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

By the method of gel-chromatography on sefadex G-200 and electrophoresis in polyacrylamid gel molecular forms of blood and liver catalase were isolated in rats with transplantable Pliss lymphosarcoma. Under study were changes in microheterogeneity of the enzyme, its activity and kinetic parameters in the kinetics of tumor growth. Quantitative and qualitative changes in the parameters under investigation were found already on the second day after tumor transplantation. These changes are enhanced with tumor progression.
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PMID:[Molecular heterogeneity of blood and liver catalase rats with tumors]. 57 62

Cell lines differing in their malignant potential have been derived from the murine BW5147 T-cell lymphosarcoma. To evaluate the involvement of chromosomal aberrations in tumor progression within this model, we have analyzed the karyotypes and the in vitro invasiveness of 13 related nonmetastatic and metastatic variants. Giemsa banding revealed the presence of several marker chromosomes, one of which was of particular importance. Depending on the cell line, four variants of this marker I were found: Marker Ia corresponds to two translocated chromosomes 3, marker Ib is a deleted Ia marker, marker Ic is a Ib translocated to small unidentified chromosome fragment, and marker Id is a further deleted Ib marker. The Ia and Id markers were characteristic for the noninvasive, nonmetastatic lines, whereas the Ib and Ic markers predominated in the invasive, metastatic variants. The results suggest that metastasis-enhancing genes are located between the D and FI band of mouse chromosome 3 and that metastasis-suppressing genes are located between the FI and H band of the same chromosome.
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PMID:Suggestive evidence that genes controlling invasion and metastasis of T-cell lymphomas are located on mouse chromosome 3. 248 51

Morphological parameters for immunoblastic lymphosarcoma (IL) subtypes: plasmocytic IL (PIL) and polymorphocellular IL (PMIL) were determined through a comparative morphological analysis of 56 sections and 64 respective diagnostic biopsies. PIL was found to more frequently affect the gastrointestinal tract. Tumors were found to be selective in damaging the organs, e.g. white pulp was affected in PIL, marginal follicular areas, in PMIL. Clinical and anatomical analyses of the death causes in patients with IL showed that they all had died of neoplastic progression (67.9%), concurrent diseases (23.2%) or complications resulted from the therapy performed (8.9%) upon tumor progression.
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PMID:[Pathologic anatomy of subtypes of immunoblastic lymphosarcoma]. 271 61

The study group included 11 patients with brain metastases of disseminated lymphosarcoma. The most common clinical course was progression of the disease which manifested itself in the advancement of general cerebral symptoms as well as focal ones indicative of hemisphere, subcortex or cerebral trunk involvement. High single intravenous doses of cyclophosphamide and rubomycin and radiotherapy or their combination appeared highly effective in cases of brain specific involvement: complete or partial regression of neurologic symptoms was observed in 7 and 3 patients, respectively. Radiation treatment was followed by COP, COAP or CAMP polychemotherapy to curb extracerebral disease progression. Low median survival of patients with brain metastases (5.1 months) was due to extracerebral tumor progression. However, brain metastases were not immediate death-causing factors.
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PMID:[Clinical picture, diagnosis and treatment of the brain lesions in lymphosarcomas]. 375 66

