Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary resection for metastatic disease in 341 patients resulted in a cumulative survival rate of 36.6% at 5 years and 26.6% at 10 years with an operative mortality of 0.9%. 5-year survival rate was 44.3% in colorectal carcinoma (n = 85), 36.2% in cervical cancer of uterus (n = 35), 40.6% in renal cell carcinoma (n = 32), 50.3% in breast cancer (n = 23), 50.0% in testicular cancer (n = 16), 17.9% in osteosarcoma (n = 33), 34.1% in soft part sarcoma (n = 38). The patients with resected metastatic pulmonary lesions from colorectal and renal cancer showed a good 5-year survival, and then the survival decreased gradually. On the other hand, the survival for testicular and breast cancer, osteosarcoma and soft part sarcoma decreased rapidly in the first 2 to 3 years, but a plateau was reached. Each primary malignancy should be analyzed individually because of the differences of their biologic behaviors. Significant factors influencing survival were (1) patients selection for pulmonary resection, (2) the biologic growth rate of each primary malignancies, and (3) effectiveness of chemotherapy for primary malignancies. Presumably, a good 5-year survival rate after thoracotomy would be a reflection of a length bias, caused by the biologic behavior of the metastatic pulmonary disease. The true benefit for the surgical approaches to metastatic neoplasm of the lung are still controversial.
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PMID:[Surgical resection of metastatic neoplasms of the lung]. 234 92

We report 28 cases of malignant disease in pregnant women. They were divided into 14 cases of intrapelvic tumors and 14 of extrapelvic tumors. The intrapelvic tumors were cervix cancer in nine and ovarian cancer in five, while the extrapelvic tumors were brain tumors in three, maxillary cancer in one, tongue cancer in one, pharyngeal cancer in one, breast cancer in one, gastric cancer in two, osteosarcoma in one Hodgkin's lymphoma in one, and leukemias in three. The prognoses of the patients with intrapelvic tumors were relatively good. But those of extrapelvic diseases were poor.
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PMID:[Malignant neoplasms in pregnancy--report of 28 cases treated in our hospital]. 377 71

Certain Lilium plants contain (25S)-spirost-5-ene-3 beta,27-diol glycosides embracing 3-hydroxy-3-methylglutaric acid at the C-27 hydroxy position. One of their derivatives, methyl ester of (25R)-27-O-[(S)-3-hydroxy-3-methylglutaryl]-spirost-5-ene-3 beta,27-diol 3-O-(O-alpha-L-rhamnopyranosyl-(1-->2)-O-[beta-D-glucopyranosyl-(1-->4)] - beta-D-glucopyranoside) was found to inhibit 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated 32P-incorporation into the phospholipids of human cervical cancer (HeLa) cells and also to inhibit the proliferation of various kinds of human malignant tumor cells, pancreatic cancer (PANC-1), osteosarcoma (OST), human gastric cancer (HGC-27), pheochromocytoma (PC-12) and HeLa cells, in vitro.
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PMID:Inhibitory effects of steroidal saponins on 12-O-tetradecanoylphorbol-13-acetate (TPA)-enhanced 32P-incorporation into phospholipids of HeLa cells and proliferation of human malignant tumor cells. 755 Jan 6

The expression of Bfl-1 gene, a novel Bcl-2 related gene, was determined by Northern blot analysis using a radiolabeled cDNA specific for Bfl-1 gene in 82 surgically resected tissue specimens of 28 gastric cancers, 15 colon cancers, nine breast cancers, eight bone and soft tissue sarcomas, five ovarian cancers, nine colon adenomas and eight gastric adenomas. A high rate of expression was observed in gastric and colon cancer, at 86 and 93%, respectively. In breast cancer, bone and soft tissue sarcoma and ovarian cancer, the expression rate was 33, 25 and 40%, respectively. In stomach cancer, the expression rate of Bfl-1 gene in metastatic lymph nodes was 82%, which was higher than 50% of the primary sites (p < 0.02). The intensity of RNA bands of the gastric cancer specimens was compared according to the stage, demonstrating that there was no difference in the expression levels of Bfl-1 gene between the stages in both primary sites and metastatic lymph nodes. Bfl-1 gene was expressed in three (33%) out of nine adenomas of the colon, while it was not detected in all eight gastric adenomas, We also examined the RNA expression of Bfl-1 gene in 22 human cancer cell lines consisting of five stomach cancer, four squamous cell carcinoma, three lung cancer, three cervical cancer, two colon cancer, two brain cancer, two leukemia and one osteosarcoma cell lines. Bfl-1 gene band was detected in one (5%) cervical cancer cell line, SiHa. The results of cancer tissue specimens indicate that Bfl-1 gene may play an important role in carcinogenesis of human cancers and may be involved in a relatively early phase of the adenoma-carcinoma sequence in colon cancer development. However, the mechanism responsible for the very low rate of expression in established cell lines is not clearly understood and further investigation is necessary to clarify the mechanism involved.
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PMID:Expression of a novel Bcl-2 related gene, Bfl-1, in various human cancers and cancer cell lines. 949 79

