Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma carcinoembryonic antigen (CEA) assay was done in 30 patients with osteosarcoma. CEA was found positive (greater 2.5 ng/ml) in 17 of 21 patients who had active evidence of disease and negative (less than 2.5 ng/ml) in all 9 patients who were in complete remission resulting from previous amputation of chemotherapy. Serial CEA determinations demonstrated a fall to normal in 7 of 9 patients following successful surgery of chemotherapy and a ruse and fall (fluctuation) of levels in 8 patients who had tumor progression while on chemotherapy. Clinical recurrence of disease in two instances preceded or coincied with CEA elevation. The CEA assay in osteosarcoma although non-specific could be used as an inportant adjunct to experienced clinical judgment, periodic x-ray examination, and laboratory study to prognosticate the course of osteosarcoma during therapy. The interpretation of a rising or falling CEA titer alone, however, must be made with caution.
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PMID:Carcinoembryonic antigen in osteosarcoma. 26 37

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

Two autopsy cases of sacrococcygeal chordoma which showed sarcomatous components in the primary and metastatic tumors are reported. Case 1 was a 48-year-old female who died 9 years after the development of the initial symptoms. Autopsy findings showed metastatic tumors consisted of malignant tumor cells similar to fibrosarcoma and osteosarcoma. Case 2 was a 63-year-old male who died 11 years after the development of the initial symptom. At autopsy only sarcomatous tumors resembling malignant fibrous histiocytoma (MFH) were observed in the metastatic lesions. Both cases were treated with irradiation. It is suggested that the appearance of sarcomatous tumor in current two cases of chordoma might be due to the phenomenon of tumor progression closely associated with irradiation therapy. These two cases can be categorized as "chordoma with a malignant spindle cell component" in a sense that highly malignant sarcomatous components existed in conjunction with chordoma in the primary tumors.
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PMID:Sacrococcygeal chordoma with a malignant spindle cell component. A report of two autopsy cases with a review of the literature. 150 5

The authors reviewed 76 magnetic resonance (MR) images of 38 patients with osteosarcoma treated with preoperative chemotherapy (intraarterial cisplatin with or without systemic chemotherapy). Histologic maps of the surgical tumor specimens in 33 cases were correlated with either late-chemotherapy or postchemotherapy MR images. There were four MR patterns--dark, mottled or speckled, homogeneous, and cystic--that corresponded to different amounts of tumor matrix, granulation tissue, hemosiderin deposits, fluid-filled cysts, and residual viable tumor. Nested foci of residual viable tumor could not be specifically identified, although tumor progression or skip metastases were accurately depicted in four patients. Other findings included (a) peritumoral edema in the soft tissues and intramedullary space that shrank with chemotherapy, (b) chemotherapy effect in the surrounding soft tissues, (c) a dark rim around the extramedullary component of the tumors corresponding to a collagenous capsule continuous with the periosteum, (d) development of metaphyseal hemorrhages and bone marrow infarcts, and (e) intramedullary vascular channels.
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PMID:Osteosarcoma: MR imaging after preoperative chemotherapy. 229 60

The curing chance of cancer disseminated to the lungs depends on the global curing chance of that specific tumor, the extent and distribution of its systemic spread and the availability of additional treatment modalities besides surgery. Of all tumors occurring in childhood and adolescence only osteosarcoma, Wilms tumor and Ewing's sarcoma preferentially disseminate to the lungs and such are the most promising candidates for successful treatment. In osteosarcoma with pulmonary dissemination surgical removal of the metastases is indispensable. In Wilms tumor chemoradiotherapy may replace or be used as an adjunct to surgery while in Ewing's sarcoma with primary pulmonary metastases chemoradiotherapy is the treatment of choice. Although metachronous lung metastases may still cured in osteosarcoma and Wilms tumor, they tend to be fatal however in Ewing's sarcoma. A small chance of success itself should not contraindicate metastasectomy but only the actual technically impossible intervention or the definite demonstration of tumor progression no longer controllable of different location. However, even palliative metastasectomy may be indicated in an individual patient.
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PMID:Surgical treatment of pulmonary metastases in childhood. 243 85

