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 significant feature of the reported case was that of a sinister-looking mandibular tumor highly suggestive of a metastatic lesion or of osteogenic sarcoma. A biopsy specimen and results of a thorough medical work-up showed the lesion to be multiple myeloma. The myeloma cells apparently have the capability to stimulate osteoblastic activity and new bone formation. This capability should be kept in mind when making the differential diagnosis of osteoblastic bony lesions of the jaws.
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PMID:A large mandibular tumor with a distinct radiological "sun-ray effect" as the primary manifestation of multiple myeloma. 27 Dec 13

Histophysiology, ultrastructure, chemical analyses of transplants and implants of Dunn and Ridgway mouse osteosarcomas demonstrate that tumorigenesis is a manifestation of deranged morphogenesis in developing mesenchymal cell populations. The end product of development is defective, incompletely calcified, disorganized bone without any inclusions of bone marrow tissue. When Dunn osteosarcoma is freeze-dried and then implanted, the tumor is resorbed and replaced by deposits of normal cartilage, bone, and bone marrow. Freeze-dried Ridgway osteosarcoma is replaced only by a fibrous connective tissue scar. Disaggregated Dunn tumor osteoblasts synthesize a trypsin-labile collagenase-resistant cell surface localized bone morphogen. Tumor matrix stroma, prepared by sequential chemical extraction of soluble non-collagenous proteins also contains significant quantities of the same bone morphogen. Tumor tissue pulverized to particle size as small as 44 micrometer3 transmitted bone morphogen more rapidly than intact tumor tissue. The total tumor cell and stroma mediated bone morphogen produces three times more normal bone than normal cortical bone matrix. Our working hypothesis is that a normal bone morphogenetic polypeptide (BMP) is synthesized by Dunn osteosarcoma cells and retained by the tumor matrix stroma. Neither the mechanism of transmission nor the mesenchymal cell receptor sites of BMP are known.
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PMID:An osteosarcoma cell and matrix retained morphogen for normal bone formation. 27 29

Metastases of osteosarcomas do not grow according to a simple exponential function, but rather according to a type of Gompertz' function where flattening with a tendency toward plateau formation sets in after a certain time. This deviation from an exponential growth type corresponds to a substantial increase in the initial tumor size--doubling time. The metastasis doubles in the period after its transfer faster than when it first becomes visible in an x-ray. Another important conclusion resulting from the use of the Gompertz model is the assumption of a tumor-specific maximum volume which cannot be exceeded over a period of infinite growth. For lung metastases of osteosarcoma this volume amounts to approximately 120 cm3. The critical volume which kills the host is, at 70 to 80 cm3, relatively close to this theoretical growth limit (only approximately one cell division below this limit). If a metastasis develops from a single cell, the number of divisions up to this point is approximately 46. Of these, 38 lie within the growth zone which is not visible via x-ray. Since cell-cycle specific agents (for example Vincristin and Methotrexate) have the greatest effect against rapidly proliferating tumors, these drugs (for example alkylantic drugs) are especially effective in the case of slowly proliferating neoplasms. Therefore, use of these drugs should be favored when the metastasis is visible in the x-ray. Since occasionally, particular when the primary tumor is still relatively small, metastasization may not necessarily have already taken place, radical operation of the primary tumor should be carried out as soon as possible. A preliminary irradiation of the primary tumor cannot prevent metastasization with certainty. Therefore delayed amputation should be avoided.
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PMID:[On the growth characteristics of human osseous sarcoma metastases: mathematical calculations and clinical consequences (author's transl)]. 27 86

Murine interferon inhibited the growth of a continuous line of osteogenic sarcoma (OGS) cells in tissue culture. Inhibition of tumor cell growth by interferon was demonstrated by: a) decreased colony formation in soft agar, b) suppression of clone formation in liquid medium, and c) reduction of tumor cell counts in monolayer cultures. This inhibition of cell growth was further documented by suppression of [3H]thymidine uptake by OGS cells exposed to interferon, which suggested inhibition of DNA synthesis of tumor cells. Exposure of tumor cells for 4 hours, 24 hours, and 2,3,4,6, and 8 days demonstrated greater activity with prolonged exposure to interferon. Inhibition of cell growth was significantly greater for OGS cells than for normal mouse embryo fibroblasts. Finally, the antitumor activity of the interferon preparation could be reversed by anti-interferon antibody.
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PMID:Antitumor activity of interferon against murine osteogenic sarcoma cells in vitro. 27 70