An important role in the immune defense against deoxyribonucleic acid virus induced tumors is mediated by T-cells, as is evident from aetiological, animal model, and clinical data. In this review the most recent observations in this field are described for three prominent members of this family of viruses, namely human papillomavirus associated with human cervical cancer, human adenovirus associated with lung infections in humans and tumors in rodents, and simian virus 40 associated with rodent tumors and human mesothelioma, osteosarcoma and ependymoma.
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PMID:Cellular immunity and immunotherapy against deoxyribonucleic acid virus-induced tumors. 968 11

E7 is the main transforming protein of human papilloma virus type 16 (HPV16) which is implicated in the formation of cervical cancer. The transforming activity of E7 has been attributed to its interaction with the retinoblastoma (Rb) tumour suppressor. However, Rb binding is not sufficient for transformation by E7. Mutations within a zinc finger domain, which is dispensable for Rb binding, also abolish E7 transformation functions. Here we show that HPV16 E7 associates with histone deacetylase in vitro and in vivo, via its zinc finger domain. Using a genetic screen, we identify Mi2beta, a component of the recently identified NURD histone deacetylase complex, as a protein that binds directly to the E7 zinc finger. A zinc finger point mutant which is unable to bind Mi2beta and histone deacetylase but is still able to bind Rb fails to overcome cell cycle arrest in osteosarcoma cells. Our results suggest that the binding to a histone deacetylase complex is an important parameter for the growthpromoting activity of the human papilloma virus E7 protein. This provides the first indication that viral oncoproteins control cell proliferation by targeting deacetylation pathways.
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PMID:The E7 oncoprotein associates with Mi2 and histone deacetylase activity to promote cell growth. 1022 59

The 50% growth inhibition toxicity (IC50 at 72 h) of 16 synthetic and 2 phytochemical natural analogs of furanonaphthoquinones (naphtho[2,3-b]furan-4,9-dione; FNQ) and 2 analogs of isofuranonaphthoquinones was assayed in vitro in respect to established human cervical cancer and lung adenocarcinoma cells in comparison with human uterine endocervical, tracheal and bronchiolar epithelial cells and fibroblasts. Prostate, cholangio, colon, laryngeal, and tongue carcinoma cell lines and two osteosarcoma cell lines were also used for the assay. The IC50 ratio of normal cells to cancer cells was estimated in order to represent preferential antitumor activity. Two analogs, 2-methylnaphtho[2,3-b]furan-4, 9-dione (FNQ3) and 2-methyl-5(or 8)-hydroxynaphtho[2,3-b]furan-4, 9-dione (FNQ13) showed 10.4 to 14.1 IC50 ratios for all carcinoma cells used, indicating a wide spectrum. Among different carcinomas, there was no difference or variety in the IC50 ratio of a single analog. A moderate IC50 ratio (3.1-4.7) was also found in nine analogs, but seven others were equally cytotoxic (less than 2.6) to both cancer and normal cells. Two isofuranonaphthoquinone derivatives were ineffective, but a thieno derivative was equally cytotoxic to all cells tested. On the basis of the IC50 ratio data and the structure of the furanonaphthoquinones, the following structural activity (selectivity) relationship can be postulated: (i) the presence of an alkyl group at position 2 enhances the IC50 ratio, particularly the methyl group; (ii) a hydroxyl group at position 5 or 8 enhances the IC50 ratio; and (iii) methylation of the phenolic hydroxyl group leads to a decrease of potency. These results indicate that FNQ3, 13, and some other analogs are more preferentially cytotoxic to human tumor cells than to normal cells, unlike mitomycin-C, adriamycin, carboplatin, and methotrexate which are cytotoxic to the both. In nude mouse xenograft tests, FNQ3 demonstrated a significant antitumor activity with T/C% values of 16. 6 to 41.6 against several human carcinoma and osteosarcoma cells.
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PMID:Furanonaphthoquinone analogs possessing preferential antitumor activity compared to normal cells. 1057 65

