages from NOS II-/- C57BL/6 mice did not. In contrast, activated macrophages produced little to no NO-mediated cytotoxicity in melanoma cells. Immunostaining analyses indicated that NOS II expression was apparent in the metastases growing in NOS H+/+ mice and correlated with increased cell proliferation in B16-BL6 lung metastases but with decreased cell proliferation in M5076 liver metastases. Our data suggest that disruption of host NOS II expression enhanced the growth and metastasis of NO-sensitive tumor cells but suppressed the metastasis of NO-resistant tumor cells, proposing that host-derived NO may differentially modulate tumor progression.
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PMID:Influence of nitric oxide synthase II gene disruption on tumor growth and metastasis. 1082 24

Malignant soft tissue tumors still represent a source of uncertainty and controversy concerning histogenetic origin and histological behavior. Considering this, chemically induced sarcomas furnish an attractive model for the elucidation of cellular alterations during tumorigenesis. This approach allows us to closely follow cyto- and histological changes within coherent stages of tumor development. The specimen under scrutiny comprised 35 rat tissue samples from day 10 up to day 200 after benzo[a]pyrene injection. Additionally, for comparison and validation two human malignant fibrous histiocytomas (MFH) were investigated. The essential biological significance of protein-carbohydrate interactions warranted the histochemical application of synthetic tools (neo-glycoproteins-NGP) and lectins in order to reveal phenotypical dynamics in this aspect throughout the process of tumor development. Namely, 6 plant lectins (carbohydrate-binding proteins with defined saccharide specificity), 7 custom-made synthetic NGP (as the corresponding ligands visualizing endogenous lectins) and additionally three antibodies were employed. Characteristic cell populations were histochemically demonstrated in four stages of tumor development: exudation (n = 5), mesenchymal proliferation (n = 7), atypical granulation tissue (n = 7) and sarcoma (n = 16). Changes of glycohistochemical binding patterns were in close phenotypic relation to cellular activity, differentiation, local distribution as well as malignant transformation and tumor progression. At present, the new glycobiological features of the malignant phenotype substantiate the assumption that not only glycosylation but also the receptor display is altered upon carcinogenesis. In conclusion, this chronological longitudinal study takes advantage of the combination of a coherent model of tumorigenesis with innovative histochemical tools whose ligands are supposed to act as mediators of cell-cell- and cell-matrix interactions. It clearly demonstrates the suitability of the glycohistochemical method for comparative approaches. The systematic analysis of glycohistochemical determinants will improve our understanding of the early tumor biological processes with potential implications for therapeutic interventions.
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PMID:Glycohistochemical monitoring of chemically induced sarcomas at different stages of tumorigenesis. 1094 65

We have recently described a novel cyclic peptide inhibitor CTTHWGFTLC (CTT) for matrix metalloproteinases (MMP)-2 and MMP-9, also called type IV collagenases or gelatinases (E. Koivunen et al., NAT: BIOTECHNOL:, 17: 768-774, 1999). As indicated by its amino acid composition, CTT is hydrophobic, and its partitioning into phospholipid films could be verified by the monolayer technique. Augmented fluorescence emission anisotropy (from 0.064 to 0.349) and reduced collisional quenching by I(-) of the Trp residue in CTT was evident in the presence of unilamellar phosphatidylcholine/phosphatidylethanolamine liposomes, revealing the association of CTT with the lipid bilayers. Gelatinases are potential targets of therapeutic intervention in cancer, and inhibitors of these enzymes can prevent tumor progression in animal models. CTT enhanced 3- to 4-fold the cellular uptake of liposome-encapsulated water-soluble fluorescent marker, rhodamine B by gelatinase-expressing cells. Gelatinase targeting seems to be essential, as modified peptides that were less potent gelatinase inhibitors were also less efficient in promoting the cellular uptake of liposomes. Augmented killing ( approximately 4-fold) of U937 leukemia and HT1080 sarcoma cells was obtained by the CTT-enhanced delivery of Adriamycin-containing liposomes, compared with control liposomes administered without the peptide. These results suggest a novel type of utility for small gelatinase inhibitors in targeted cancer therapy.
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PMID:Binding of novel peptide inhibitors of type IV collagenases to phospholipid membranes and use in liposome targeting to tumor cells in vitro. 1135 15