Twelve consecutive unselected patients (aged 6 to 18 years) with osteogenic sarcoma underwent 19 thoracotomies for resection of pulmonary metastases. Wedge excisions of 41 metastatic nodules, one bilobectomy, and one pneumonectomy were performed. Six patients each required one thoracotomy, five patients underwent two thoracotomies, and one patient required three. Serious surgical complications were limited to one patient who required reoperation for closure of a bronchopleural fistula following bilobectomy. Initial pulmonary metastasis occurred 9 months (mean) after amputation (range 1 to 21 months). Complete excision of all identifiable metastatic tumor was possible in 17 of 19 thoracotomies. All patients received intensive cyclical chemotherapy after initial definitive amputation, after thoracotomy, or both. Tumor doubling time (TDT) during chemotherapy (mean 74 days) was significantly prolonged (p = 0.017) compared to TDT during intervals of no therapy (mean 22 days). Five patients received pulmonary radiotherapy prior to thoracotomy and five after thoracotomy. Four patients died during the observation period, having survived 10 to 30 months after amputation. Two patients are alive with known extrapulmonary metastases. Six patients are free of disease. The survival rate is 91.7 percent 1 year after amputation, 82.5 percent at 2 years, and 57.8 percent at 3 years. These results suggest improved survival when aggressive surgical resections of pulmonary metastases are combined with chemotherapy and radiotherapy. Thoracic surgical procedures in this group of patients are safe and associated with a low incidence of complications despite the potentially increased risks owing to antecedent chemotherapy and pulmonary irradiation.
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PMID:Pulmonary resection in children with metastatic osteogenic sarcoma: improved survival with surgery, chemotherapy, and irradiation. 27 31

Forty-five cases of osteosarcoma were studied for transepiphyseal spread of the lesion because of the current interest in local resection and chemotherapy as treatment of this disease. In 17 cases, the epiphyseal plate had closed and all 17 had transepiphyseal extension of the tumor. In 28 cases, the epiphyseal plate was open; 21 showed growth or microscopic evidence of transepiphyseal extension of the lesion. The most common method of extension was directly through the epiphyseal plate along vascular channels, or less commonly, about the epiphyseal plate beneath the perichondrium and into the epiphysis along the epiphyeal vascular channels. The majority of these extensions were not detectable by either conventional radiography or radioisotope scanning. Local resection with preservation of the epiphysis will, in all likelihood, leave residual disease despite the oft-quoted statement that an open epiphyseal plate is a biologic barrier to the extension of bone tumors.
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PMID:Transepiphyseal extension of osteosarcoma: incidence, mechanism, and implications. 27 69

Cytotoxicity of lymphocytes from T1 or T2 bladder cancer patients and patients with other diseases was tested in 44-hour microcytotoxicity assay against 3 different target cell lines: 1) HU 456, derived from human bladder carcinoma and established in our laboratory, 2) HU 609, a line derived from normal human bladder tissue and established in our laboratory and 3) SAOS-2, a human osteosarcoma cell line from the Memorial Sloan-Kettering Cancer Institute. Lymphocyte concentrations ranging from 7.8 time 10(4) to 2.5 times 10(6) lymphocytes per ml. were tested against each cell line. Lymphocytes from both groups of patients demonstrated a cytotoxicity against all 3 target cell lines, proportional to the lymphocyte concentration used. There was no difference in reactivity to HU 609 or to SAOS-2 between bladder cancer and control patients but the lymphocytes of bladder cancer patients showed a statistically greater cytotoxicity for HU 456, demonstrating a tumor type-specific cellular immune reaction superimposed on a background of non-specific cytotoxicity.
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PMID:The specificity of the microcytotoxicity assay for cell-mediated immunity in human bladder cancer. 27 6