The retinoblastoma protein (pRb), the gene product of the first reported tumour suppressor gene, is functionally inactivated by the E7 protein of high-risk human papillomavirus (HPV) found in most human cervical cancers. We have, in this study, constructed an adenoviral vector expressing wild-type pRb (Ad5-Rb) and used the constructed Ad5-Rb to transfect the osteosarcoma cell line Saos-2, and three cervical cancer cell lines HeLa, SiHa and C-33A. Our results showed that pRb caused G1 arrest in Saos-2 cells after transfection with Ad5-Rb. The number of colonies formed by the Ad5-Rb-transfected Saos-2 cells in soft agar was also found to be significantly lower (P<0.05) than those transfected with the adenoviral control expressing Escherichia coli beta-galactosidase (Ad5-LacZ). The transfection of Ad5-Rb caused an increase in the population of SiHa and C-33A cells in the G1 phase from 53.0 and 52.9% to 72.4 and 64.3%, respectively, but not in the HeLa cells. However, Ad5-Rb did not show any inhibitory effect on the growth of SiHa, HeLa and C-33A cells, and inhibition of colony formation in soft agar was not observed either. In contrast, flow cytometric analysis showed that Ad5-p53, a p53-expressing adenovirus, induced apoptosis, i.e. the appearance of sub-G1 peak, in all three tested cervical cancer cell lines. Nevertheless, the Ad5-p53-induced apoptosis was partially inhibited when Ad5-Rb was added simultaneously. These findings suggested that pRb may not be a good candidate for cervical cancer gene therapy. Our data also showed that the use of full-length pRb in combination with TP53 might not be a suitable strategy for cancer gene therapy.
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PMID:pRb-expressing adenovirus Ad5-Rb attenuates the p53-induced apoptosis in cervical cancer cell lines. 1172 Aug 46

Human papillomavirus type 16 (HPV-16) is the major risk factor for development of cervical cancer. The major oncoprotein E7 enhances cell growth control. However, E7 has in some reports been shown to induce apoptosis suggesting that there is a delicate balance between cell proliferation and induction of cell death. We have used the osteosarcoma cell line U2OS cells provided with E7 and the cdk2 inhibitor p21 (cip1/waf1) under inducible control, as a model system for the analysis of E7-mediated apoptosis. Our data shows that simultaneous expression of E7 and p21 proteins induces cell death, possibly because of conflicting growth control. Interestingly, E7/p21-induced cell death is associated with the activation of a newly identified mediator of apoptosis, namely cathepsin B. Activation of the cellular caspases is undetectable in cells undergoing E7/p21-induced apoptosis. To our knowledge, this is the first time a role for cathepsin B is reported in HPV-induced apoptotic signalling.
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PMID:Simultaneous human papilloma virus type 16 E7 and cdk inhibitor p21 expression induces apoptosis and cathepsin B activation. 1501 52

The fragility of the evidence for SV40 association with human cancer is seen in studies of NHL. A publication in 1999 stated that SV40 is rarely present in NHL. In 2002, two laboratories reported SV40 sequences in 42% to 43% of cases of NHL . One of these laboratories also detected SV40 sequences in small proportions of pediatric tumors (e.g., Wilm's tumor, hepatoblastoma, rhabdomyosarcoma, medulloblastoma, osteosarcoma, and retinoblastoma) and adult carcinomas (e.g., lung, colon, breast, and prostate) These positive results were not confirmed in subsequent studies published in 2003. Capello et al and Mackenzie et al failed to detect SV40 sequences in NHL tissues. Sanjose et al examined sera from patients with NHL and from controls for antibodies reactive to SV40 VLPs, and they detected no significant differences between the two groups. The association of SV40 with NHL is in doubt. An etiologic link between a virus and a cancer becomes plausible when evidence from different lines of enquiry (e.g., epidemiology, pathogenesis, and molecular mechanisms) is mutually reinforcing and together provides a coherent picture that can connect the biology the virus to the characteristics of the disease. The associations of human papillomaviruses with cervical cancer and hepatitis B and C viruses with hepatocellular carcinoma are examples in which the etiologic link is clear. With SV40 and mesothelioma, the data on viral sequences in tumors is inconsistent and disputed, and serologic evidence does not support any association. The epidemiologic data do not show that documented exposures tt SV40 increase the risk of mesothelioma. It seems improbable that a single virus (which cannot be conclusively demonstrated to be present in the community) contributes to the development of such a wide variety of tumors, spanning all age groups and histologic types. The weaknesses in the evidence linking SV40 with mesothelioma are summarized in Box 11 It seems unlikely that infection with SV40 contributes to the development of human mesothelioma or any other human cancer.
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PMID:Causality of mesothelioma: SV40 question. 1555 56


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