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)

Contemporary clinical research is actively engaged at the conquest of residual neoplastic disease. The preliminary results of combined treatment modalities for osteogenic sarcoma, Ewing's sarcoma, rhabdomyosarcoma, breast cancer, malignant melanoma and Hodgkin's disease have shown a significant decrease in the incidence of distant metastases. In some neoplasias the decreased relapse rate was associated to improved survival. Since the problem of long-term carcinogenesis does exist, the use of prolonged adjuvant chemotherapy, at present moment, is best limited to patients at high risk of early relapse when treated only with local or local-regional modalities.
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PMID:Treatment of residual neoplastic disease in solid tumours. 106 17

Soluble chromium (VI) compounds either alone or in combination with 3-methylcholanthrene (MC) were used to transform non-tumorigenic osteoblast-like human osteosarcoma cells (HOS TE85). The Cr(VI) compounds were highly toxic to these cells with LC50 values in the range of approximately 0.5-1.0 microM. Continuous passaging of the treated cells resulted in sustained increase in anchorage-independent (AI) colony formation. Treatment with Cr(VI) and MC resulted in substantial increase in AI growth. At the XVth passage, a number of individual AI colonies were expanded in culture and used for further studies. The cells are refractory in appearance and grow as 'nests' rather than as monolayers. The cell lines have relatively high plating efficiency (PE) in soft agar and respond to promotional effect of phorbol-12-myristate-13-acetate by an increase in PE and in the size and number of AI colonies. While the isolated cells are not tumorigenic when tested in athymic nude mice, most of the lines possess higher levels of plasminogen activator (PA) activity, considered as one of the markers of transformation. This is also reflected in the increase in the steady state level of urokinase type PA mRNA. These results show that Cr(VI) compounds are capable of promoting human cells to an altered phenotype characteristic of a stage in the carcinogenesis cascade.
Carcinogenesis 1992 Nov
PMID:Transformation of non-tumorigenic osteoblast-like human osteosarcoma cells by hexavalent chromates: alteration of morphology, induction of anchorage-independence and proteolytic function. 142 71

Amplification and rearrangement of cellular proto-oncogenes are two of the several possible genetic alterations implicated in carcinogenesis and tumor progression. Although morphologically similar tumors may be heterogeneous at the level of the genome, some tumor types have shown relatively frequent and consistent abnormalities of specific oncogenes. In order to determine the frequency of oncogene amplification and rearrangement in several types of human sarcomas and to determine if histologically similar tumors have common genetic alterations, we analyzed 26 primary sarcomas by Southern hybridization. The oncogene probes utilized were N- and H-ras, sis, EGF-R (erb-B-1), neu (erb-B-2), fos, N- and c-myc, mos, and yes. The tumors studied included: five rhabdomyosarcomas (one alveolar, four embryonal), six malignant fibrous histiocytomas, six leiomyosarcomas, four liposarcomas, two Ewing's sarcomas, one osteosarcoma, and two fibrosarcomas. Oncogene abnormalities were identified in three tumors. One rhabdomyosarcoma showed 12-fold amplification and concurrent rearrangement of sis. This particular tumor also revealed rearrangement of H-ras and 15-fold amplification of c-myc. A second rhabdomyosarcoma revealed rearrangement of neu. A liposarcoma had a sis rearrangement. These findings suggest that many sarcomas show no common structural oncogene abnormalities. The presence of differing oncogene alterations within the rhabdomyosarcoma group indicates genetic heterogeneity among histologically similar sarcomas. The finding of a sis rearrangement in both a liposarcoma and a rhabdomyosarcoma, however, may suggest common oncogenesis among different tumor types.
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PMID:Genomic alterations in sarcomas: a histologic correlative study with use of oncogene panels. 149 46

Inactivation of two tumor suppressor genes, RB and p53, is associated with tumor formation. To elucidate the molecular basis of the tumorigenesis of human osteosarcoma, structural and expressional alterations of these two genes were examined in five human osteosarcoma cell lines, two of which were from Japanese patients. In addition, I analyzed two adenovirus E1A-binding proteins, p107 and p300, putative "tumor suppressor gene products", which share similar properties with the RB protein in binding to the E1A oncoprotein. Detailed analyses of DNA, mRNA, and protein showed that (1) 3 lines including both Japanese lines lost the expression of the RB protein due to either the absence or the alteration of mRNA caused by DNA rearrangement, (2) abnormality of p53 gene was detected in all cell lines : 4 lines lost p53 expression due to either gene loss or the absence of mRNA, and one line expressed an abnormal form of the protein without detectable DNA and mRNA alterations and (3) no significant alteration of p107 or p300 was detected in all cell lines. These results further confirm that inactivating mutations of p53 and RB genes are deeply involved in the carcinogenesis of human osteosarcoma and suggest that p107 and p300 may not play a role in the tumorigenesis.
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PMID:[Roles of tumor suppressor genes in human osteosarcoma cells]. 182 50

