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)

Chemotherapeutic agents are used in increasingly high dosages to treat patients with refractory cancers. An in vitro clonogenic assay was used to investigate the effects of melphalan on cultures of human neuroblastoma, Ewing's sarcoma, and osteosarcoma cells, as well as on normal bone marrow cells. A 1-hr incubation with 10(-5) M melphalan significantly inhibited tumor colony growth of both fresh neuroblastoma and osteosarcoma cells (p less than 0.01) while Ewing's sarcoma cells and normal bone marrow appeared resistant to melphalan even at a 100-fold higher concentration. Incubation with melphalan for 8 hr did not significantly increase the sensitivity of neuroblastoma and osteosarcoma or the relative resistance of Ewing's sarcoma cells; however, normal bone marrow which had remained resistant to melphalan after 1 hr of incubation, showed significant inhibition of colony growth after an 8-hr incubation with the agent. Repeated exposure to melphalan increased the degree of inhibition of both tumor and normal marrow colonies. Fresh neuroblastoma cells were significantly more sensitive than long-term cultured neuroblastoma cells at all drug doses tested. HPLC studies demonstrated that the loss of melphalan followed first-order kinetics with a half-life of 69 min, and that in addition to the 2 known breakdown products, mono- and dihydroxy-melphalan, several other peaks were present which were not attributable to the tissue culture medium or the buffer solutions.
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PMID:In vitro studies with melphalan and pediatric neoplastic and normal bone marrow cells. 345 79

We have characterized the distribution, expression, and hormonal regulation of gap junctions in primary cultures of rat osteoblast-like cells (ROBs), and three osteosarcoma cell lines, ROS 17/2.8, UMR-106, and SAOS-2, and a continuous osteoblastic cell line, MC3T3-E1. All cell lines we examined were functionally coupled. ROS 17/2.8 were the more strongly coupled, while ROB and MC3T3-E1 were moderately coupled and UMR-106 and SAOS-2 were weakly coupled. Exposure to parathyroid hormone (PTH) for 1 h increased functional coupling in ROB cells in a concentration-dependent manner. Furthermore, PTH(3-34), an analog of PTH with binds to the PTH receptor and thus attenuates PTH-stimulated cAMP accumulation, also attenuated PTH-stimulated functional coupling in ROB. This suggests that PTH increases functional coupling partly through a cAMP-dependent mechanism. A 1 h exposure to PTH did not affect coupling in ROS 17/2.8, UMR-106, MC3T3-E1, or SAOS-2. To examine whether connexin43 (Cx43), a specific gap junction protein, is present in functionally coupled osteoblastic cells, we characterized Cx43 distribution and expression. Indirect immunofluorescence with antibodies to Cx43 revealed that ROS 17/2.8, ROB, and to a lesser extent MC3T3-E1 and UMR-106, expressed Cx43 immunoreactivity. SAOS-2 showed little if any Cx43 immunoreactivity. Cx43 mRNA and Cx43 protein were detected by Northern blot analysis and immunoblot analysis, respectively, in all cell lines examined, including SAOS-2. Our findings suggest that acute exposure to PTH regulates gap junction coupling, in a cell-line dependent manner, in osteoblastic cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cell-to-cell communication in osteoblastic networks: cell line-dependent hormonal regulation of gap junction function. 757 12

The cytotoxic activity of the imidazoacridinone C1311 was assessed on two ovarian cancer cell lines (A2780, OAW42) and one osteogenic sarcoma cell line (U2-OS) and their sublines (A2780Cp8, OAW42-MER and U2-OS-R) with experimentally induced resistance to cisplatin. A 1-h exposure to C1311 significantly inhibited the growth of all cell lines, with IC50 values ranging from 0.50 +/-0.11 to 4.10+/-0.36 microM. No or only partial cross-resistance was found between C1311 and cisplatin in the different cell lines. Treatment with equitoxic (IC50) C1311 concentrations consistently induced accumulation of cells in the G2M phase. The cyclin B1-associated p34(cdc2) kinase activity in cells arrested in G2M was superimposable to that of control cells in the OAW42-MER and U2-OS cell lines, whereas a reduction of cdc2 catalytic activity was observed in OAW42 and U2-OS-R cells. Exposure to C1311 (IC50) induced apoptosis in the U2-OS and U2-OS-R cell lines, whereas in the OAW42 and OAW42-MER cell lines there was a negligible percentage of apoptotic cells. In U2-OS, U2-OS-R and OAW42 cells, C1311 induced an increase in p53 expression and an increase in p21waf1 protein, whereas p53 failed to transactivate p21waf1 in OAW42-MER cells. An almost complete abrogation of bcl-2 was observed in U2-OS-R cells in correspondence with the peak of apoptosis induction. Our results indicate that C1311 is active against human ovarian cancer and osteogenic sarcoma cells and is not cross-resistant with CDDP. Moreover, C1311 blocks cells in the G2M phase and induces apoptosis in a small percentage of osteogenic sarcoma cells.
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PMID:Cell growth inhibition, G2M cell cycle arrest and apoptosis induced by the imidazoacridinone C1311 in human tumour cell lines. 1157 53

A seven-and-a-half-year-old dog presented with anorexia, lethargy and haematurla. A 1.8 kg abdominal mass was excised and determined to be a primary renal osteosarcoma. Haematuria was observed five months after surgery and the tumour was radiographically determined to have recurred locally. The dog was euthanased 12 days later due to refractory pain and anorexia. Although osteosarcomas are expected to develop distant metastases, this dog was euthanased due to clinical evidence of local tumour recurrence. Haematuria was an indication both of initial tumour development and later recurrence.
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PMID:Renal osteosarcoma in a dog. 1560 Feb 74

We conducted a case-control study to investigate the role of common SNPs in ERCC2 (rs13181 and rs1799793) and ERCC3 (rs4150441 and rs4150506) in the development of osteosarcoma. A 1:2 matched case-control study was conducted. Between January 2012 and December 2013, 141 patients with pathologically diagnosed osteosarcoma and 282 controls were recruited in our study. Genotyping of ERCC2 rs13181 and rs1799793 as well as ERCC3 rs4150441 and rs4150506 were performed using polymerase chain reaction coupled with restriction fragment length polymorphism. The genotype distributions of ERCC2 rs13181 and rs1799793 as well as ERCC3 rs4150441 and rs4150506 showed no significant difference between patients with osteosarcoma and controls, as analyzed by c2 tests. Multivariate logistic regression analysis did not reveal significant associations between ERCC2 rs13181/rs1799793 or ERCC3 rs4150441/ rs4150506 gene polymorphisms and the development of osteosarcoma in codominant, dominant, and recessive models. In conclusion, we did not find any association between ERCC2 or ERCC3 gene polymorphisms and the development of osteosarcoma. Future studies with larger sample sizes may contribute in elucidating the impact of ERCC2 and ERCC3 gene polymorphisms on osteosarcoma risks.
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PMID:Role of ERCC2 and ERCC3 gene polymorphisms in the development of osteosarcoma. 2705 Oct 24