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Query: UMLS:C0279530 (bone cancer)
 1,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bone cancer can be induced by radionuclides that localize in the skeleton. Histologically, these experimentally induced tumors resemble those found naturally in man; they range from densely ossified osteogenic sarcomas to osteolytic tumors with giant cells and only a small osteoid component. Fibrosarcomas and hemangiosarcomas also can occur in some species. It has not been possible to determine the dose in terms of absorbed energy necessary for bone-tumor induction because radionuclides are not deposited uniformly, and they diminish in amount with time. Also, the precise time when irreversible noeplastic change occurs is not known. With X-rays, however, 500 rads delivered to the endosteal surface of a mouse femur has been shown to cause osteogenic sarcoma. Bone tumors can be induced in mice by viruses. FBJ osteosarcoma virus and RFB osteoma virus were obtained from spontaneous tumors; FBR osteosarcoma virus came from a radiation-induced tumor. All three are RNA viruses with C-type particle morphology, and they are propagated by injecting cell-free extracts of virus-induced tumor. All three are RNA viruses with C-type particle morphology, and they are propagated by injecting cell-free extracts of virus-induced tumor into newborn mice. Interaction studies with bone-seeking radionuclides and these viruses have led to the hypothesis that radiation produces cancer by inactivating a viral inhibitor. There is also evidence of a bone tumor virus in the human disease. The injection of cell-free extracts of human bone cancer into newborn Syrian hamsters has induced a variety of mesenchymal tumors at a rate significantly higher than in the control hamsters. Sixty tumors of this type, including 20 osteosarcomas, 11 fibrosarcomas, and 9 osteomas, have been diagnosed so far in experimental animals; in control hamsters there has been only one, a fibrosarcoma. Immunofluorescence assays and cytotoxicity studies indicated that these hamster tumors carried a human antigen.
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PMID:Pathogenesis of radiation and virus-induced bone tumors. 18 72

In dogs, osteosarcoma is markedly more frequent in giant breeds than in small ones. Ewing's tumor rarely occurs in species other than man. In children, both osteosarcoma dne Ewing's tumor appear to be related to the rate of bone growth. Nonradiogenic osteosarcoma occurs excessively in persons with the heritable form of retinoblastoma, and in certain malformation syndromes, some of which are known to be genetically induced. Osteosarcoma may also be of the heritable type when it is multicentric or aggregates in families. The neoplasm may occur excessively in certain families with specific cancers not involving bone. By contrast, the only evidence of a genetic influence on Ewing's tumor is its near-absence among blacks in the United States and in Africa. The only exogenous agent known to induce osteosarcoma (but not Ewing's tumor) in man is ionizing radiation in substantial doses. There is no epidemiologic evidence for the virus etiology of bone cancer in man. Despite the epidemiologic differences between osteosarcoma and Ewing's tumor, both histologic types occasionally occur in different portions of the same neoplasm.
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PMID:Etiology of childhood bone cancer: epidemiologic observations. 107 Jul 24

A limited long-term experiment has been completed in which the chronic toxicity resulting from a single intravenous injection of 31.4 kBq of a poly-disperse 239Pu colloid sol per kg of body weight was tested in Beagle dogs. The Pu deposited mostly in the phagocytic cells of liver, spleen and to a lesser degree in lung and bone marrow. Slow solubilization of the Pu particles by endogenous ligands caused translocation of the nuclide and redeposition mostly as monomeric Pu in the skeleton and in liver hepatocytes. Thus, the deposit behaved as expected from a pulmonary or wound contamination in humans with a moderately soluble depot of Pu such as Class W hot particles. Therefore, this type of deposit provided the basis for a practical model to study the ensuing radiation effects under various experimental conditions. The dogs were divided into three groups of four animals each, and the following conditions were applied: (a) no further treatment was given, allowing free translocation of the Pu to its secondary deposition sites; (b) interception of the Pu translocation by weekly injections of 30 mumol of Ca-DTPA/kg of body weight (Ca-chelate of diethylene-triaminepentaacetic acid); and (c) interception of translocation by daily injections of 30 mumol/kg body weight of Zn-DTPA. For each of the groups (b) and (c), three dogs were used in a lifetime study, and one was sacrificed for nuclide distribution studies. Free translocation and subsequent deposition in the skeleton resulted in the death of each of the non-chelated dogs from osteosarcoma between 1267 and 1594 days after injection. Weekly treatment with Ca-DTPA reduced the total Pu burden significantly, but these dogs also died with osteosarcoma between 1462 and 1783 days. Daily injections with Zn-DTPA reduced the total Pu burden more efficiently than Ca-DTPA and prevented continuous deposition of solubilized Pu on bone surfaces. The mean post-injection survival of these dogs was 3520 days or about 2.1 times that of the animals receiving Ca-DTPA, while the latent period for bone tumour induction was about 2.6 times longer. This treatment reduced the severity of liver lesions and eliminated the occurrence of persistent leukopenia, but it did not prevent the formation of bone cancer.
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PMID:Effectiveness of DTPA treatments following the injection of particulate plutonium. 168 Sep 51

