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 amino acid sequence of the vitronectin receptor alpha subunit deduced from cDNA is presented. The sequence defines a 1047-amino-acid polypeptide precursor with a putative signal sequence, a large extracellular domain with several sites homologous to calcium binding sites in other proteins, a transmembrane domain, and a 32-amino-acid cytoplasmic domain. The 7-kilobase vitronectin receptor alpha subunit mRNA was found to be expressed in all cell lines examined, including endothelial cells, K562 and HEL leukemia cells, and osteosarcoma cells. In the two leukemia cell lines, the expression of the vitronectin receptor mRNA, as well as that of the fibronectin receptor, was enhanced in the presence of phorbol ester, a treatment known to increase the adhesiveness of these cells. The HEL cells were the only ones among the cell lines tested that also contained the mRNA of the platelet adhesion receptor alpha subunit, glycoprotein IIb. The expression of glycoprotein IIb was slightly enhanced by treatment of the cells with phorbol ester. These results complete the partial cDNA sequence of the vitronectin receptor alpha subunit published previously (Suzuki, S., Argraves, W. S., Pytela, R., Arai, H., Krusius, T., Pierschbacher, M. D., and Ruoslahti, E. (1986) Proc. Natl. Acad. Sci. U.S.A., 83, 8614-8618), confirm that the vitronectin receptor, and not IIb, is expressed in endothelial cells, and show that changes in the level of its expression correlate with changes in cell adhesiveness.
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PMID:Amino acid sequence of the vitronectin receptor alpha subunit and comparative expression of adhesion receptor mRNAs. 244

Children with acute leukemia often have erythrocytes with "fetal-like" features. To examine the relationship of the type and phase of the leukemia to this observation, we studied 39 children with newly diagnosed acute lymphocytic leukemia (ALL) and 5 with acute nonlymphocytic leukemia (ANLL). In addition, 22 patients were evaluated during chemotherapy, 3 off therapy, and 12 at the time of relapse. Macrocytosis and/or anisocytosis was noted in 70% of patients with ALL at the time of first diagnosis, 80% of patients with new ANLL, and greater than 90% of patients with ALL while on treatment. F cells were increased in 25% of ALL and 80% of ANLL at diagnosis and in 60% of ALL during chemotherapy. Hb F levels were elevated in 8, 40, and 30% of these groups, respectively. Nonleukemic controls for chemotherapy (six patients with osteogenic sarcoma) all had macrocytosis and/or anisocytosis, and 80% had increased F cell proportions. Features at relapse on chemotherapy were similar to those during treated remissions. Abnormal RBCs are more frequent at the time of diagnosis in ANLL, in which they may belong to the malignant clone, than in ALL, in which stress erythropoiesis and/or leukemic factors may be contributory. During chemotherapy, drug-related erythrocyte changes are added to those of leukemia itself. Thus, leukemia, chemotherapy, and the combination lead to erythrocytes with fetal-like features.
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PMID:Erythrocyte characteristics in childhood acute leukemia. 246 41

Clomesone was evaluated for antitumor activity against a spectrum of animal tumor models. Clomesone exhibited significant antitumor activity against the murine L1210 leukemia implanted i.p., s.c., and intracerebrally (i.c.). Activity against s.c.-implanted tumor was largely independent of schedule and route of administration. Therapeutically optimal single-dose treatment (for tumored mice) was less toxic to nontumored mice than therapeutically optimal prolonged treatment. Clomesone also exhibited activity against other murine tumors (P388 leukemia, B16 melanoma, Lewis lung carcinoma, and M5076 sarcoma). It was active against P388 leukemia sublines resistant to cyclophosphamide, L-phenylalanine mustard, and cis-diamminedichloroplatinum(II). No activity was observed against a P388 subline resistant to N,N'-bis(2-chloroethyl)-N-nitrosourea or against Ridgway osteogenic sarcoma, a nitrosourea-resistant murine solid tumor. Clomesone is generally as effective as the chloroethylnitrosoureas against experimental tumor models. Since clomesone does not have the hydroxyethylating and carbamoylating activities of the chloroethylnitrosoureas (which do not appear to contribute to antitumor activity), it would likely be a more toxicologically selective compound. It may prove to be less carcinogenic than the chloroethylnitrosoureas, and it may contribute less target organ toxicity and less interference with the actions of other drugs when used in combinations.
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PMID:Antitumor activity of 2-chloroethyl (methylsulfonyl)methanesulfonate (clomesone, NSC 33847) against selected tumor systems in mice. 253 44