The effect of aminohexyl-2-hydroxyethylmethacrylate polymer (HEMA-Hex) with sorbed methotrexate (MTX) or 3',5'-dibromoaminopterin (BrAP) on the survival of C3H mice with Gardner lymphosarcoma was studied. The measured bits of HEMA-Hex-MTX or HEMA-Hex-BrAP were implanted into the solid tumor growing 4 to 8 8 days. The doses of sorbed antimetabolites amounting in MTX 4.3 to 13.5 mg.kg-1 and in BrAP 5.1 and 12.6 mg.kg-1 were calculated from the area of the carrier and mean weight of animals. Following implantation i. p. injections of leucovorin or anhydroleucovorin were applied. The treatment of early tumors showed better results than that of advanced ones if evaluated either as prolonged survival or as a number of mice surviving the observation period. The 18-hr. interval between implantation of HEMA-Hex-MTX and anhydroleucovorin injection was optimum if considered both the protection of mice from lethal MTX toxicity and therapeutic effect measured as prolonged survival. Doses of leucovorin or anhydroleucovorin close to MTX doses in term mg.kg-1 resulted in best results. In case leucovorin was applied to tumor-bearing mice pretreated with HEMA-Hex with nonlethal dose of MTX, the survival of mice was shortened. Folic acid did not show this effect. Intra-tumorous implantation of HEMA-Hex-BrAP toxicity even if applied into an advanced tumor. The therapeutic effect of the sorbed BrAP seemed to decrease with tumor progression at a lower rate than of that the sorbed MTX. The application of anhydroleucovorin after implantation of HEMA-Hex-BrAP shortened the survival of tumor-bearing mice.
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PMID:Localized chemotherapy of Gardner's lymphosarcoma of C3H mice using combinations of carrier-sorbed antifolics and detoxicating tetrahydrofolates. 697 53

The paper presents a detailed clinical, hematological, morphological, ultrastructural and immunological characterisation of T-cell lymphosarcoma with prolymphocytic-lymphocytic leukemic transformation (PLLT). In PLLT the proportion of T-cell immunological subvariant of lymphosarcoma came to 15% being detected only in 8 out of 52 examinees. The patients (6 males and 2 females) varied in age from 24 to 76 years (median 49 years) and had the following histological forms of primary tumor tissue: lymphoblastic lymphosarcoma (n = 3), pleiomorphic small cell lymphosarcoma (n = 1), large-cell anaplastic lymphosarcoma (n = 1), prolymphocytic lymphosarcoma. Immunological characteristics of these 8 cases were heterogeneous: in lymphoblastic variant there was immature T-immunological phenotype. In pleomorphic small-cell lymphosarcoma there were also signs of T-cell activation. In large-cell anaplastic lymphosarcoma an immunological phenotype of lymphoid cells from the primary tumor tissue and bone marrow differed in more advanced immunological differentiation of bone marrow tumor cells. In prolymphocytic variant tumor cells had features of T-helpers or T-suppressors. Most of the patients received polychemotherapy according to the schemes for high-grade lymphosarcomas despite PLLT though the latter is not a universal indicator of late tumor progression, more aggressive course of the disease and poor prognosis.
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PMID:[The prolymphocytic-lymphocytic leukemization of T-cell lymphosarcomas]. 748 4

An ascitic lymphosarcoma (LS-A) of Swiss mice that regressed spontaneously on subcutaneous (s.c.) transplantation was investigated for the mechanism of its progressive growth and host mortality on intraperitoneal (i.p.) transplantation. In vitro studies indicated significant inhibition of LS-A proliferation seeded at higher cell density (>10(4)/ml). Culture supernatants of LS-A caused bi-modal growth effects, the early supernatants (24 h) caused stimulation and the late (72 h) supernatants inhibited LS-A proliferation. The 72-h supernatants also suppressed T and B cell response to mitogens in a dose-dependent manner. Pan anti-transforming growth factor-beta antibody abrogated the inhibitory effects of supernatants. The supernatants contained both latent as well as bio-active form of transforming growth factor-beta1 (TGF-beta1) as determined by ELISA. Mice bearing i.p. ascites tumor had elevated serum TGF-beta1, hemoglobulinemia, splenic lymphopenia, impaired response of the T cells to mitogen and reduced expression of transferrin receptor (CD71) on the bone marrow cells. However, mice which rejected s.c. transplants, did not show significant changes in these parameters. Our studies indicated profound influence of site of tumor growth on tumor progression and host immune system mediated by tumor-derived TGF-beta1. It is possible that human tumors which secrete TGF-beta1 may exhibit similar patho-physiological effects in the host depending on the anatomical site of the tumor.
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PMID:Role of tumor-derived transforming growth factor-beta1 (TGF-beta1) in site-dependent tumorigenicity of murine ascitic lymphosarcoma. 1572 58