To study the late consequences of primary bone cancer, we interviewed 82 osteosarcoma and 29 Ewing's sarcoma survivors regarding their health, fertility and offspring, employment, annual income, and activities of daily living. All subjects had been diagnosed before age 20 (mean age, 14.6 years), had survived at least 5 years from diagnosis, and were at least 21 years of age. On average, they were 32.5 years of age at interview. As controls, 151 siblings were interviewed. During the follow-up period, eight survivors had died, and eight survivors had been diagnosed with a second malignancy (7.2%; P = .002). No other health condition distinguished survivors from controls. Although the survivors were more likely than controls to have some difficulty climbing stairs and to have had employment disability, employment status and annual income at follow-up were similar. Deficits in marriage and fertility were not significant. Adult survivors of primary bone tumors diagnosed during childhood or adolescence are at high risk for second malignancies and premature death, making continued medical follow-up of utmost importance. Despite the physical impairment following limb amputation for many, the majority of outcomes we measured did not differ from controls, suggesting few adverse psychosocial outcomes in this group of cancer survivors.
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PMID:Late effects of therapy in adult survivors of osteosarcoma and Ewing's sarcoma. 810 65

Silver-stained nucleolar proteins (AgNORs) were counted in a variety of bone tumors. In osteosarcomas, the number of AgNORs was also quantified before and after chemotherapy. Malignant bone tumor cells possessed more than five small AgNORs (5.85 +/- 1.39). Nuclei of benign bone tumor cells had less than three (2.61 +/- 0.51). A significant difference in the number of AgNORs between osteosarcomas before chemotherapy (6.10 +/- 1.22) and after chemotherapy (4.20 +/- 1.07) was observed. (p less than 0.001). The number of AgNORs in osteosarcoma patients with better prognoses was smaller than that of osteosarcoma patients showing poor prognoses, but without significant difference. The results of the present study indicate that the AgNOR count might help in determining malignancy, evaluating the effect of chemotherapy, and deciding the prognosis.
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PMID:Nucleolar organizer regions in bone tumors. 193 46

Canine appendicular osteosarcoma is a highly malignant primary bone cancer that closely resembles the same disease in humans. Although amputation alone usually controls local disease, metastatic cancer is common and is the cause of death or euthanasia in 90% of dogs by 1 year. Cisplatin (+/- doxorubicin) chemotherapy appears to improve survival time in dogs; however, metastatic cancer remains a problem. Pulmonary metastasectomy may prolong survival in carefully selected dogs. Limb-sparing, although involved and potentially fraught with complications, can result in local disease control and a functional, pain-free limb in selected dogs without adversely affecting their survival. Studies are ongoing to improve local disease control with limb-sparing and improve disease-free survival in dogs with appendicular osteosarcoma. In conclusion, dogs with osteosarcoma were previously thought to have a hopeless prognosis, but the outlook is beginning to appear more optimistic. Limb-sparing in dogs is still evolving; however, it is possible in selected cases to optimize survival and preserve limb function.
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PMID:Management of canine appendicular osteosarcoma. 219 34

Osteosarcoma is the most frequent childhood bone cancer (Tebbi, C. K., and Gaeta, J. Pediatr. Ann., 17:285-300, 1988). Using Southern blot mapping, we found that 11 of 60 (18%) osteosarcomas had altered restriction patterns of the p53 gene and that six of these had loss of the other p53 allele. In contrast, no alteration of the p53 gene was detected in 50 samples from other types of sarcomas. Fifty % of osteosarcoma cell lines (4 of 8) also had gross rearrangements of one p53 allele with loss of the second allele, and these had no detectable p53 mRNA. Osteosarcoma cell lines with no detectable alteration of the p53 gene contained abundant p53 transcripts. Taken together, data show that human osteosarcomas can have rearrangements of the p53 gene; these rearrangements may cause loss of normal constraints on cellular growth.
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PMID:Frequency and structure of p53 rearrangements in human osteosarcoma. 225 37

