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Digitale Medien

Phase II study of 10-ethyl-10-deaza-aminopterin (10-EdAM; CGP 30 694) for stage IIIB or IV non-small cell lung cancer (1990)

Lee, Jin S. ; Libshitz, Herman I. ; Murphy, William K. ; [weitere]

Springer

Investigational new drugs 8 (1990), S. 299-304

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ISSN: 1573-0646

Schlagwort(e): non-small cell lung cancer ; chemotherapy ; 10-ethyl-10-deaza-aminopterin ; 10-EdAM

Quelle: Springer Online Journal Archives 1860-2000

Thema: Chemie und Pharmazie , Medizin

Notizen: Summary Thirty-one patients with stage IIIB or IV non-small cell lung cancer (NSCLC) were treated with intravenous 10-EdAM on a weekly basis. The starting dose was 80 mg/m2, with subsequent doses adjusted depending on evidence of toxicity. There were 20 men and 11 women with a median age of 58 years (range, 33–75). Response was evaluated in 30 patients, 5 with evaluable but not measurable tumors and 25 with measurable indicator lesions. There were no complete remissions; 3 patients achieved partial remission. Nine patients had a minor response, 6 showed no change, and 12 had progressive disease. Median survival for all 31 patients was 43 weeks (range, 12–65+). During the first 3-week period, the 10-EdAM dose was reduced or withheld in 19 patients (because of stomatitis in 12, SGPT elevation in 3, skin rash in 2, and granulocytopenia in 2), escalated in 11 patients, and unchanged in 1 patient. A mean of 34–88 mg/m2of 10-EdAM (median, 50) was given per week during the first 5-week period. Myelotoxicity was infrequent and there was no significant nephrotoxicity. Considering the modest side effects of this treatment and the conservative dose-modification schedule which mandated substantial dose reductions, we conclude that 10-EdAM is a promising antitumor agent for NSCLC.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00171841

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Digitale Medien

Intermediate biomarkers in upper aerodigestive tract and lung chemoprevention trials (1992)

Benner, Steven E. ; Hong, Waun K. ; Lippman, Scott M. ; [weitere]

New York, N.Y. : Wiley-Blackwell

Journal of Cellular Biochemistry 50 (1992), S. 33-38

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ISSN: 0730-2312

Schlagwort(e): chemoprevention ; field cancerization ; intermediate biomarker ; premalignant lesions ; upper aerodigestive tract cancer ; Life and Medical Sciences ; Cell & Developmental Biology

Quelle: Wiley InterScience Backfile Collection 1832-2000

Thema: Biologie , Chemie und Pharmazie , Medizin

Notizen: Chemoprevention trials in lung and upper aerodigestive tract (UADT) cancer are guided by the field cancerization hypothesis. Inhaled carcinogens place the entire epithelial lining at risk for the development of cancer. The hypothesis is supported by the occurrence of premalignant lesions, such as leukoplakia or squamous metaplasia, and multiple primary tumors within the field. The concept of carcinogenesis as a multistep process suggests the possibility of blocking or reversing the progression to invasive cancer with systemic treatment. A series of ongoing clinical trials will determine the efficacy of retinoid chemoprevention and will attempt to develop intermediate biomarkers. Biomarkers which reliably reflect progression towards cancer could be used to dramatically improve the efficiency of chemoprevention trials and also would aid in screening potential chemoprevention agents. Genomic biomarkers include non-specific estimates of ongoing DNA injury, such as micronuclei, as well as development of aneuploidy and alterations in oncogenes. A class of biomarkers of increasing importance assess proliferation and growth regulation, and include proliferating cell nuclear antigen (PCNA), TGF-β, EGFR and retinoid receptors. Other markers, such as the blood group antigens, reflect differentiation and may be associated with the development of premalignant lesions. Preliminary data from several of these markers has suggested and association with carcinogenic exposures and premalignant lesions, but none of these markers either alone or in panels have yet been validated as a reliable surrogate for the development of invasive cancer. © 1992 Wiley-Liss, Inc.

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