Using a somatic cell hybridization technique, four murine monoclonal antibodies (three immunoglobulin M and one immunoglobulin G3) were produced against a human neuroblastoma cell surface glycolipid antigen. They reacted strongly with all human neuroblastoma tumor-containing specimens and six of eight human neuroblastoma cell lines. More than 98% of each neuroblastoma cell population possessed this surface antigen, and in the presence of complement, 100% of them were killed. While melanoma and osteogenic sarcoma carried this antigen, leukemia and most Ewing's and Wilms' tumors did not. There was no cross-reaction with 30 normal or remission bone marrow samples and none with normal human tissues other than neurons in vitro. This antigen was neuraminidase sensitive, separable on thin-layer chromatogram, and did not modulate after combining with the monoclonal antibodies. These antibodies could detect less than 0.1% tumor cells deliberately seeded in the bone marrow samples. Because of their unique properties, these monoclonal antibodies may have diagnostic and therapeutic potentials.
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PMID:Monoclonal antibodies to a glycolipid antigen on human neuroblastoma cells. 258 Jun 25

Introduction of an exogenous retinoblastoma (RB) gene in RB-deficient retinoblastoma or osteosarcoma cells has been shown to suppress their neoplastic phenotype. In experiments designed to explore the potential mechanism of RB tumor suppression, we report here that the phosphorylation state of RB protein is modulated during normal cellular events. In resting cells, RB protein is present in its least phosphorylated form; in rapidly proliferating cells, RB protein is highly phosphorylated. Maximal phosphorylation is associated with S phase of the cell cycle. Induction of differentiation in several human leukemia cell lines by treatment with phorbol ester or retinoic acid leads to dephosphorylation of RB. Time course studies indicate that RB dephosphorylation precedes the total arrest of cell growth during differentiation. These observations strongly suggest that the function of RB protein is modulated by a phosphorylation/dephosphorylation mechanism during cell proliferation and differentiation.
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PMID:Phosphorylation of the retinoblastoma gene product is modulated during the cell cycle and cellular differentiation. 267 46

Between 1950 and 1984 out of 57.393 women who delivered at the First Department of Obstetrics and Gynecology, Catania University Medical School, Catania, Italy, 40 cases of malignant neoplasia were diagnosed with an incidence of one case in 1.434 deliveries. The most frequent neoplasias is cervix carcinoma (21 cases; 52.5%), followed by breast cancer (6 cases; 15%), ovarian cancer (4 cases; 10%) and leukemia (4 cases; 10%). There was very rare association with Hodgkin disease (2 cases; 5%), osteosarcoma (1 case; 2.5%), medulloblastoma (1 case; 2.5%), and skin melanoma (1 case; 2.5%). Since cancer of the uterine cervix is the most frequent neoplasia (one cases out of 2.733 deliveries), cervical smear should be performed during pregnancy in women that never performed it.
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PMID:[Cancer and pregnancy. Retrospective study on the frequency in 57,393 deliveries]. 276 32

