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)

The dosimetry of alpha-emitting radionuclides in bone is discussed. Results are presented for average dose rates to tissues close to endosteal surfaces and to haematopoietic bone marrow from thin plane sources of radionuclides buried to different depths in bone and emitting alpha-particles with energies in the range 3-8 MeV. These results are used to demonstrate that on an activity basis 239Pu is unlikely to be more than fifteen times as toxic as 226Ra with respect to osteosarcoma and leukaemia induction in man.
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PMID:Aspects of the dosimetry of alpha-emitting radionuclides in bone with particular emphasis on 226Ra and 239Pu. 26 72

Osteogenic sarcoma developed in a 14-year-old boy 13 years after he had partially recovered from chloramphenicol-induced aplastic anemia. A possible relationship is considered between aplastic anemia, chloramphenicol, testosterone, prednisone, and osteogenic sarcoma. Leukemia has been reported following chloramphenicol-induced aplastic anemia and liver tumors have been associated with testosterone therapy. Certain chemicals have caused osteogenic sarcoma in animals. Thus, we believe there are sufficient a priori reasons to question an etiologic relationship between the cause or treatment of aplastic anemia and osteogenic sarcoma.
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PMID:Osteogenic sarcoma in a patient with aplastic anemia. 26 29

Three brothers had separate childhood cancers--osteogenic sarcoma, acute lymphoblastic leukemia, and bilateral malignant neurilemoma. Comprehensive family history showed a total of 16 cases of cancer among the descendants of the proband's great-great-great-grandmother, including a previously unsuspected cluster of similar neoplasms in an distant branch. The constellation of tumors in the family included bony and soft-tissue sarcomas, brain and neural tumors, leukemia, and breast carcinoma, occurring in a pattern suggesting the action of an incompletely penetrant autosomal dominant gene with pleiotropic effects. In some cases the genetic predisposition may have interacted with environmental determinants to produce particular tumors.
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PMID:Genealogy of cancer in a family. 28 40

cis-Dichlorodiammineplatinum(II) (cis-platinum) has no more than additive, and often much less than additive, lethal toxicity for mice when given in combination with other anticancer agents representing several of the major functional classes of clinically useful anticancer drugs. The previously reported broad spectrum of anticancer activity of cis-platinum against tumors in laboratory animals has now been extended to promisingly useful therapeutic synergism in combination with other active anticancer drugs, including advanced-staged tumors in mice; eg, cis-platinum plus cyclophosphamide against advanced Ridgway osteogenic sarcoma and advanced P388 leukemia, and as surgical adjuvant chemotherapy against advanced colon tumor 26; cis-platinum plus Adriamycin against advanced P388; and cis-platinum plus VP-16-213 against advanced P388. Therapeutic synergism was also seen with cis-platinum plus carminomycin (an Adriamycin analog) against early colon tumor 26. Resistance and cross-resistance studies using sublines of L1210 and P388 selected for resistance to various alkylating agents (cyclophosphamide, melphalan, BCNU, or cis-platinum) indicate a variety of resistance and cross-resistance patterns which further support the growing body of evidence that wide differences in mechanism of cytotoxic activity exist among alkylating agents having experimentally and clinically useful anticancer activity. These data support the observed therapeutic synergisms with combinations of alkylating agents seen against a broad spectrum of murine tumors, and they suggest other drug combinations that might be considered for experimental and clinical trial based on a growing number of logical differences in biochemical mechanism of action of alkylating agent anticancer drugs that have been reported.
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PMID:cis-Dichlorodiammineplatinum(II): combination chemotherapy and cross-resistance studies with tumors of mice. 29 80

Parabiosis of rats permits one partner to survive 1000 R X-radiation if the other is shielded. This dose to the previously shielded partner after intervals of 5, 10 or 30 days tests the ability of the first irradiated partner to recover and, in turn, support the second. The effectiveness of this can be measured by the late effects induced in the pair. Lifespan was shortened by 100--150 days following a 5-day interval, by 30 days following a 10-day interval and not shortened following a 30-day interval. The incidence of leukaemia was about 6 per cent in each group, close to that in control pairs. Shortening the interval between the irradiations decreased the average age of death from leukaemia. No solid lymphoid tumours were induced in the doubly irradiated pairs. The incidence of osteogenic sarcoma was 1.6 per cent in controls and 12.9 per cent in the pairs with both partners irradiated.
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PMID:Late effects of successive massive doses of radiation on parabiont rat pairs. 30 53

Cancer chemotherapy has developed rapidly over the last twenty years. The majority of patients with cancer die from metastatic disease, so the major therapeutic advance now must be better systemic therapy. From its early beginning in the 1940's with oestrogen therapy for prostatic cancer, nitrogen mustards in the lymphomas, and folic acid antagonists in childhood leukaemia, there are now between thirty and forty active anti-cancer agents in clinical use. The main clinical pharmacological points of the major agents are briefly reviewed, together with their main dose-limiting toxic effects and their activity as single agents. Clinical chemotherapy has developed by the introduction of newer agents from the drug screening programmes and a better understanding of the scheduling to avoid serious toxicity. Although drug-resistance is still a major problem, by combining different active agents there has been a dramatic improvement in survival of patients with selected tumours. More recently, treatment of patients early, before they have gross clinical recurrence, has already shown some benefit in pre-menopausal patients with carcinoma of the breast and in patients with osteosarcoma. The limitations of clinical measurements in monitoring therapy are clear, and a major improvement could well be realised if therapy could be monitored on the basis of quantitative markers. The clinical impact of cancer chemotherapy has already been dramatic in drug-sensitive tumours, but these only contribute a small proportion of the total. Some of the common tumours fall into the group that are relatively drug sensitive where the lives of patients can be prolonged, but there is still a significant fraction of tumours which are insensitive to existing drugs and which will probably require the development of newer agents before chemotherapy can make any impact on the survival of patients with these tumours.
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PMID:The current role of cancer chemotherapy. 36 Nov 39

