The expression of c-myc, bcl-2 and p53 proteins in adenocarcinomas of lung.
OBJECTIVE
c-myc, bcl-2 and p53 are known to regulate apoptosis. There has been growing interest in analyzing their contribution to the pathogenesis and prognosis in a variety of human cancers. This study was undertaken to investigate the expression of these proteins in pulmonary adenocarcinomas and to determine their relationship with clinicopathologic parameters and survival.


METHODS
Archival tumor tissues from 61 patients with adenocarcinoma of lung were analyzed by immunohistochemistry for the expression of c-myc, bcl-2 and p53 proteins. Clinical information was obtained through the computerized retrospect database from the tumor registry.


RESULTS
Of 61 patients, 32 were men and 29 women with the median age 63 years. 4 had stage I disease, 2 had stage II disease and 55 had stage III disease. The expression of c-myc protein was identified in 13% (8/61) tumors, bcl-2 protein was detected in 1.6% tumors (1/61) and p53 was detected in 77% (47/71) tumors. The association of the expression of c-myc, bcl-2 and p53 was not detected. The survival time was longer in patients expressing c-myc protein than in patients without the c-myc protein expression (p=.045). Neither bcl-2 nor p53 showed the correlation to clinicopathologic variables.


CONCLUSIONS
Our data suggest the involvement of p53 alteration in the pathogenesis of lung adenocarcinoma. The c-myc expression in some tumors indicates that c-myc alone may not contribute critically to the development and/or the progression of these tumors. It, however, correlated to the survival time, suggesting the c-myc expression as a favorable prognostic factor possibly through the apoptosis pathway.
Yoo
Jinyoung
J
Department of Pathology, St Vincent's Hospital, Catholic University, Suwon, Korea.
Jung
Ji Han
JH
Choi
Hyun Joo
HJ
Kang
Seok Jin
SJ
Kang
Chang Suk
CS
Cancer. 1994 Apr 15;73(8):2013-26
8156506
Radiat Res. 1993 Dec;136(3):307-12
8278571
Br J Cancer. 1993 Feb;67(2):205-8
8431353
Cancer Res Treat. 2001 Aug;33(4):343-9
26680806
Oncogene. 1993 May;8(5):1183-93
8479742
Eur Respir J. 1989 May;2(5):461-9
2547647
Blood. 1992 Aug 15;80(4):879-86
1498330
N Engl J Med. 1994 Jun 16;330(24):1757-8
8190145
Br J Cancer. 1986 Mar;53(3):331-7
3964537
J Clin Invest. 1987 Jun;79(6):1629-34
3034978
Histopathology. 1996 Jul;29(1):45-50
8818693
Cancer. 1987 Apr 1;59(7):1289-95
3545431
Adv Cancer Res. 1991;56:1-48
2028839
N Engl J Med. 1993 Sep 2;329(10):690-4
8393963
Proc Natl Acad Sci U S A. 1992 May 15;89(10):4495-9
1584781
Br J Cancer. 1998 Feb;77(4):663-9
9484827
Nature. 1992 Oct 8;359(6395):552-4
1406975
Nature. 1991 Jul 25;352(6333):345-7
1852210
Anticancer Res. 1992 Jan-Feb;12(1):11-20
1348920
Cell Growth Differ. 1993 Feb;4(2):57-65
8494784
Anticancer Res. 1990 May-Jun;10(3):623-8
2164348
Anticancer Res. 1993 Sep-Oct;13(5A):1373-85
8239508
Cancer Res. 2000 Jan 1;60(1):143-9
10646866
Hum Pathol. 1997 Sep;28(9):1079-82
9308733