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Heterogenous amplification of myc family oncogenes in small cell lung carcinoma

✍ Scribed by Masayuki Noguchi; Setsuo Hirohashi; Futoshi Hara; Akira Kojima; Yukio Shimosato; Tetsu Shinkai; Ryosuke Tsuchiya

Publisher: John Wiley and Sons
Year: 1990
Tongue: English
Weight: 687 KB
Volume: 66
Category: Article
ISSN: 0008-543X
DOI: 10.1002/1097-0142(19901115)66:10<2053::aid-cncr2820661002>3.0.co;2-k

No coin nor oath required. For personal study only.

✦ Synopsis

One hundred forty-two foci of small cell lung carcinoma (SCLC) from 47 patients were examined for amplification of myc family oncogenes (c-myc, N-myc, and L-myc), by dot blot hybridization using formalin-fixed and paraffin-embedded materials which were resected surgically or obtained at autopsy. Some selected patients were also examined by in situ hybridization. Amplification of myc family genes was detected in 11 patients (23.4%) (c-myc in one, N-myc in five, and L-myc in five). Two of the 11 patients (one with N-myc and one with L-myc) had heterogenously amplified clones. In the patient with N-myc amplification, amplification was detected in metastatic tumors in the pancreas, lung, and pleura, but not in the liver and lymph node metastases. In the primary tumor, areas with and without N-myc amplification were seen. In the patient with L-myc amplification, although amplification was not detected in the surgically resected primary lesion, mediastinal lymph node metastatic lesions obtained at autopsy showed L-myc gene amplification. These two cases, together with previously reported evidence, suggest that myc gene amplification plays an important role in malignant progression, rather than development, of SCLC. In Stage I11 and IV groups, patients with over ten-fold myc gene amplification were suggested to survive for a shorter time than patients without such amplification (P = 0.06). Cancer 66:2053-2058,1990.

MPLIFICATION OF ONCOGENES has been studied by

A using cell lines and fresh surgical materials from various kinds of tumors, and about 10% to 20% of all human malignant tumors showed amplification of various kinds of oncogenes which had been identified.'-5 In particular, N-myc gene amplification in neuroblastomas6-8 and c-erb-B2 in breast carcinoma^^^'^ was studied in detail

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