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Critical analysis of tumors

Author Year Implant Time interval (yrs) Tumor type [Pg.536]

6 osteosarcomas, 1 chondrosarcoma, 1 angiosarcoma, 1 fibrosarcoma. Direct contact with the underlying tumor was noted in 15 of the 19 cases in which sufficient information is known from which to make such determinations. In three of the cases, particulate metal matter was determined to be present in the tumor including one case of a soft tissue sarcoma that appeared on image and exploration to be remote from the implant but had obvious evidence of nickel present within the tumor cells. [Pg.537]

Many of these tumors have not had an appropriate latent interval between implantation and development to be seriously considered implant induced. Given that the interval to tumor induction from bone stimulation should be at least as long as the accepted five year interval from radiation therapy to sarcoma degeneration, 15 of the 28 patients would qualify, all of whom have had tumours around total hip arthroplasties. [Pg.537]

Trademark, Howmedica, Inc. (cobalt-chromium alloy). M.F.H. = malignant fibrous histiocytoma. [Pg.537]


Gordon et al. (48) recently performed a pathway-based pharmacogenomic study on rectal cancer treated with chemoradiation in which they evaluated 21 polymorphisms in 18 genes involved in the critical pathways of cancer progression (drug metabolism, tumor microenvironment, cell cycle control, and DNA repair). They applied the CART analysis and found that a classification tree with four genes (lL-8, lCAM-1, TGF-, and... [Pg.361]

A 5-year course of tamoxifen treatment provides protection superior to 1-2 years of treatment. Currently, 5 years of adjuvant tamoxifen is recommended to be optimal, since extending treatment beyond 5 years provides no further improvement [137,138], There are reports of tamoxifen-stimulated tumor growth occurring during the treatment of advanced (metastatic stage IV) breast cancer [139,140], but there is currently no evidence that extending tamoxifen beyond 5 years of adjuvant therapy increases the risk of tumor recurrence. Critically important, the protective effects of tamoxifen on breast cancer recurrence and mortality are persistent long after tamoxifen therapy is stopped. A meta-analysis of 15 years of follow-up of 10,386 women shows that 5 years of adjuvant tamoxifen in ER-positive disease versus not... [Pg.137]

BCG has also been studied in several experimental models. Maximum tumor inhibition and prevention of pulmonary metastases in animals with methylcholanthrene sarcoma followed BCG plus live tumor vaccine inoculated intralesionally. 6,47 Bansal and Sjogren have shown that BCG must be given before the tumor reaches a critical size otherwise BCG enhances the blocking effects on the enlarging tumor.Finally BCG decreases the tumor size in Moloney sarcoma virus Infected mice which had been immunosup-pressed by cytoxan. Analysis of the guinea pig hepatoma model revealed that both the BCG cell wall suspension in oil and isolated BCG cell wall components were as effective as the live organisms.50 Another BCG product, methanol-extraction residue (MER) has also been extensively studied and shown to stimulate a positive host response towards tumor rejection.51... [Pg.153]

What is our key hint in linking these skin cancer cases to UV irradiation Analysis of the p53 tumor suppressor gene from basal and squamous ceU carcinomas showed in more than 30% of all investigated cases deleterious mutations in this critical gene, which is the guardian of the cell. Approximately 68% of the detected mutations are C —> T transitions, which in over 90% of cases, are present at dipyrimidine sites. ° Tandem-transition mutations CC —> TT make up about 14% of all detected p53 muta-tions. These C to T transitions, particularly at dipytimidine sites, are so-called fingerprint mutations. They are formed due to DNA replication mistakes made by the cell in the presence of UV-induced DNA lesions. The main mechanisms believed to be responsible for these mutations are also covered in this review. [Pg.2730]


See other pages where Critical analysis of tumors is mentioned: [Pg.536]    [Pg.537]    [Pg.536]    [Pg.537]    [Pg.536]    [Pg.537]    [Pg.536]    [Pg.537]    [Pg.301]    [Pg.6]    [Pg.164]    [Pg.209]    [Pg.366]    [Pg.244]    [Pg.37]    [Pg.484]    [Pg.2482]    [Pg.391]    [Pg.107]    [Pg.2349]    [Pg.2377]    [Pg.521]    [Pg.158]    [Pg.661]    [Pg.182]    [Pg.83]    [Pg.143]    [Pg.381]    [Pg.438]    [Pg.924]    [Pg.528]    [Pg.107]    [Pg.419]    [Pg.3058]    [Pg.370]    [Pg.16]    [Pg.381]    [Pg.249]    [Pg.150]    [Pg.274]    [Pg.541]    [Pg.13]    [Pg.173]    [Pg.2799]    [Pg.120]    [Pg.129]    [Pg.157]    [Pg.1390]   


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Critical analysis

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