The study of bone cancer has been difficult in part due to a lack of appropriate in vitro osteosarcoma model systems. The development of such systems is essential if a clearer understanding of the biology of and mechanisms behind the formation and progression of bone cancers is to be obtained. We report here the development of an in vitro model system which demonstrates important characteristics generally associated with osteosarcoma. The chick periosteal osteogenesis model was infected with the Fujinami Sarcoma Virus (FSV) containing the v-fps oncogene which encodes for a P140gag-fps protein-tyrosine kinase. Under the appropriate conditions FSV infected cultures developed bone and cartilaginous tissues which showed histopathological findings consistent with osteosarcoma. Biochemical data indicating massive increases in alkaline phosphatase activity, protein content, 3H-Thymidine incorporation as well as expression of active P140gag-fps confirm that transformation has occurred in FSV infected cultures. This novel in vitro model system should prove most useful in the study of bone cancer.
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PMID:In vitro transformation of osteoblasts: putative formation of osteosarcoma in vitro. 282 12

Two prepubertal sisters of American Indian origin developed osteosarcoma at 8 and 12 years of age. This familial occurrence, tumor onset prior to puberty, unusual tumor location in one who also had short stature, and ethnic background all suggest an inborn predisposition to bone cancer rather than a chance occurrence. Rearrangements involving chromosomes #13 and #14 were found in both the surviving proband and mother. Comparison of the arm ratio and prometaphase G-banding patterns of the rearranged chromosomes suggests either deletion of band 14q11.2 or pericentric inversion (with breakpoints at 13q12 and 14q11.2) in the proband's rearranged chromosome, but not in her mother's. Her mother, who had no malignancy, had a typical Robertsonian translocation [t(13;14)(p11;q11)]. Three previously reported children with chromosomal abnormalities developed osteosarcoma at unusually young ages, younger even than in reported sibships with osteosarcoma. The most frequently detected cytogenetic abnormalities in sarcoma tumor cells involve chromosomes #13 and #14. In addition, some cases of bilateral retinoblastoma and familial unilateral retinoblastoma, which are known to be at increased risk for osteosarcoma, are associated with tiny deletions on chromosome #13. Thus, there may be a causal relationship between constitutional loss or rearrangement of genetic material at these breakpoints on chromosomes #13 or #14 and development of osteosarcoma in this family that is similar to that seen in patients with small constitutional chromosomal deletions who develop Wilms' tumor and retinoblastoma.
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PMID:Familial osteosarcoma associated with 13;14 chromosomal rearrangement. 385 64

The relative effectiveness of nine bone-seeking radionuclides with their progeny for the production of malignant skeletal tumors (mostly osteogenic sarcoma), principally by chronic alpha-particle irradiation, is examined with available data obtained from lifetime studies at three laboratories of pure-bred beagles exposed to graded dosages in controlled experiments. The lifetime tumor dose-rate/time-response relationships observed in beagles injected with 226Ra at the University of California at Davis, in which 123 cases of bone cancer (98% osteosarcoma) have been observed for dose rates between 0.05 and 20 rad/day, provide the basis for comparing the induction of bone cancer by the other radionuclides. All nine radionuclide studies were found to demonstrate with high precision (sigma g less than 1.2) a three-dimensional lognormal response relationship represented in two dimensions by the equation of the time to death from bone cancer t = KD-s, where t is the elapsed time to death, D is the average skeletal dose rate, K is a parameter characteristic of the radionuclide, risk level and exposure details, and S observed to be 0.29 (0.01 SE) and suggested to be exactly one-third for all the nine radionuclides. The results show the relative biological effectiveness (RBE) for bone-cancer induction potency with respect to radiation exposure from 226Ra to be 3.0 for 228Ra , 6.4 for 241Am, 6.6 for 249Cf , 252Cf and 253Es , 9.0 for 239Pu, 10.7 for 228Th , and 15.5 for 238Pu. The observed RBE values are interpreted in terms of the relative exposure of sensitive cells of the skeleton since they all involve primarily alpha irradiation. Scaling to people is accomplished using a response ratio (RR) of 3.6 with respect to beagles.
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PMID:Comparison of the carcinogenicity of radium and bone-seeking actinides. 632 74


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