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Cancer doubling time

Derenzini M, Sirri V, Trere D, Ochs RL (1995) The quantity of nucleolar proteins nucleolin and protein B23 is related to cell doubling time in human cancer cells. Lab Invest 73 497—502 Derenzini M, Trere D, Pession A, Govoni M, Sirri V, Chieco P (2000) Nucleolar size indicates the rapidity of cell proliferation in cancer tissues. J Pathol 191 181—186 Derenzini M, Trere D, Pession A, Montanaro L, Sirri V, Ochs RL (1998) Nucleolar function and size in cancer cells. Am J Pathol 152 1291-1297... [Pg.140]

Despite these initial promising results, further studies are needed to determine the exact indications for using [ F]-fluorocholine in the diagnostic algorithm of patients with prostate cancer and to assess the influence of different factors including hormonal therapy, PSA level and PSA doubling time on the uptake of the tracer in the cancer lesions. [Pg.178]

Human colon cancer cell growth (LoVo) is effected by protease inhibitors. In the presence of 62.5 pM BB both the doubling time and saturation density are considerably... [Pg.285]

Tumors with doubling time more than 60 days (epidermoid cancer of head and neck) have less sensitivity of chemiotherapy ... [Pg.90]

Tumors with doubling time more than 90 days (cancer of colon) have low sensitivity to cytostatic agents). [Pg.90]

Non-small cell lung cancer (NSCLC) isdiagnosed inthe majority (80%) of lung cancer patients. NSCLC typically has a slower growth rate and doubling time than small cell lung... [Pg.2365]

Derenzini, M., Sirri, V., Trere, D and Ochs, R. L. (1995b). The quantity of nucleolar proteins nucleolin and protein B23 is related to cell doubling time in human cancer ceils. Lab. Invest. 73, 497-502. [Pg.319]

P388 and B16 population doubling time by the acyclic monoterpene geraniol. Cancer Res., 51 37-42. [Pg.279]

Okazaki N, Yoshino M, Yoshida T, et al (1989) Evaluation of the prognosis for small hepatocellular carcinoma based on tumor volume doubling time. A preliminary report. Cancer 63 2207-2210... [Pg.176]

The parenchyma must be carefully screened for the presence of primary or secondary malignant disease. Most patients awaiting transplantation are cirrhotic, with a high risk of developing hepatoma, and as many as 20% of these patients will develop HCC (Fig. 4.2.6). Patients diagnosed with small hepatic cancer are moved up the transplantation list. On the basis of the natural doubling time of hepatoma, it has... [Pg.116]

Given the clear antiapoptotic and antimetastatic properties of NO donors, together with their low-toxicity profile, it is perhaps surprising that few clinical trials have been initiated to date. One study is currently under way, in which the NO donor GTN was administered via slow release dermal patch to men with a PSA recurrence after primary therapy for localised prostate cancer (Seimens et al. 2007) PSA levels are used as a biomarker for efficacy. GTN markedly and significantly increased PSA doubling time to 32 months compared with 13 months in the control group, in the absence of any serious adverse events. [Pg.396]

Etoposide causes multiple DNA double-strand breaks by inhibiting topoisomerase II. The pharmacokinetics of etoposide are described by a two-compartment model, with an a half-life of 0.5 to 1 hour and a (5 half-life of 3.4 to 8.3 hours. Approximately 30% of the dose is excreted unchanged by the kidney.16 Etoposide has shown activity in the treatment of several types of lymphoma, testicular and lung cancer, retinoblastoma, and carcinoma of unknown primary. The intravenous preparation has limited stability, so final concentrations should be 0.4 mg/mL. Intravenous administration needs to be slow to prevent hypotension. Oral bioavailability is approximately 50%, so oral dosages are approximate two times those of intravenous doses however, relatively low oral daily dosages are used for 1 to 2 weeks. Side effects include mucositis, myelosuppression, alopecia, phlebitis, hypersensitivity reactions, and secondary leukemias. [Pg.1288]


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See also in sourсe #XX -- [ Pg.2285 ]




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Doubling time

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