Molecular and cellular biology of small cell lung cancer

被引:69
作者
Sattler, M [1 ]
Salgia, R [1 ]
机构
[1] Harvard Univ, Sch Med, Brigham & Womens Hosp,Dept Med Oncol, Dana Farber Canc Inst,Div Thorac Oncol Program, Boston, MA 02115 USA
关键词
D O I
10.1053/sonc.2003.50019
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
For any tumor to become cancerous, various genetic mutations and biologic alterations must occur in the cell that in combination render it a malignant neoplasm. Small cell lung cancer (SCLC) is a neoplasm associated with several molecular and cellular abnormalities. SCLC is associated with early and frequent metastasis as well as a poor ultimate response to chemotherapy. New and novel therapies based on understanding the mechanisms of transformation are needed. SCLC is associated with multiple chromosomal abnormalities, the most common of which is chromosome 3p deletion, as well as with abnormal oncogenes and tumor-suppressor genes. Along with the genetic alterations, SCLC has been shown to overexpress various cell surface receptors, including receptor tyrosine kinases (RTKs), G-protein-coupled receptors, integrins, and others. Some downstream molecules are also activated, such as phosphatidylinositol 3′-kinase, and would serve as good candidates for therapeutic strategies. Copyright 2003, Elsevier Science (USA). All rights reserved.
引用
收藏
页码:57 / 71
页数:15
相关论文
共 158 条
[1]
Structure and function of the type 1 insulin-like growth factor receptor [J].
Adams, TE ;
Epa, VC ;
Garrett, TPJ ;
Ward, CW .
CELLULAR AND MOLECULAR LIFE SCIENCES, 2000, 57 (07) :1050-1093
[2]
Role of redox potential and reactive oxygen species in stress signaling [J].
Adler, V ;
Yin, ZM ;
Tew, KD ;
Ronai, Z .
ONCOGENE, 1999, 18 (45) :6104-6111
[3]
SURFACE RUFFLES AS MARKERS FOR STUDIES OF CELL TRANSFORMATION BY ROUS-SARCOMA VIRUS - (SCANNING ELECTRON MICROSCOPY CHICK EMBRYO FIBROBLAST-PROTEIN SYNTHESIS) [J].
AMBROS, VR ;
CHEN, LB ;
BUCHANAN, JM .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1975, 72 (08) :3144-3148
[4]
The biology of stem cell factor and its receptor C-kit [J].
Ashman, LK .
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 1999, 31 (10) :1037-1051
[5]
Potent blockade of hepatocyte growth factor-stimulated cell motility, matrix invasion and branching morphogenesis by antagonists of Grb2 Src homology 2 domain interactions [J].
Atabey, N ;
Gao, Y ;
Yao, ZJ ;
Breckenridge, D ;
Soon, L ;
Soriano, JV ;
Burke, TR ;
Bottaro, DP .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2001, 276 (17) :14308-14314
[6]
Banerjee D, 1999, CURR OPIN MOL THER, V1, P404
[7]
A peptide representing the carboxyl-terminal tail of the met receptor inhibits kinase activity and invasive growth [J].
Bardelli, A ;
Longati, P ;
Williams, TA ;
Benvenuti, S ;
Comoglio, PM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (41) :29274-29281
[8]
Fhit, a putative tumor suppressor in humans, is a dinucleoside 5',5'''-P-1,P-3-triphosphate hydrolase [J].
Barnes, LD ;
Garrison, PN ;
Siprashvili, Z ;
Guranowski, A ;
Robinson, AK ;
Ingram, SW ;
Croce, CM ;
Ohta, M ;
Huebner, F .
BIOCHEMISTRY, 1996, 35 (36) :11529-11535
[9]
Roles of superoxide radical anion in signal transduction mediated by reversible regulation of protein-tyrosine phosphatase 1B [J].
Barrett, WC ;
DeGnore, JP ;
Keng, YF ;
Zhang, ZY ;
Yim, MB ;
Chock, PB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (49) :34543-34546
[10]
THE POTENTIAL OF PROTEIN-KINASE-C AS A TARGET FOR ANTICANCER TREATMENT [J].
BASU, A .
PHARMACOLOGY & THERAPEUTICS, 1993, 59 (03) :257-280