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 search for new structures in tumors by genomics and proteomics methods is a major goal in tumor biology and may lead to the detection of markers or antigens for the generation of tumor vaccines. The aim of this study was to identify proteins that have been predicted so far based upon their nucleic acid sequence only or show poor identity to known proteins in tumor cell lines. Cell lines of neuroblastoma, colorectal, cervix carcinoma, adenocarcinoma of the ovary, lung and breast cancer, promyelocytic leukaemia, rhabdomyosarcoma, osteosarcoma and malignant melanoma were used. Cell lysates were run on 2D gel electrophoresis with subsequent in-gel digestion and MALDI-TOF-TOF analysis. A series of 10 hypothetical proteins (HPs) were observed and three of these proteins, hypothetical protein (Q9BTE6), CGI-83 protein (Q9Y392) and similar to CG11334 (Q9BV20), were so far described in tumors exclusively. The other seven proteins were already detected at the transcriptional level in normal and tumor cell lines or tissues. In conclusion, the three HPs observed in lung cancer and malignant melanoma may be candidates for development of tumor markers and generation of tumor vaccines.
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PMID:Detection of hypothetical proteins in 10 individual human tumor cell lines. 1568 Feb 40

Hypoxia induces Hif-1alpha and selects for loss of wild-type p53 function, both of which can promote tumor cell survival. We evaluated the ability of TRAIL to induce apoptosis of human tumor cell lines exposed to hypoxia. H460 lung cancer cells express low levels of Hif-1alpha, stabilize wild-type p53 during hypoxia, and undergo TRAIL-induced apoptosis. In U2OS osteosarcoma or PA1 ovarian teratocarcinoma cells, high levels of Hif-1alpha and low levels of stable p53 are detected during hypoxia, and cells undergo low levels of TRAIL-induced apoptosis as compared to H460 cells. H460 cells are sensitized to TRAIL-induced apoptosis, whereas U2OS are protected, and little apoptosis is observed in relatively TRAIL-resistant PA1 during hypoxia. Forced expression of Hif-1alpha is also surprisingly a potent inducer of apoptosis in wild-type p53 expressing H460 cells and further promotes TRAIL-induced apoptosis. TRAIL-sensitive wild-type p53-expressing HCT116 colon carcinoma cells modestly elevate Hif-1alpha levels and are equally or slightly more sensitive to TRAIL during hypoxia. In contrast, p53-null HCT116 have higher levels of Hif-1alpha during normoxia and are extremely sensitive to TRAIL, but are protected from TRAIL-induced apoptosis during hypoxia. We hypothesize that a hypoxic tumor microenvironment may alter sensitivity to TRAIL, which may be impacted by Hif-1alpha levels and p53 status. These findings suggest that particular attention to hypoxic regions of tumors and sensitizers to hypoxia-induced cell death may be required to optimize therapeutic combinations using TRAIL.
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PMID:Modulation of TRAIL-induced tumor cell apoptosis in a hypoxic environment. 1629 25

Malignant tumours of the chest wall are uncommon. The purpose of this pictorial essay is to describe the CT and MRI findings of malignant neoplasms affecting the bony skeleton of the chest wall and the costal cartilages. The most common primary malignant neoplasms involving the bony skeleton of the chest wall are chondrosarcoma, osteosarcoma and Ewing's sarcoma/primitive neuroectodermal tumour. Metastases, multiple myeloma and invasive primary lung cancer are the most frequent secondary lesions. We performed a retrospective review of the radiology and pathology archive at our institution from 1 July 2000 to 31 December 2004 and identified 31 of these lesions. Several of these tumours have distinctive radiological features, allowing a confident radiological diagnosis to be suggested.
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PMID:Malignant chest wall neoplasms of bone and cartilage: a pictorial review of CT and MR findings. 1679 48