Experimental animal model of tumor progression based on mice lymphosarcoma (LS) and resistant lymphosarcoma (RLS) has been developed. LS tumor displays high sensitivity to cyclophosphamide, which is widely used in anticancer therapy. RLS tumor was derived from LS by passaging in mice receiving low concentration of cyclophosphamide (20 mg/kg) and display resistance to cyclophosphamide (up to dose 150 mg/kg). The primary cultures of LS and RLS tumors display different expression levels of the genes related to apoptosis and multiple drug-resistant phenotype: in RLS tumor high levels of mdr1b and bcl-2 genes and low level of p53 gene expression were found. A total of 10% of cells in RLS primary culture display multiple drug-resistant phenotype and survive even at high dose of cytostatics. Cultivation of RLS primary culture in the presence of increasing vinblastine concentrations gives RLS(40) cell culture, which exhibits high levels of mdr1a/1b genes expression as compared to RLS and 20-fold increase of resistance to cytostatics. Drug-resistant RLS(40) cells were transplanted into CBA mice and sensitivity of the tumors to anticancer drugs was tested. RLS(40) tumors were resistant to a number of cytostatics used in anticancer therapy (cyclophosphamide, cysplatin, vinblastine, rubomycinum). Thus, RLS(40) tumor can be used as model, which corresponds to tumor status observed in patients after one or several courses of chemotherapy and can be useful for testing conventional therapy alone or together with newly developed gene-targeted therapeutics.
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PMID:Animal model of drug-resistant tumor progression. 1734 38

It is widely accepted that the majority of cancers result from multiple cellular events leading to malignancy after a prolonged period of clinical latency, and that the immune system plays a critical role in the control of cancer progression. Bovine leukemia virus (BLV) is an oncogenic member of the Retroviridae family. Complete genomic sequences of BLV strains isolated from peripheral blood mononuclear cells (PBMC) from cattle have been previously reported. However, a detailed characterization of the complete genome of BLV strains directly isolated from bovine tumors is much needed in order to contribute to the understanding of the mechanisms of leukemogenesis induced by BLV in cattle. In this study, we performed a molecular characterization of BLV complete genomes from bovine B-cell lymphosarcoma isolates. A nucleotide substitution was found in the glucocorticoid response element (GRE) site of the 5' long terminal repeat (5'LTR) of the BLV isolates. All amino acid substitutions in Tax previously found to be related to stimulate high transcriptional activity of 5'LTR were not found in these studies. Amino acid substitutions were found in the nucleocapsid, gp51 and G4 proteins. Premature stop-codons in R3 were observed. Few mutations or amino acid substitutions may be needed to allow BLV provirus to achieve silencing. Substitutions that favor suppression of viral expression in malignant B cells might be a strategy to circumvent effective immune attack.
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PMID:A detailed molecular analysis of complete bovine leukemia virus genomes isolated from B-cell lymphosarcomas. 2350 7

Tumor-associated cell-free DNAs (cfDNAs) are found to play some important roles at different stages of tumor progression; they are involved in the transformation of normal cells and contribute to tumor migration and invasion. DNase I is considered a promising cancer cure, due to its ability to degrade cfDNAs. Previous studies using murine tumor models have proved the high anti-metastatic potential of DNase I. Later circulating cfDNAs, especially tandem repeats associated with short-interspersed nuclear elements (SINEs) and long-interspersed nuclear elements (LINEs), have been found to be the enzyme's main molecular targets. Here, using Lewis lung carcinoma, melanoma B16, and lymphosarcoma RLS40 murine tumor models, we reveal that tumor progression is accompanied by an increase in the level of SINE and LINEs in the pool of circulating cfDNAs. Treatment with DNase I decreased in the number and area of metastases by factor 3-10, and the size of the primary tumor node by factor 1.5-2, which correlated with 5- to 10-fold decreasing SINEs and LINEs. We demonstrated that SINEs and LINEs from cfDNA of tumor-bearing mice are able to penetrate human cells. The results show that SINEs and LINEs could be important players in metastasis, and this allows them to be considered as attractive new targets for anticancer therapy.
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PMID:Targeting Circulating SINEs and LINEs with DNase I Provides Metastases Inhibition in Experimental Tumor Models. 3214 18


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