Among a cohort of 10,106 three-year survivors of childhood cancer, 90 second primary tumours (SPTs) were observed. Within 25 years of 3-year survival about 4% developed a SPT, about 6-fold expected, the relative risk not varying much with increasing follow-up. Following genetic retinoblastoma we observed 30-fold the expected number of SPTs, and over 400-fold the expected number of osteosarcomas. The risk of SPT in the absence of radiotherapy and chemotherapy (inherent risk) following genetic retinoblastoma was 13-fold expected and over 200-fold the expected number of osteosarcomas were observed. There was evidence that both radiotherapy and cyclophosphamide were associated with an increased risk of SPT. After all first primary tumours (FPTs) excluding retinoblastoma we observed almost 5-fold the expected number of SPTs. The inherent risk was 4-fold expected, the relative risks associated with radiotherapy but no chemotherapy, and both radiotherapy and chemotherapy were 6- and 9-fold expected respectively. There were about 20-fold the number of malignant bone tumours expected, most were osteosarcoma; also 7-fold the number of central nervous system tumours expected. There were 8 basal cell carcinomas and it seems likely that radiotherapy was involved in the development of some of these. Radiotherapy appears to have been involved in the development of many of the SPTs observed following all FPTs excluding retinoblastoma, particularly after CNS tumours, Wilms' tumour and Hodgkin's disease. Currently there is insufficient follow-up to examine the risk following chemotherapy. After acute leukaemia there was 20-fold the expected number of central nervous system tumours, though this is based on only 3 cases; whether therapy is directly involved in their development is uncertain. The risks we report are rarely greater than those reported in previous large-scale studies; in most instances they are substantially less. It is very unlikely that many SPTs were missed with our follow-up system so alternative explanations require further investigation; in particular it is possible the lower risks in our data compared to series treated in the United States may be explained, in part, by less combination therapy and lower doses of radiotherapy.
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PMID:Incidence of second primary tumours among childhood cancer survivors. 282 73

Internal irradiation of mice using bone seeking radionuclides results in the activation of endogenous retroviruses and in the subsequent development of bone tumors. Genomic DNA from an osteosarcoma cell line, derived from an 90Sr-induced bone tumor, was cotransfected with the plasmid pSV2-neo into NIH/3T3 cells and G418-resistant transfectants gave rise to colonies in soft agar. Southern blot analysis of these first cycle transformants revealed the presence of extra copies of c-ras. We have analysed the arrangement of ecotropic murine leukemia proviral sequences in seven 90Sr-induced bone tumors and one osteosarcoma cell line of CF1-mice. Integration of ecotropic and/or ecotropic recombinant proviruses seems to be involved in rearrangements of 3' provirus cellular junction fragments occurring in all tumor DNAs analysed, but no indication for site-specific integration was found. We also determined the primary structure of FBR-MuSV, a transforming retrovirus able to induce bone tumors in newborn mice. FBR-MuSV contains sequences from all four exons of the murine c-fos gene, but lacks sequences encoding the first 24 and the last 98 amino acids of the c-fos gene product. The coding region of FBR-MuSV has also undergone two small in frame deletions. Thus, the v-fosFBR-MuSV retains 236 amino acids of the 380 amino acids of the murine c-fos product. In FBR-MuSV-transformed cells two fos-containing mRNAs have been detected: a 3.3-kb full-size genomic RNA and a 2.2-kb subgenomic mRNA as revealed by both fos- and MuLV-hybridization probes.
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PMID:Oncogene involvement in radiation- and virus-induced mouse osteosarcomas. 301 18

We isolated the full length provirus of human T cell leukaemia virus type I (HTLV-I) from MT-2, a lymphoid cell line producing HTLV-I. In three non-lymphoid cell lines (COS7, human osteosarcoma HOS cells, and HeLa) this provirus expressed a trans-acting activity after co-transfection with a recombinant plasmid carrying a bacterial chloramphenicol acetyltransferase gene under the control of a long terminal repeat of HTLV-I provirus. The trans-acting protein p40 was detected by immunoprecipitation in transfected HOS cells. Structural proteins of HTLV-I, the gag and env products, were also formed and processed in the same manner as observed in MT-2 cells. In transfected HeLa cells, the p40 protein was mainly localized in the nucleus, while other structural proteins were detected in the cytoplasm and/or the membrane by indirect immunofluorescence. Syncytium formation was observed in HeLa cells after transfection. These results demonstrated that non-lymphoid cells could produce the major proteins of HTLV-I after DNA transfection of the cloned provirus.
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PMID:Expression of a provirus of human T cell leukaemia virus type I by DNA transfection. 302 87

A patient with well-differentiated monoblastic leukemia (ANLL FAB-M5b) is described in whom acute leukemia was diagnosed 25 months after having completed postoperative adjuvant chemotherapy for osteogenic sarcoma of the femur. All analyzed metaphases showed 48xy, dup 1(q12), +3, +9.
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PMID:Acute monoblastic leukemia as a second malignancy following chemotherapy for osteogenic sarcoma: a case report. 315 50


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