Postradiation sarcoma is a rare late complication of external radiotherapy. We herein present two cases with this disease. A 54-year-old man had undergone a lobectomy and chest wall resection for Pancoast type lung cancer 7 years previously. He had undergone irradiation with a total dose of 50 Gy. Computed tomography (CT) demonstrated a tumorous expansion of the right lateral thoracic wall. A pathological examination confirmed a diagnosis of osteosarcoma. A 60-year-old woman had undergone a resection of the lateral chest wall mass, which was diagnosed to be Hodgkin's disease in 1991. Chemotherapy was given postoperatively. A tumorous lesion arose again and irradiation was performed with a total dose of 110 Gy. In 2000, two tumors appeared in the irradiation field. A pathological examination showed a sarcoma with divergent differentiation. In 2003, a tumor recurred and was diagnosed to be a liposarcoma. Patients who have received radiotherapy should therefore be followed up while taking into consideration the possible development of postradiation sarcoma.
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PMID:Postradiation sarcoma of the chest wall: report of two cases. 1712 40

Many researchers have reported that proteasome inhibitors could induce apoptosis in a variety of cancer cells, such as breast cancer cell, lung cancer cell, and lymphoma cell. However, the effect of proteasome inhibitors on osteocsarcoma cells and the mechanisms are seldom studied. In this study, we found proteasome inhibitor MG132 was an effective inducer of apoptosis in human osteosarcoma MG-63 cells. On normal human diploid fibroblast cells, MG132 did not show any apoptosis-inducing effects. Apoptotic changes such as DNA fragment and apoptotic body were observed in MG132-treated cells and MG132 mostly caused MG-63 cell arrest at G(2)-M-phase by cell cycle analysis. Increased activation of caspase-8, accumulation of p27(Kip1), and an increased ratio of Bax:Bcl-2 were detected by RT-PCR and Western blot analysis. Activation of caspase-3 and caspase-9 were not observed. This suggests that the apoptosis induced by MG132 in MG63 cells is caspase-8 dependent, p27 and bcl-2 family related.
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PMID:Caspase-8 dependent osteosarcoma cell apoptosis induced by proteasome inhibitor MG132. 1749 42

Sesamin is a major lignan constituent of sesame and possesses multiple functions such as antihypertensive, cholesterol-lowering, lipid-lowering and anticancer activities. Several groups have previously reported that sesamin induces growth inhibition in human cancer cells. However, the nature of this growth inhibitory mechanism remains unknown. The authors here report that sesamin induces growth arrest at the G1 phase in cell cycle progression in the human breast cancer cell line MCF-7. Furthermore, sesamin dephosphorylates tumor-suppressor retinoblastoma protein (RB). It is also shown that inhibition of MCF-7 cell proliferation by sesamin is correlated with down-regulated cyclin D1 protein expression, a proto-oncogene that is overexpressed in many human cancer cells. It was found that sesamin-induced down-regulation of cyclin D1 was inhibited by proteasome inhibitors, suggesting that sesamin suppresses cyclin D1 protein expression by promoting proteasome degradation of cyclin D1 protein. Sesamin down-regulates cyclin D1 protein expression in various kinds of human tumor cells, including lung cancer, transformed renal cells, immortalized keratinocyte, melanoma and osteosarcoma. Furthermore, depletion of cyclin D1 protein using small interfering RNA rendered MCF-7 cells insensitive to the growth inhibitory effects of sesamin, implicating that cyclin D1 is at least partially related to the antiproliferative effects of sesamin. Taken together, these results suggest that the ability of sesamin to down-regulate cyclin D1 protein expression through the activation of proteasome degradation could be one of the mechanisms of the antiproliferative activity of this agent.
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PMID:Sesamin, a lignan of sesame, down-regulates cyclin D1 protein expression in human tumor cells. 1764 Feb 97

Non-traumatic osteonecrosis of bone is recognized as a potential complication in solid-tumour cancer patients receiving treatment with cytotoxic chemotherapy. This review summarizes recent reports of osteonecrosis associated with chemotherapy in cancer patients, and describes the possible underlying pathophysiology and options available for its diagnosis, prevention and treatment. Fifty-four reported cases of non-traumatic osteonecrosis in adult patients with solid tumours receiving chemotherapy were identified by searching for reports in the medical literature. Osteonecrosis was observed most commonly in men receiving chemotherapy for testicular cancer. Osteonecrosis was also seen in patients receiving chemotherapy for breast, ovarian, small-cell lung cancer and osteosarcoma. Most patients had received corticosteroids, had femoral head involvement and had delayed onset of osteonecrosis. It appears that patients at higher risk for osteonecrosis with chemotherapy are identifiable. As the long-term survival of patients with solid tumours receiving chemotherapy increases, the prevalence of treatment-related osteonecrosis may also increase. Patients should be informed that osteonecrosis is a potential complication of cancer treatment. Measures to reduce risk should be taken, and patients should be monitored for early symptoms. Routine screening for chemotherapy-associated osteonecrosis is not recommended; however, a high index of clinical suspicion in patients at risk may allow for early intervention and preservation of the joints.
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PMID:Chemotherapy-associated osteonecrosis in cancer patients with solid tumours: a systematic review. 1842 77