Well documented examples of primary malignant giant cell tumor of bone (giant cell tumor and concurrent sarcoma arising de novo) are exceedingly rare in the literature. We report a case arising in the left ischium of a 44-yr-old man. He had no previous history of radiation therapy or multiple resections. Histologically, the tumor was a typical giant cell tumor of bone juxtaposed to a malignant fibrous histiocytoma (MFH). The juxtaposition of a high grade sarcoma (MFH) and a locally aggressive nonmalignant neoplasm such as giant cell tumor is analogous to several other tumors of bone and soft tissue in which a low grade malignant or locally aggressive tumor can be associated with MFH or fibrosarcoma de novo, namely chondrosarcoma, chordoma, liposarcoma, and well differentiated intraosseous and parosteal osteosarcoma. The presence of a high grade malignant component in each of the aforementioned neoplasms generally portends a more ominous prognosis, although this is not invariably true. Recognition of the phenomenon of "dedifferentiation" (or tumor progression) in some bone tumors and sarcomas is important to ensure appropriate treatment. Distinction from secondary malignant giant cell tumors which are usually radiation induced is also important, since the latter have a much worse prognosis than those with dedifferentiation occurring de novo.
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PMID:Primary malignant giant cell tumor of bone: "dedifferentiated" giant cell tumor. 255 83

The determination and comparison of genotypic combinations at genomic loci in constitutional and tumor tissues from patients with various types of cancer have defined the chromosomal locations of loci in which recessive mutations play a role in disease development. The predisposing nature of some of these mutant alleles is exemplified by studies of retinoblastoma and osteogenic sarcoma, two clinically associated diseases that share a pathogenetically causal predisposition mapping to 13q14. Genomic alteration of chromosome 10 is apparent in glioblastomas and mixed tumors of glioblastoma/astrocytoma grade III but not in homogeneous astrocytoma grades II or III; this suggests the definition of a locus involved in tumor progression and, perhaps, an approach to molecular genetic staging of tumors.
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PMID:Loss of heterozygosity in stages of malignancy. 266 35

Thirteen clones were established from a Dunn osteosarcoma by means of limiting dilution. The heterogeneity of four parameters (in vivo and in vitro growth rates, alkaline phosphatase activity and metastatic capacity) was clearly demonstrated. Statistical analysis does not reveal a high correlation between the four parameters. The highly metastatic clones 5 and 10 lost tumorigenicity at the primary site. The presence of these clones suggests that the microenvironment of the host is able to control tumor growth and that metastasis should be considered as a differentiated phenotype in tumor progression.
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PMID:Establishment of highly metastatic clones without tumorigenicity derived from Dunn osteosarcoma. 320 8

The authors evaluated a new protocol of neoadjuvant chemotherapy for osteosarcoma, easier to manage and different from T10. The good results obtained with the postoperative ADR-CDDP association led us to undertake a pilot study between 1982 and 1984, using ADR-CDDP as preoperative chemotherapy. The records of sixteen patients were available for follow-up. The average age of the patients was 19.9 years. Patients received two or three preoperative courses, and a total of six identical courses. Tolerance was good. Pain usually disappeared but this was often misleading because associated with radiological and/or clinical tumor progression, low histological necrosis or poor outcome. The continuous disease-free survival actuarial rate was less than 57 and 40% at 18 months and two years respectively. The actuarial survival rate was 87% at one year and 65% at two years respectively. Disappointing results of this preoperative protocol, compared to results with the SO4 78 or T10 protocols for example, led to publish these data early in order to underline their potential dangers. As a result, we stopped our study. The charter of pilot studies justifies this publication. As well, these data point out the necessity of very close follow-up of neoadjuvant chemotherapy by sophisticated medical imaging. Neoadjuvant chemotherapy, if ineffective, must be stopped early, and should lead to surgery, followed by adequate postoperative chemotherapy.
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PMID:[Pre and postoperative chemotherapy of osteosarcoma with an adriamycin-cisplatin combination. Risks of a neoadjuvant chemotherapy which is not sufficiently effective]. 346 71

Stromal-epithelial interaction has a fundamental role in determining normal prostate development. Aberrant interaction between stroma and epithelium in the prostate is thought to contribute to neoplastic progression. Using a cell-cell interaction model, we observed that an inductive fibroblast cell line derived from fetal urogenital sinuses can confer growth responsiveness to androgen in both prostate and non-prostate epithelial cells in vivo. This concept was applied to test whether inductive stromal cells from bone or prostate alter cancer growth and metastasis. We observed that when a non-tumorigenic stromal cell line derived from a human osteosarcoma interacted with a non-tumorigenic androgen dependent prostate cancer cell line (LNCaP) in vivo, there was a marked alteration of both genotypes and phenotypes of the subsequently derived LNCaP sublines. One such subline, C4-2, acquired androgen independence as well as osseous-metastatic potential. These results support the concept that "genomic adaptation" is the most likely mechanism to explain the phenomenon of prostate cancer cell lines being permanently altered as a result of stromal-epithelial interaction in vivo. The establishment and further refinement of this cell-cell interaction model will allow us to define the roles of growth factors, growth factor receptors and extracellular matrices in prostate carcinogenesis. This approach could lead to the development of new therapeutic modalities that influence the rate of human prostate cancer progression.
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PMID:The role of stromal-epithelial interaction in normal and malignant growth. 762 72


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