Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Studies were made to determine if examination with multiple radiopharmaceuticals would improve the sensitivity and specificity of colloid liver spleen scans. Increased uptake of Ga-67 citrate and In-111 bleomycin was found in most Tc-99m sulfur colloid scan defects caused by hepatocellular hepatoma or lymphoma. Increased uptake of these agents was found in some defects caused by malignant melanoma, breast carcinoma and carcinoma of the lung, and was rarely seen in defects caused by cholangiocarcinoma or gastrointestinal neoplasms. Gallium was useful in the followup of patients with hepatoma. Procedures designed to evaluate the gall bladder fossa, renal impression, or blood pool activity of an apparent tumor were found to be helpful and simple to perform. Iodine-131 as NaI was useful in studying functioning liver metastases from thyroid carcinoma as were bone scanning agents in evaluating hepatic metastases from osteogenic sarcoma. Multiple radiopharmaceutical evaluation of the physiologic and biochemical characteristics of liver lesions supplements current radiologic examinations and increases diagnostic specificity.
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PMID:A study of filling defects in the liver and spleen with multiple radionuclides. 21 17

Cancer chemotherapy was purely palliative until the early sixties. Tumor cures have been since obtained, first in malignant trophoblastoma and Burkitt's lymphoma, and more recently in Hodgkin's disease, diffuse histiocytic lymphoma, acute lymphocytic leukemia in children, Wilms's tumor and osteosarcoma. Preliminary data are suggestive of tumor cures in testicular teratomas and, possibly, in small cell carcinoma of the lung. Five patients with trophoblastoma, Hodgkin's disease, melanoma, chronic myelocytic leukemia and anaplastic carcinoma of the lung are briefly presented, all without evidence of tumor relapse 3 years or more after chemotherapy. Theoretical bases for improvement of the curative effect of cancer chemotherapy are discussed, including the development of new agents, and new pharmacological problems concerning drug interactions, complexes of drugs with macromolecules or immunoglobulins and liposomes are considered.
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PMID:[Curability of malignant neoplasms: value and limitations of chemotherapy]. 21 68

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

N-Trifluoroacetyladriamycin-14-valerate (AD-32) is superior to Adriamycin in murine L1210 and P388 leukemias and in a number of solid tumor systems, including Ridgway osteogenic sarcoma and Lewis lung carcinoma. In preclinical toxicology studies, AD-32 was less toxic than Adriamycin in both tumor- and non-tumor-being mice and in rabbits. An initial clinical trial was carried out in 23 patients who received a total of 74 courses of AD-32 over a dose range of 100--700 mg/m2 administered at 21-day intervals. Hydrocortisone given during the period of infusion prevented all clinical manifestations of acute toxicity. The AD-32 dose-limiting toxicity, leukopenia, was comparable to that of Adriamycin at a dose of 10:1, but at these equivalently myelosuppressive doses, AD-32 induced less gastrointestinal toxicity and alopecia than Adriamycin and it did not cause local tissue damage following inadvertent paravenous extravasation. Although two responses are reported, the therapeutic activity of AD-32 cannot be assessed because of an inadequate number of patients in any given tumor type. A phase II study is being initiated at a dose of 600 mg/m2 given at 21-day intervals.
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PMID:Initial clinical evaluation of N-trifluoroacetyladriamycin-14-valerate (AD-32), an adriamycin analog. 45 34

Screening for retinoic acid-binding protein (RABP) in experimental tumors revealed the presence of this protein in three mammary tumors, two metastatic colon tumors, B16 melanoma. Lewis lung carcinoma, Ridgway osteogenic sarcoma, and keratoacanthoma. RABP was below the limits of detection in two weakly metastatic colon tumors and in Sarcoma 180. After s.c. implantation of RABP-containing tumors into mice, this protein could be traced in the lungs due to pulmonary metastasis. Following implantation of Lewis lung tumors, RABP was detected in the lung on the 6th day. On the 15th day after implantation, RABP was present in lung and brain, but not in other tissues where this protein was normally lacking. In primary cultures of Lewis lung carcinoma, the lower limit for detection of RABP by sucrose gradient sedimentation technique corresponded to 0.12 mg protein that was extractable from 3 X 10(5) cells. Both chick embryo skin and rabbit ear skin extracts contained RABP; the level of cellular retinol-binding protein was high in chick embryo skin but only marginal in rabbit ear. The amounts of these proteins on chick embryo skin and rabbit ear skin correlate with the biological potency of retinol and retinoic acid, as observed by others.
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PMID:Retinoic acid-binding protein in experimental tumors and in tissues with metastatic tumor foci. 56 58