Retinoblastoma (Rb), the most common intraocular tumor in childhood, is caused by the loss of function of both retinoblastoma susceptibility gene (RB1 or Rb1) alleles. In 1971, Alfred Knudson proposed his "two-hit" theory based upon empiric observations of the clinical genetics of Rb, revealing the role of tumor-suppressor genes in human cancer. Knudson proposed that: "In the dominant inherited form of Rb, one mutation is inherited via germ line and the second occurs in somatic cells. In the nonhereditary form, both mutations occur in somatic cells." The Knudson hypothesis was validated later with the cloning of RB1, the first tumor-suppressor gene to be identified. A few years later, Harbour extended these findings to small-cell lung cancer, showing that the RB1 locus was disrupted in tumors other than Rb and osteosarcoma. Since then, it has been found that most, if not all, tumors have defects in their RB1 pathway through genetic lesions in the RB1 gene itself or other genes in the pathway. The history of Rb research highlights how basic research on a rare childhood cancer can have a much broader effect on a disease that affects millions of people each year worldwide.
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PMID:Molecular biology of retinoblastoma. 1862 66

It has been reported that blocking Notch signaling in tumor-bearing mice results in abortive angiogenesis and tumor regression. However, given that Notch signaling influences numerous cellular processes in vivo, a comprehensive evaluation of the effect of Notch inactivation on tumor growth would be favorable. In this study, we inoculated four cancer cell lines in mice with the conditional inactivation of recombination signal-binding protein-Jkappa (RBP-J), which mediates signaling from all four mammalian Notch receptors. We found that whereas three tumors including hepatocarcinoma, lung cancer, and osteogenic sarcoma grew slower in the RBP-J-deficient mice, at least a melanoma, B16, grew significantly faster in the RBP-J-deficient mice than in the controls, suggesting that the RBP-J-deficient hosts could provide permissive cues for tumor growth. All these tumors showed increased microvessels and up-regulated hypoxia-inducible factor 1alpha, suggesting that whereas defective angiogenesis resulted in hypoxia, different tumors might grow differentially in the RBP-J-deleted mice. Similarly, increased infiltration of Gr1(+)/Mac1(+) cells were noticed in tumors grown in the RBP-J-inactivated mice. Moreover, we found that when inoculated in the RBP-J knockout hosts, the H22 hepatoma cells had a high frequency of metastasis and lethality, suggesting that at least for H22, deficiency of environmental Notch signaling favored tumor metastasis. Our findings suggested that the general blockade of Notch signaling in tumor-bearing mice could lead to defective angiogenesis in tumors, but depending on tumor cell types, general inhibition of Notch signaling might result in tumor regression, progression, or metastasis.
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PMID:Blockade of Notch signaling in tumor-bearing mice may lead to tumor regression, progression, or metastasis, depending on tumor cell types. 1910 29

Primary pulmonary osteosarcoma is very rare. Most cases are secondary deposits from primaries arising in the appendicular skeleton. Four cases of primary osteogenic sarcoma of the lung are described and the literature reviewed for previously reported cases. These pulmonary tumors occur in patients who are in their fourth to seventh decades, that is, an older age group than their primary bone equivalent. There is a slight male predominance. There appears to be a propensity for the left lung, especially the left upper lobe. The clinical presentation is similar to primary (epithelial) lung cancer. Differentiation from pleomorphic carcinomas and other sarcomas is discussed. We know of no predisposing factor(s) in our cases for the development of this tumor.
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PMID:Primary pulmonary osteosarcoma: a report of 4 cases and a review of the literature. 1928 94


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