PMID- 10498884
OWN - NLM
STAT- MEDLINE
DCOM- 19991005
LR  - 20071114
IS  - 0950-9232 (Print)
IS  - 0950-9232 (Linking)
VI  - 18
IP  - 38
DP  - 1999 Sep 20
TI  - Modeling human lung cancer in mice: similarities and shortcomings.
PG  - 5318-24
AB  - Lung cancer kills more Americans yearly than any other neoplastic process.
      Mortality rates have changed little over the past several decades, despite
      improvements in surgical techniques, radiation therapy and chemotherapy. The
      identification of mutations in oncogenes and tumor suppressor genes in human lung
      tumor specimens, including K-ras, p53, p16INK4a and Rb, offers molecular
      explanations for tumor development and resistance to therapy. Mouse models of
      human lung cancer may advance our understanding of this disease. The examination 
      of mice which develop lung cancer either spontaneously or due to carcinogen
      exposure, and the creation of mouse strains harboring the specific genetic
      mutations found in human lung cancer are among strategies being pursued.
FAU - Tuveson, D A
AU  - Tuveson DA
AD  - Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts, MA 02115, 
      USA.
FAU - Jacks, T
AU  - Jacks T
LA  - eng
GR  - T32CA71345/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - England
TA  - Oncogene
JT  - Oncogene
JID - 8711562
SB  - IM
MH  - Animals
MH  - *Disease Models, Animal
MH  - Humans
MH  - Lung Neoplasms/*genetics/pathology
MH  - Mice
RF  - 109
EDAT- 1999/09/28 00:00
MHDA- 1999/09/28 00:01
CRDT- 1999/09/28 00:00
PHST- 1999/09/28 00:00 [pubmed]
PHST- 1999/09/28 00:01 [medline]
PHST- 1999/09/28 00:00 [entrez]
AID - 10.1038/sj.onc.1203107 [doi]
PST - ppublish
SO  - Oncogene. 1999 Sep 20;18(38):5318-24. doi: 10.1038/sj.onc.1203107.