Dunn osteosarcomas synthesize 2 times more alkaline phosphatase than do Ridgeway osteosarcomas, 3 times more than do HeLa cells, and 4 to 5 times more than do rat or mouse fibroblast cell cultures. Implants of killed freeze-dried Dunn cell cultures into the thigh muscles are resorbed and replaced by normal cartilage, bone, and bone marrow tissue, while implants of freeze-dried Ridgeway cells are resorbed and replaced by fibrous tissue only. Outgrowths of normal muscle septum connective tissue cells onto the stroma of Ridgeway tumors differentiate into fibrous tissue. Cultures of either tumor on a substratum of bone matrix stroma prepared from normal bone proliferate, assume a spherical shape, and perpetuate the transformed osteoblast-like cell without forming attachments or adapting to the contour of the substratum. Outgrwoths of muscle mesenchymal cells on the Dunn tumor stroma differentiate into cartilage. Dunn osteosarcoma cell cultures proliferate on the inside and produce deposits of normal bone (not tumorous bone) on the outside of diffusion chambers. Killed freeze-dried cell cultures produce transfilter deposits of normal bone and bone marrow, but the quantity is significantly lower. On a substratum of cellulose acetate, outgrowths of muscle connective tissue will differentiate into cartilage when cell-free Dunn stroma is present under the organ culture grid. Tumorigenesis and normal cartilage and bone morphodifferentiation are antithetic, but tumor cells transfer a bone morphogen similar to the bone morphogenetic protein (BMP) of normal bone matrix. BMP recruits mesenchymal cells to proliferate and differentiate into cartilage and bone.
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PMID:Osteogenesis and chondrogenesis in transplants of Dunn and Ridgway osteosarcoma cell cultures. 27 82

The latency period, success rate, and minimal cell inoculum size required for transplantation of continuously passaged human tumor lines into congenitally athymic (nude) mice, antilymphocyte serum (ALS)-treated congenitally athymic (nude) mice, and congenitally athymic-asplenic (lasat) mice were compared. The 11 tumor lines studied included examples of breast adenocarcinoma, transitional cell carcinoma, osteosarcoma, fibrosarcoma, Hodgkin's disease, malignant melanoma, and rhabdomyosarcoma. Of these 11 tumor lines, 3 were successfully transplanted into nude mice, compared to 5 of 10 tumor lines in ALS-treated nude mice and 9 of 11 lines in lasat mice. Moreover, the latency period was shorter and the minimal cell inoculum size was lower for lasat mice than for either nude or ALS-treated nude mice. Despite this enhancement of heterotransplantation into lasat mice and despite the growth of large local masses, no evidence of distant metastases was found.
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PMID:Enhancement of heterotransplanted human tumor graft survival in nude mice treated with antilymphocyte serum and in congenitally athymic-asplenic (Lasat) mice. 27 31

Results on seven cases of osteosarcoma are reported, based on new morphologic methods and quantitative procedures. Tumor tissue was embedded without prior decalcification in plastic and sectioned. Imprint cytology preparations were produced from fresh tumor tissue, and cell nuclei were measured with an electronic image analysing computer system. The loss of differentiation seen in osteosarcomas differs among osteoblasts, osteocytes, and osteoclasts. The differentiation of osteoclasts, namely their resorptive characteristics, disappears relatively early. Tumor osteocytes show loss of differentiation in their osteocyte processes. The new formation of tumor bone tissue remains in the near normal range of volume density when nuclear polymorphy is limited. The formation of ground substance and mineralization are apparently closely couplet to one another, since in our cases mostly ordered osteoid seams were observed. The capacity for mineralization of bone tissue is lost with marked polymorphy. The significance of these results for diagnostic statements and therapeutic consequences will be further discussed in long term studies.
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PMID:Morphology of osteosarcoma: new qualitative and quantitative investigations. 27 49


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