Intraoperative radiotherapy has been employed in human cancer research for over a decade. Since 1979, trials to assess the acute and late toxicity of IORT have been carried out at the National Cancer Institute in an adult dog model in an attempt to establish dose tolerance guidelines for a variety of organs. Of the 170 animals entered on 12 studies with a minimum follow-up of 2 years, 148 dogs received IORT; 22 control animals received only surgery. Animals were sacrificed at designated intervals following IORT, usually at 1, 6, 12, 24, and 60 month intervals. 102 of 148 irradiated dogs were sacrificed less than 24 months; 46 dogs were followed greater than or equal to 24 months after IORT. To date, 34 of the 46 animals have been sacrificed; the 12 remaining animals are to be followed to 5 years. These 12 animals have minimum follow-up of 30 months. In the irradiated group followed for greater than or equal to 24 months, 10 tumors have arisen in 9 animals. One animal developed an incidental spontaneous breast carcinoma outside the IORT port, discovered only at scheduled post-mortem exam. The remaining nine tumors arose within IORT ports. Two tumors were benign neural tumors--a neuroma and a neurofibroma. One animal had a "collision" tumor comprised of grade I chondrosarcoma adjacent to grade III osteosarcoma arising in lumbar vertebrae. Two other grade III osteosarcomas, one grade III fibrosarcoma, and one grade III malignant fibrous histiocytoma arose in retroperitoneal/paravertebral sites. An embryonal rhabdomyosarcoma (sarcoma botryoides) arose within the irradiated urinary bladder of one animal. No sham irradiated controls nor IORT animals sacrificed less than 24 months have developed any spontaneous or radiation-induced tumors. The time range of diagnoses of tumors was 24-58 months (median 40 months). The IORT dose range associated with tumor development was 20-35 Gy (median 30 Gy). The carcinogenesis capability of single fraction, high dose radiation in animals is discussed, as are the implications of these data for continued research and clinical usage of IORT in the treatment of humans.
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PMID:Tumor induction following intraoperative radiotherapy: late results of the National Cancer Institute canine trials. 212 Jan 59

Several familial cancer syndromes have been identified. The syndrome of sarcomas, breast cancer and other neoplasms, known as Li-Fraumeni syndrome, is characterized by several different neoplasms presenting at young ages with autosomal dominant transmission and a high incidence of second primaries. In this paper, we studied six generations (51 people) of the family of a 24-year-old man with osteogenic sarcoma of the mandible. Twelve malignancies in 11 people, including several rare tumors, were revealed. Mean age of presentation was 24 years old. Nine of the 11 patients died of disease. One developed a second primary. Two tumors presented in the head and neck. Transmission was autosomal dominant. The karyotypes of two family members were normal. Identification of Li-Fraumeni syndrome in a family is important in determining appropriate follow-up for the patient and family. Such families are models for studying carcinogenesis.
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PMID:Family cancer syndrome: a study of the kindred of a man with osteogenic sarcoma of the mandible. 224 14

Increased energy intake and physical inactivity have been shown to heighten the risk of breast, large bowel, and other cancers. Large body size and fatness, as measured by adult stature, body weight and body mass indices, are positively related to a variety of cancers, including breast, colorectum, prostate, endometrium, kidney, and ovary, as well as to total cancer incidence or mortality in many investigations, although conflicting reports exist. Adult weight gain has also been specifically implicated in a few etiologic studies of breast and large bowel cancer. Furthermore, increased birthweight and childhood stature have been linked to increased risk of leukemia, lymphoma, osteogenic sarcoma, and central nervous system malignancies between infancy and young adulthood. Greater body weight also adversely affects breast cancer survival. These findings are complementary and support a role for positive energy balance in promoting human carcinogenesis. Potential mechanisms are discussed.
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PMID:Energy balance, body size, and cancer. 225 89

Vitamin A is known to be able to modulate cell growth and differentiation and to act as an inhibitor of the process of carcinogenesis in some experimental models. Here we have studied the effect of different concentrations of vitamin A on chemotactic and chemoinvasive behaviour of a metastatic osteosarcoma cell line. The cell proliferation was partially inhibited in the presence of 10(-5) M retinol after 4 days of incubation. Retinol effect on chemotactic and chemoinvasive activity of osteosarcoma cells seemed to be dose-dependent. The highest retinol concentration used (10(-5) M) had an inhibitory effect on migratory and invasive cell response. Lower retinol concentrations seemed to be able to enhance (10(-8) M) both chemotactic and chemoinvasive activity of osteosarcoma cells. Chemotaxis and chemoinvasion assays provide rapid and quantitative tools to study the "in vitro" behaviour of metastatic cells. Furthermore, they represent a mean to screen for drugs, hormones and other substances able to alter the metastatic phenotype.
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PMID:Effect of vitamin A on chemotactic and chemoinvasive behaviour of an osteosarcoma cell line. 239 Feb 27

Some human tumor cell lines express the c-sis gene, the proto-oncogene of the transforming gene v-sis, and produce platelet-derived growth factor, which may contribute to carcinogenesis by autocrine or paracrine mechanisms. Here we demonstrate that c-sis expression in some human glioma and osteosarcoma cell lines can be blocked by agents that increase cellular cyclic adenosine monophosphate (cAMP). Forskolin, 8-bromocyclic AMP, cholera toxin, and prostaglandin E1 reduced c-sis mRNA in these cells by up to 90%. c-sis transcription rates were reduced by agents that increase cAMP; the stability of c-sis mRNA was unaffected. The possible therapeutic value of blocking the expression of tumor growth factor genes pharmacologically warrants further study.
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PMID:Cyclic AMP blocks expression of the c-sis gene in tumor cells. 254 92

The authors describe a case of post radiation osteogenic osteosarcoma secondary to Hodgkin's disease. 14 similar cases were found in literature. They discuss the predisposition to the carcinogenesis due to the association of the chemotherapy and the radiotherapy for the treatment of Hodgkin's disease.
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PMID:[Post-radiation osteosarcoma following Hodgkin's disease. Apropos of a case and review of the literature]. 266 Jan 99


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