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

Amygdalin MF was evaluated alone and in combination with an activating agent, beta-glucosidase, against three transplantable rodent tumors; Ridgway osteogenic sarcoma, Lewis lung carcinoma, and P388 leukemia. In dose-response studies up to the LD20 in normal mice, amygdalin MF alone did not demonstrate significant antitumor activity against any of these three tumor systems. Similarly, at doses not exceeding the LD10 in normal mice, amygdalin MF plus beta-glucosidase did not demonstrate antitumour activity against any of these three tumor systems. Potentiation of the lethal toxicity of amygdalin MF by beta-glucosidase was observed in all studies where the two agents were given in simultaneous combination.
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PMID:Experimental studies of the antitumor activity of amygdalin MF (NSC-15780) alone and in combination with beta-glucosidase (NSC-128056). 106 May 11

N-(Phosphonacetyl)-L-aspartate (PALA) is an analog of the transition state for the aspartate transcarbamylase reaction and has been reported previously to be a potent and specific inhibitor of de novo pyrimidine nucleotide biosynthesis. It is now shown that PALA has considerable antitumor activity against certain transplantable tumors in mice. PALA, unlike other antimetabolites, was less effective against ascitic leukemias than against two solid tumors, B16 melanoma and Lewis lung carcinoma. Another solid tumor, Ridgway osteogenic sarcoma, which is sensitivie to many established chemotherapeutic agents, did not respond to PALA. Daily or intermittent treatment with PALA did not significantly increase the life-span of mice bearing i.p. leukemia L1210. The survival time of mice bearing i.p. P388 leukemia was prolonged by PALA treatment by up to 64%. In a number of experiments mice bearing i.p. B16 melanoma survived 77 to 86% longer than did controls when treated with PALA (490 mg/kg) on Days 1, 5, and 9. Lewis lung carcinoma, a tumor refractory to most established antineoplastic agents, was highly sensitive to PALA. Treatment on Days 1, 5, and 9 following s.c. implantation of Lewis lung carcinoma was curative to 50% of the mice. If treatment was delayed until s.c. Lewis lung tumors had reached about 500 mg, PALA neither cured the mice nor produced significant tumor regression. However, extensive delay of tumor growth and prolongation of survival were still observed.
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PMID:Antitumor activity of N-(phosphonacetyl)-L-aspartic acid, a transition-state inhibitor of aspartate transcarbamylase. 106 66

Cyclophospamide was given in two dose schedules to 25 patients with a variety of nonlymphoid solid tumors. Eleven patients were given 18 courses of cyclophosphamide at a total dose of 60 mg/kg. Sixteen patients received 26 courses at a total dose of 100 mg/kg. Two patients were treated with both regimens. Partial responses were achieved in two patients treated with 60-mg/kg dose of cyclophosphamide. One of these patients had osteogenic sarcoma and the other had renal carcinoma. The higher dose also produced two partial responses, one in a patient with anaplastic carcinom a of the lung and the other in a patient with anaplastic carcinoma of the lung and the other in a patient with embryonal testicular carcinoma. Mean leukocyte counts fell to a nadir of 1400 cells/mm after 60 mg/kg while they dropped to below 1000 cells/mm for 5 days after 100 mg/kg of cyclophosphamide. Mean platelet counts remained above 150,000 platelets/mm after both cyclophosphamide schedules. In fective complications were documented aftter three of the 18 courses at 60 mg/kg and after ten of the 26 courses at 100 mg5kg. In the latter group, there were three episodes of bacteremia, including one death from pseudomonas sepsis. Nonhematologic toxicity noted with the 100-mg/kg dose of cyclophosphamide included rare instances of electrocardiogram changes and serum enzyme alterations compatible with myocardial toxicity. The intensive cyclophosphamide therapy did not appear to result in an increased antitumor response in malignancies usually considered to be refractory to alkylating agents.
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PMID:Intensive cyclophosphamide (NSC-26271) therapy for solid tumors. 109

Partially thiolated polycytidylic acid (5-mercaptopolycytidylic, MPC) and its double-stranded complex with polyinosinic acid [poly (I)].poly(I).MPC, were assayed in both antiproliferative and cytotoxicity tests against human cell lines: lung carcinoma A549, colon carcinoma HT-29, osteosarcoma HOS, and amnion cells (WISH). Inhibitory effects of MPC were noted in the antiproliferative assay with ID50 of 7, 24, 33, and 35 micrograms.ml-1, and in the cytotoxicity test with ID50 of 164, 174, 210, and 290 micrograms.ml-1 against the HOS, A549, HT-29, and WISH cells respectively. Comparison with the corresponding partially thiolated mononucleotide (5-mercapto-CMP + CMP) and the nucleoside (5-mercapto-cytidine) demonstrated that MPC was a more potent antiproliferative agent than either of its monomeric constituents. The inhibitory effect of MPC upon the incorporation of [3H]thymidine into the DNA of growing A549 cells paralleled its antiproliferative activity.
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PMID:Inhibition of human cancer cell lines in vitro with mono- and polynucleotides containing 5-mercaptocytosine bases. 177 73


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