Skip Navigation

JNCI Journal of the National Cancer Institute 1999 91(21):1796-1799; doi:10.1093/jnci/91.21.1796
© 1999 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Request Permissions
Google Scholar
Right arrow Articles by Hittelman, W. N.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hittelman, W. N.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 91, No. 21, 1796-1799, November 3, 1999
© 1999 Oxford University Press


EDITORIALS

Clones and Subclones in the Lung Cancer Field

Walter N. Hittelman

Correspondence to: Walter N. Hittelman, Ph.D., Department of Clinical Investigation, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030 (e-mail: Hittelman/MDACC@MDACC).

Based on a variety of clinical (1,2), histologic (3,4), cytogenetic (5-7), and molecular (8-10) data, lung cancer, like many other epithelial cancers, is suggested to develop as a multistep tumorigenesis process in a field of cancerization (11,12). Carcinogen exposure (e.g., tobacco) is believed to induce genetic damage in target cells that accumulates over years of exposure. Moreover, chronic tissue injury leads to chronic wound healing, whereby cells carrying genetic alterations that are important for survival and preferential regrowth expand at the expense of their neighbors. These surviving colonies continue to accumulate new tissue-relevant genetic alterations and eventually evolve into an invasive lesion. Since the whole aerodigestive tract is similarly exposed to carcinogen, one might predict that such clonal outgrowths develop throughout the exposed tissue.

Until recently, characterization of the fine . . . [Full Text of this Article]

NOTES

REFERENCES


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
JNCI J Natl Cancer InstHome page
W. N. Hittelman, D. D. Liu, J. M. Kurie, R. Lotan, J. S. Lee, F. Khuri, H. Ibarguen, R. C. Morice, G. Walsh, J. A. Roth, et al.
Proliferative Changes in the Bronchial Epithelium of Former Smokers Treated With Retinoids
J Natl Cancer Inst, November 7, 2007; 99(21): 1603 - 1612.
[Abstract] [Full Text] [PDF]


Home page
Clin. Cancer Res.Home page
S. M. Lippman and J. V. Heymach
The Convergent Development of Molecular-Targeted Drugs for Cancer Treatment and Prevention
Clin. Cancer Res., July 15, 2007; 13(14): 4035 - 4041.
[Abstract] [Full Text] [PDF]


Home page
Eur Respir JHome page
G. Sutedja
New techniques for early detection of lung cancer
Eur. Respir. J., January 1, 2003; 21(39_suppl): 57S - 66s.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
S. Laconi, P. Pani, S. Pillai, D. Pasciu, D. S. R. Sarma, and E. Laconi
A growth-constrained environment drives tumor progression invivo
PNAS, June 20, 2001; (2001) 131210498.
[Abstract] [Full Text] [PDF]


Home page
Proc. Natl. Acad. Sci. USAHome page
S. Laconi, P. Pani, S. Pillai, D. Pasciu, D. S. R. Sarma, and E. Laconi
A growth-constrained environment drives tumor progression invivo
PNAS, July 3, 2001; 98(14): 7806 - 7811.
[Abstract] [Full Text] [PDF]