The study was concerned with growth of sarcoma M-1 and basic morphological characteristics of proliferative activity of cells of this strain as well as apoptosis of cells at different stages of tumor progression in rats before and after a single gamma irradiation at 30 Gy. At the parenchymal periphery which determines tumor growth, the PCNA index of proliferating cells was 76.5%; spontaneous cell death--0.28%. During post-irradiation period, the sarcoma PCNA index fell to 62.3% while the apoptotic index rose five-fold. These findings support the concept of radiation-induced apoptosis being a major pathogenetic factor responsible for effectiveness of radiotherapy of tumors. Indirect evidence on PCNA immunostaining suggested that synthesis of this cyclin is sensitive to the level of oxygen input in the cell, yet it offers sufficient resistance to gamma-radiation.
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PMID:[Growth kinetics and functional morphology of M-1 sarcoma in rats before and after gamma-irradiation]. 1154 33

The aims of this study were to compare genetic aberrations in primary soft-tissue sarcomas and their local recurrences and to evaluate the genetic changes occurring during tumor progression. A primary soft-tissue sarcoma and its subsequent local recurrence were analyzed in 20 tumor pairs by comparative genomic hybridization. The samples were obtained before application of radio- or chemotherapy. Copy number aberrations were detected in 50% of the primary tumors and in 70% of the local recurrences. In primary tumors, the mean number of changes was 2.45 (range, 0 to 11) whereas in local recurrences, it was 5.05 (range, 0 to 17). The mean increase of changes from primary tumor to local recurrence was 2.6 per tumor pair (P =.02). Gains predominated over losses in both primary tumors and their local recurrences. The number of high-level amplifications was twofold in local recurrences. The most frequent gain affected 5p14-p15.1 (10% of primary tumors, 25% of local recurrences) and the most frequent loss, 9p (9p21-pter in 5% of primary tumors; 9p22-pter in 30% of local recurrences). In conclusion, our results show an increase in the number of genetic changes in local recurrences, due to tumor progression. Loss at 9p and gains at 5p and 20q were more frequent in local recurrences, and high-level amplification of 18p11.3 was not detected in any of the primary tumors. Although all these alterations were not specific to local recurrences, they may represent changes important during tumor progression.
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PMID:Primary soft tissue sarcoma and its local recurrence: genetic changes studied by comparative genomic hybridization. 1159 67

The effectiveness of combined chemoimmunotherapy with ifosfamide derivative CBM-4A and granulocyte-macrophage colony-stimulating factor (GM-CSF) was investigated in two experimental tumor models, 3MC-induced MHC class I+ sarcoma Mc12 and HPV16 E6/E7 oncogene-induced MHC class I- carcinoma MK16, transplanted in syngeneic mice. Treatment of Mc12 and MK16 tumor-bearing mice with GM-CSF or CBM-4A alone produced moderate anti-tumor effects. However, when the tumor-bearing mice were first treated i.p. with a single dose of CBM-4A (150 mg/kg) and three days later peritumorally with five daily doses of GM-CSF (100 ng/day), substantially stronger tumor-inhibitory effects were observed. The results indicate that in both, MHC class I+ and MHC class I- tumors, the combined chemoimmunotherapy can inhibit tumor progression more effectively than GM-CSF therapy or chemotherapy alone, and they suggest that GM-CSF should be considered as adjuvant to chemotherapy in clinical trials with HPV 16-associated neoplasms.
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PMID:Chemoimmunotherapy of cancer: potentiated effectiveness of granulocyte-macrophage colony-stimulating factor and ifosfamide derivative CBM-4A. 1160 69