1,4-Dihydroxy-5,8-bis(((2[(2-hydroxyethyl)amino]ethyl)amino))-9,-10-anthracenedione dihydrochloride (CL 232315; NSC 301739D), a representative of a new chemical class of compounds with antineoplastic properties, has been evaluated for antitumor activity in experimental mouse tumor systems. The compound produced significant increases in life span (ILS) and long-term survivors when tested against the P388 and L1210 leukemias as well as the solid neoplasms, B16 melanoma and Colon Tumor 26. The optimal treatment regimens resulted in a 173 to greater than 200% ILS with 20 to 80% 60-day survivors in mice with P388 leukemia, A 205% ILS with 55% 60-day survivors in mice with L1210 leukemia, and an ILS of greater than 300% with 80% 90-day survivors in mice with B16 melanoma. In contrast to Adriamycin, CL 232315 was active against the i.v. implanted L1210 leukemia and demonstrated moderate activity against P388/Adria, a subline of P388 resistant to Adriamycin. The compound was ineffective when tested against the Lewis lung carcinoma and the Ridgway osteogenic sarcoma. CL 232315 was active i.p., s.c., and i.v., but p.o. activity was not demonstrated. Schedule dependency was not observed when the compound was administered once daily for nine days, once every four days, or as a single dose.
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PMID:Activity of a novel anthracenedione, 1,4-dihydroxy-5,8-bis(((2-[(2-hydroxyethyl)amino]ethyl)amino])-9,10-anthracenedione dihydrochloride, against experimental tumors in mice. 42 98

While structure-activity relationships for vinblastine (VLB), vincristine, deacetyl-VLB, and deacetyl-VLB amide (vindesine, VDS) in several tumor and leukemia models have been reported previously, the present study explores these relationships for a series of N-substituted vindesine analogues. These compounds were prepared from the reaction of deacetyl-VLB acid azide with the appropriate amines and were characterized by mass spectral analysis, 1H and 13C NMR spectra, electrometric titration, and infrared spectra. N-Alkylvindesines have reduced activity compared to that of VDS against the Gardner lymphosarcoma (GLS). N-beta-Hydroxyethyl-VDS surpasses vindesine in its activity against the Ridgway osteogenic sarcoma and the GLS, whereas against the B16 melanoma it is less active than VDS. N-beta-(4-Hydroxyphenethyl)-VDS, envisaged as a substrate for the enzyme tryosinase, was shown to be more active than VDS against the B16 melanoma but has only marginal activity against the GLS. In terms of collective antitumor activity against the model systems used, vindesine emerges as the congener with optimum qualities. Bis(N-ethylidenevindesine) disulfide, the first example of a bridged bisvindesine and comparable to VDS in its antitumor profile, shows evidence of activity against a P388/VCR leukemia strain known to be resistant to maytansine as well as to vincristine.
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PMID:Structure-activity relationships of dimeric Catharanthus alkaloids. 2. Experimental antitumor activities of N-substituted deacetylvinblastine amide (vindesine) sulfates. 43 Apr 77

Except for oral administration, there was no grossly observed toxicity from carefully administered high doses of amygdalin in the experimental systems used. The compound in high doses was ineffective against the DMBA-induced rat mammary carcinoma and the following transplanted experimental tumors: Sarcoma 180, plasma cell tumor LPC-1, leukemia L1210, Mecca lymphosarcoma, Ridgway osteogenic sarcoma, sarcoma T241, mammary carcinoma E0771, Taper liver tumor, Ehrlich carcinoma (solid and ascites), and Walker carcinosarcoma 256. Amygdalin did not noticeably influence the toxicity or impair the efficacy of these chemotherapeutic agents in their respective systems: Cytosine arabinoside, methotrexate, cytoxan, or 5-fluorouracil in L1210; the latter two in LPC-1; 6-mercaptopurine in Ridgway osteogenic sarcoma; estradiol-17beta or 2alpha-methyldihydrotestosterone propionate in the DMBA-induced rat mammary carcinoma.
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PMID:Antitumor tests of amygdalin in transplantable animal tumor systems. 64 16

With the object of examining the anti-tumour effect of exogenous interferon therapy in man a research programme has been initiated at the Karolinska Hospital. Established cell lines obtained from patients with Burkitt's and other types of lymphoma, leukaemia, osteosarcoma, mammary carcinoma and fibrosarcoma and from fibroblast cultures displayed a variable sensitivity to the cell multiplication inhibitory activity of interferon. All the monolayer cultures tested were found to be sensitive to interferon at concentrations between 10 and 300 units/ml. Some lymphoma cell lines were not sensitive to interferon even at concentrations as high as 10.000 units/ml, while others were sensitive at concentrations between 2 and 300 units/ml. The interferons tested appeared to show a degree of tissue specificity. Controlled studies in vivo are being performed on osteosarcoma, juvenile papilloma of the larynx, multiple myeloma and small-cell carcinoma of the lung. The clinical results of this research obtained to date, together with the results obtained in model experiments, would appear to warrant accelerated production of human interferon.
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PMID:Interferon therapy for neoplastic diseases in man in vitro and in vivo studies. 72 40


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