The study comprised newly synthesized sesquiterpenoid analogs of taxol. The synthesis of the compounds was performed at the Institute of Organic Chemistry, Polish Academy of Sciences. Cytotoxicity of the compound was assessed using formazan method. In in vitro studies the cell cultures were infected with HSV-1MC. The tested compounds were added in different concentrations to the cell culture after viral infection. Titer of the virus was expressed in TCID50/ml at particular stages of the experiments. In in vivo experiments NMRI mice were infected intramuscularly with a Moloney murine sarcoma virus (Mo-MSV). Tested compounds were administered to the mice intravenously on the day of virus inoculation. In Mo-MSV-infected mice dynamics of tumor progression and regression was assessed, as well as a mean time interval of tumor disappearance. Among the compounds tested: isovellerol-13-N-benzoyl-(2'R,3'S)-3'-phenylisoserinate, 5-deoxy-lactarolid B 8-[N-benzoyl-(2'R,3'S)-3'-phenylisoserinate] and isolactarorufin 8-epi-[N-benzoyl-(2'R,3'S)-3'-phenylisoserinate] showed significant antiviral activity in in vitro experiments. In in vivo experiments only lactarorufin A 8-[N-benzoyl-(2'R,3'S)-3'-phenylisoserinate] significantly inhibited the development of tumors and shortened the time of their total regression in the course of Mo-MSV infection.
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PMID:[Influence of newly synthesized sesquiterpenes--analogs of taxol on multiplication of herpes simplex virus (HSV-1MC) and retrovirus (Mo-MSV)]. 1178 86

Malignant fibrous histiocytoma (MFH) has come to be regarded as the most common malignant neoplasm of the mesenchymal soft tissues. It designates a spectrum of tumors which share morphologic features that allow their inclusion in a distinct clinicopathologic setting, although being not uniform in their histogenesis and pathogenesis. Clinicopathologic variants include the following: the storiform-pleomorphic form of MFH, the myxoid type of MFH, the giant cell type of MFH and the inflammatory type. The latter group, the angiomatoid variant, has been reclassified within the fibrohistiocytic tumors of low malignant potential. Tissue culture, ultrastructural and immunohistochemical studies have both endorsed or refuted the validity of the concept. As a whole, these morphologic studies which attempted to characterize MFH were not able to delineate specific markers or to describe the phenotype of this sarcoma of supposed fibrohistiocytic lineage. There is growing evidence that MFH is a second component in another sarcoma and represents a morphologic modulation resulting from tumor progression. Recent cytogenetic and molecular genetic investigations are consistent with that hypothesis: a comparative analysis between the most frequent genomic imbalances observed in series of MFH and leiomyosarcomas (LMS) demonstrated that both tumors had similar recurrent imbalances. Immunohistochemical and molecular biologic investigations have shown similar targets of chromosome deletions in both tumors. A new classification of soft tissue sarcoma based on molecular parameters is nevertheless premature. The morphologic characterization of MFH and its sub-types provides the clinician with unique information in the management of these tumors, by identifying a spectrum of tumors with well-recognized clinical profiles.
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PMID:[Does malignant fibrous histiocytoma exist?]. 1193 97

The development of an effective antitumor immune response to control tumor growth is influenced by the tumor cell itself and/or by the tumor microenvironment. Tumor invasion and tumor cell spreading require a finely tuned regulation of the formation and loosening of adhesive contacts of tumor cells with the extracellular matrix (ECM). In our laboratory, a rat tumor cell line derived from a spontaneous rat sarcoma revealed, by flow cytometry, a high frequency of intercellular adhesion molecule-1 (ICAM-1, 70.1 +/- 8.7%) and urokinase-type plaminogen activator receptor (uPAR, 51.2 +/- 5.2%) positive cells, while a weak expression of MHC class II (IA, 2.2 +/- 0.2% and IE, 17.4 +/- 3.7%) and B7 (12.1 +/- 2.2%) antigens was detected. In our tumor experimental model, after implantation of tumor cells, visible tumor masses were present at days 5-7 with a relatively fast tumor growth until day 15 (progressive phase) followed by a suppression of the tumor growth (regressive phase). Here we present data that correlates a significant decrease in the frequency of ICAM-1 and uPAR expressing tumor cells with the appearance of tumor cells in sites distant from that of the primary tumor. In addition we describe the development of a cellular immune response which controls the tumor progression and is associated with an increase in the expression of major histocompatibility complex (MHC) class II IA antigen during tumor development. The histological examination at tumor progressive and regressive time points revealed the relevant presence of polymorphonuclear neutrophils (PMNs) evidencing colliquative necrosis in tumor growth areas. Taken together, these results support the idea that the balance between adhesive interactions, proteolytic activity and tumorigenicity may lead to a tumor invasive phenotype.
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PMID:Decreased expression of intercellular adhesion molecule-1 (ICAM-1) and urokinase-type plasminogen activator receptor (uPAR) is associated with tumor cell spreading in vivo. 1219 72


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